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Case 1-06-cv-14199-LAK D ocument 9 Filed 04/02/2007 Page 1 of 75
UNITED STATES DISTRICT COURT
SOUTHERN DISTRICT OF NEW YORK
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IN RE PFIZER INC. MASTER FILE No. 06-CV-14199
SECURITIES LITIGATION AND RELATED CASES
AMENDED CLASS ACTION
THIS DOCUMENT RELATES TO: COMPLAINT
ALL CASES JURY TRIAL DEMANDED
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Plaintiffs Uniformed Sanitationmen's Association Compensation Accrual Fund and
Teamsters Local 617 Welfare & Pension Funds (collectively, "Plaintiffs"), individually and on
behalf of all other persons similarly situated, by their undersigned attorneys, for their complaint
against defendants, allege the following based upon personal knowledge as to themselves and
their own acts, and information and belief as to all other matters based upon, inter alia, an
investigation conducted by and through their attorneys. This investigation included, among other
things: (i) the review of academic literature and research concerning cardiology, pharmacology,
the inhibition of Cholesteryl Ester Transfer Protein ("CETP")', the impact of changes in systolic
blood pressure on coronary heart disease risk, and pertinent statistics; (ii) the review of
disclosures made by a former Pfizer Inc. ("Pfizer," "PFE" or the "Company") senior medical
officer on December 8, 2006 concerning internal Pfizer views of adverse prospects for
torcetrapib clinical trials, as more fully described in paragraphs 43-44 herein ; (iii) the interview
of a clinician who administered torcetrapib Phase III clinical trials; and (iv) the review of public
filings and other public disclosures concerning tortcetrapib or Pfizer, including transcripts of
analyst conference calls, filings with the Securities and Exchange Commission ("SEC") and
Food and Drug Administration ("FDA"), press releases issued by or regarding Pfizer, securities
For the convenience of the Court, a glossary of terms is attached at the end of the
Amended Class Action Complaint herein.
Case 1-06-cv-14199-LAK Document 9 Filed 04/02/2007 Page 2 of 75
analyst reports about Pfizer, and other information readily obtainable on the Internet regarding
Pfizer and/or torcetrapib.
SUMMARY AND NATURE OF ACTION
A. Background
This is a federal class action brought on behalf of all persons who purchased or
otherwise acquired Pfizer securities between January 19, 2005 and December 2, 2006, inclusive
(the "Class Period") for violations of Sections 10(b) and 20(a) of the Securities Exchange Act of
1934 (the "Exchange Act"), 15 U.S.C. §§ 78j(b), 78t(a). It is alleged herein that Defendants, in a
desperate effort to avert significant market loss due to the impending loss of patent protection by
principal Pfizer drugs, engaged in a common course of conduct and scheme designed to
artificially inflate the price of Pfizer securities during the Class Period by misrepresenting to
investors that blood pressure side effects found in the clinical trials of its next "blockbuster" drug
torcetrapib were of little concern and that the clinical trials showed positive results when they
clearly did not.
2. By 2002, it had become readily apparent to Pfizer and the financial markets that,
while Pfizer held its place as the world's largest manufacturers and distributors of
pharmaceutical products, there was a severe chink in its armor: Pfizer derived a substantial
portion of its annual revenue from drugs which were soon to lose patent exclusivity. This meant
that, from that point in time, Pfizer's revenue would be substantially curtailed by competition
from generic drug companies. The most prominent example of this financial weakness was
reflected in Pfizer's dependence on Lipitor, a "statin" drug which combated coronary heart
disease by reducing cholesterol found in low density lipoproteins (`LDL").2 Lipitor accounted
LDL and high density lipoproteins ("HDL") are proteins with fatty parts to which
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for approximately 20% of Pfizer's annual revenue in 2003, and that percentage grew to 23% in
2005 and 28.6% in 2006. Not only was patent exclusivity due to end for Lipitor in 2010, but
patent exclusivity for Lipitor's competitor Zocor (manufactured by Merck & Co., Inc.
("Merck")) was due to end even earlier, in 2006, posing a further threat to continued Lipitor sales
as generic (and therefore substantially less expensive) Zocor would be substituted in the
marketplace for Lipitor.
Faced with the enormous pressure from the financial markets to provide a way to
ameliorate the upcoming substantial loss of Lipitor and other drug revenues short of a substantial
restructuring of the Company, Pfizer falsely touted to investors torcetrapib as the next "$11
billion" "blockbuster" drug. Torcetrapib was described as a drug which reduced coronary heart
disease by increasing HDL-c for a population who did not respond to Pfizer's Lipitor drug.
Cholesterol molecules are fatty substances produced in the body which contribute to the
formation of plaque in the arteries. One of the mechanisms by which statins such as Lipitor
reduce cardiovascular events is by reducing LDL-c. However, Pfizer stated that not all patients
suffering from coronary heart disease respond to statins - indeed, Pfizer claimed that between
60%-65% of the population do not. Pfizer posited that, since people with healthy heart profiles
exhibit high levels of cholesterol associated with high HDL-c in addition to low levels of LDL-c,
the balance of the market of people at risk for heart disease could be treated by increasing HDL
cholesterol. Torcetrapib was intended to do just that.
cholesterol can attach. "LDL-c" refers to the cholesterol which is attached to LDL proteins.
Similarly, "HDL-c" refers to the cholesterol which is attached to HDL proteins. The amount of
cholesterol attached to an LDL or HDL particle is variable in the same way the amount of
garbage that can be placed in a garbage truck is variable. High LDL-c correlates generally with
high cardiovascular risk. Conversely, when HDL-c is high, this correlates generally with low
cardiovascular risk. It is the amount of LDL-c or HDL-c in the blood (rather than amount of
LDL or HDL) that correlates with cardiovascular health.
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4. The fundamental risk torcetrapib posed as a therapeutic treatment however, was
not its ultimate ability to increase HDL-c, but the mechanism by which it increased it.
Torcetrapib increased HDL levels by inhibiting the activity of the enzyme known as CETP,
whereby cholesterol is transferred from HDL-c to LDL molecules, forming LDL-c. By blocking
CETP, cholesterol would potentially accumulate in HDL particles, thereby increasing the
patient's HDL-c level. However, CETP is also involved in the process of cholesterol removal
known as reverse cholesterol transport ("RCT"). In RCT, cholesterol molecules are collected
and transferred to the liver for excretion from the human body. Thus, while inhibiting CETP
may cause increases in HDL-c levels - since blocking CETP reduces the transfer of cholesterol
from HDL to LDL - this same inhibition may also impair the RCT processes.
Indeed, an entire body of clinical studies reported in academic literature prior to
the commencement of the Class Period in 2005 (¶¶ 63-76, infra) showed that persons who had a
genetic CETP deficiency, while exhibiting increased HDL-c levels, actually suffered increased
coronary heart risk as compared with those without CETP inhibition. Other human and animal
studies confirmed this same correlation linking CETP inhibition with increased HDL-c levels
and increased adverse coronary heart risks. (Id.) These studies, though never referred to by
Pfizer, became highly relevant to Pfizer investors during the Class Period, as the torcetrapib
clinical trials revealed that while the drug appeared to increase HDL-c levels, it did not provide
any clinical benefit or improve cholesterol removal through RCT but did produce the serious
adverse side effect of increased blood pressure.
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B. Material Omissions and Misrepresentations
6. During the Class Period, Pfizer misrepresented both that the trials produced
evidence that torcetrapib improved the processes of cholesterol removal and that side effects
caused by torcetrapib were of little concern.
7. Specifically, Pfizer repeatedly discounted the significance of torcetrapib's adverse
blood pressure side effect, stating in April 2005 that it " is not really an issue" as seen in Phase I,
but "pretty much evaporated" with "no significant outlier "3 in Phase II trials. In January
2006, Pfizer stated that "we wouldn't have launched an $800 million study withoutfeeling
pretty confident that we have that issue well analyzed and addressed;" and in February 2006,
Pfizer stated that the blood pressure side effect is "easily monitored and managed clinically. "
(Emphasis supplied).
Further, in October 2006, Pfizer violated American Heart Association ("AHA")
rules, which preclude pre-announcing results that are to be presented at the its conferences, by
pre-announcing torcetrapib Phase III and clinical trial results that showed an even larger blood
pressure increase of "3 to 4 millimeters" in those patients taking the drug. The pre-
announcement - which Pfizer directed at investors - was clearly done to put a false and
misleading spin on the blood pressure side effect, with Pfizer emphasizing that the effect "will
not alter the favorable clinical profile of torcetrapib/ atorvastatin in the treatment of
cardiovascular disease ." (Emphasis supplied).
9. Pfizer's statements regarding the blood pressure side effect were blatantly false.
First, blood pressure increases during the Phase II trial were "2 to 3 millimeters" as announced
by Pfizer in October 2006 - not the nearly "evaporated" Phase II blood pressure increases
An "outlier" is defined as any value that is markedly smaller or larger than other values.
Case 1-06-cv-14199-LAK D ocument 9 Filed 04/02/2007 Page 6 of 75
claimed in April 2005 (¶ 104); nor the "1 to 2 milligram" [sic] Phase II increases claimed in
January 2006 (¶ 125); nor the "2 millimeter" Phase II blood pressure increases claimed in
February 2006 (¶ 132). Moreover the Phase II data showed dramatic "outliers:" 4% of the
population receiving torcetrapib experienced blood pressure increases in excess of 15 mm.
Further, the Phase III trial data reflected that the percentage of "outliers" had expanded by
over 132.5%: in the Phase III trials 9.3% of the torcetrapib patients experienced blood
pressure increase ofgreater than 15mm compared to 4% in the Phase II trials. (¶ 154).
Studies have linked a 15 millimeter increase in systolic blood pressure with a 75% increase in
stroke mortality risk, and even a 2 millimeter increase was linked to a 10% increase in stroke
mortality risk. (¶¶ 77-82).
10. Further, Pfizer concealed its belief that the cause of the high blood pressure was
torcetrapib's potentially lethal inhibition of monoamine oxidase ("MAO"), a compound that
controls the body's secretion of adrenaline-like substances called monoamines, which raise blood
pressure. (¶¶ 85-87). The inhibition of MAO would leave monoamines uncontrolled, leading to
higher blood pressure, and could be lethal to any patient who ingested food (cheese) or drink
(wine) that already contained monoamines. However, even if such a risk could be controlled,
none of the torcetrapib clinical trial results provided the slightest justification for doing so since
no clinical benefit such as improved cholesterol removal had been shown. In fact, as noted infra
(¶ 11), the best that could be said of torcetrapib's effect on RCT cholesterol removal was that it
was not impaired - not that cholesterol removal in any way had been enhanced..
11. Further, on November 15, 2005 (¶¶ 106-16), November 25, 2005 (¶¶ 117-24),
March 14, 2006 (¶¶ 136-37) and October 31, 2006 (¶¶ 142-47), Pfizer repeatedly touted to
investors that the torcetrapib clinical trials demonstrated dramatic increases in HDL-c levels.
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Pfizer immediately followed that claim with the description of HDL's normal function of
removing cholesterol from the body (which is the RCT process). However, significantly,
torcetrapib's increase in HDL-c was not ever shown in either the Phase II or III clinical trials to
increase the removal of cholesterol from the body. For example, a specific examination of
patient feces during the Phase II trials found no evidence that patients taking torcetrapib excreted
any more cholesterol than those who did not take torcetrapib. Moreover, given the fact that the
mechanism by which torcetrapib achieved the increase in HDL-c levels - i.e., the inhibition of
CETP - had historically been linked in many studies to increased coronary heart disease,
investors should have been told not only of the fact that the increase in HDL-c did not produce
positive results in terms of increased cholesterol removal, but that the increased HDL-c from
CETP-inhibition or deficiency was associated with increased or worsened coronary heart disease
(even beyond torcetrapib ' s increased blood pressure side effect described infra). Put simply, far
from touting the fact that torcetrapib increased HDL-c levels, Pfizer should have warned
investors that, because that increase was being achieved by CETP inhibition, based on clinical
studies it was at least equally as likely that torcetrapib would have adverse effects, as had been
seen in many other instances where HDL-c had been increased by way of CETP inhibition. (See
¶¶ 58-76).
12. Pfizer's other statements concerning the clinical trial results were similarly
misleading. In November 2005, Pfizer again sought to claim that torcetrapib increased the
removal of cholesterol (i.e., the RCT process) by stating that Phase II clinical trial results showed
"increased ability to transport cholesterolfrom cells - an effect seen to be functionally similar
to patients with naturally occurring high levels ofHDL-cholesterol' (¶ 112) (emphasis
supplied). This was also false. In fact, what the Phase II trial showed was that torcetrapib did
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not "compromise" (i.e., worsen) the cholesterol removal process, and that the only "increased
ability" Pfizer could have referred to was only a very preliminary step in the RCT process which
did not evidence actual cholesterol removal.
13. Further, in January 2005, Pfizer, after describing its extensive Phase III trial
program, touted a specific recent rabbit study where torcetrapib was shown to reduce arterial
lesions. (¶ 99). However, Pfizer did not disclose that, in a human torcetrapib trial funded by
Pfizer and completed by October 2004, torcetrapib failed to increase cholesterol removal - a
benefit Pfizer falsely suggested torcetrapib provided.
14. Pfizer further falsely touted in October 2006 that torcetrapib was only one of
many drugs which could emerge from Pfizer's successful "CETP franchise" (¶ 140), and on
November 30, 2006 -just days before the halting of the torcetrapib trials - Pfizer stated that
torcetrapib research represented the "most important new development in cardiovascular
medicine in years." (¶ 148). In fact, the trials as of that date had demonstrated no clinical
benefit and also showed a clear clinical risk of increased blood pressure (on average of 3-4
millimeters ). (¶¶ 106-16).
C. Unnecessary Extension Of Clinical Trials In The Face Of Mortality
15. Pfizer's desperation to keep the torcetrapib ball in the air until the absolute last
second also was reflected in the design of the torcetrapib Phase III clinical trials. Pfizer designed
the trials so as to ensure that they would not be halted absent a statistical certainty in excess of
99% that any deaths could not be attributed to chance - a so-called "P value" of 0.01. Pfizer
permitted the Phase III trials to continue in this manner. While such a degree of certainty might
have application where a patient population is terminally ill - and therefore the risk of death
from continuation of the trial is lessened - it clearly had no application here where the patient
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population was generally healthy. Using a 95% certainty level that adverse results were caused
by torcetrapib would have had no negative impact on the study other than to end it earlier and
potentially save lives. (¶¶ 94-98).
16. Pfizer designed and implemented the Phase III trials in a manner which served its
financial interest and violated the fundamental guideline that less proof of harm or risk should be
required in considering termination of a clinical trial, thereby permitting obedience to a pre-set
statistical P value to dictate ethical conduct. (Id.). The net effect of Pfizer allowing the trial to
continue to the 99% certainty level meant that Pfizer, until just days before the trial was halted
on December 2, 2006, could continue its false and misleading statements about torcetrapib to
investors.
D. Pfizer's Common Stock Price Declines Upon Adverse Disclosures
17. As a result of Pfizer's hype as to the clinical success of torcetrapib and
discounting of the serious adverse incidents in those clinical trials, the market reacted
dramatically to the sudden news on December 2, 2006 that the clinical trials were being halted
due to deaths (¶¶ 151-53). On December 4, 2006, Pfizer's stock price plummeted to $24.90 per
share from its prior day close of $27.86 per share on December 1, 2006, a 10.62% drop in one
day on massive volume of 289,209,504 shares, more than seven times the prior day's volume of
40,177, 600, and more than nine times its average daily volume for the prior year, representing a
market of loss of $855,984,640. The following day, December 5, 2006, Pfizer's stock price
further declined $0.08 per share, again on large volume of 118,558,300 shares traded,
contributing to a two- day market capitalization loss of $865 ,471,704
18. Also, the exact set of circumstances that Pfizer sought to avoid by hyping
torcetrapib actually occurred after the drug ' s failure : Pfizer announced on January 22, 2007 that
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it would lay off 10% of its workforce and close at least five facilities as part of an effort to slash
its annual costs by up to $2 billion by the end of 2008. (¶¶ 160-61).
JURISDICTION AND VENUE
19. The claims asserted herein arise under and pursuant to Sections 10(b) and 20(a) of
the Exchange Act [15 U.S.C. §§ 78j(b) and 78t(a)] and Rule lOb-5 promulgated thereunder by
the SEC [17 C.F.R. § 240.10b-5].
20. This Court has jurisdiction over the subject matter of this action pursuant to
Section 27 of the Exchange Act [15 U.S.C. § 78aa] and 28 U.S.C. § 1331.
21. Venue is proper in this District pursuant to Section 27 of the Exchange Act [ 15
U.S.C. § 78aa] and 28 U.S.C. § 1391(b). Many of the acts and transactions alleged herein,
including the preparation and dissemination of materially false and misleading information,
occurred in substantial part in this Judicial District. Additionally, Pfizer maintains its executive
offices in this Judicial District.
22. In connection with the acts alleged in this complaint, defendants, directly or
indirectly, used the means and instrumentalities of interstate commerce, including, but not
limited to, the mails, interstate telephone communications and the facilities of the national
securities markets.
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PARTIES
23. Lead Plaintiff Uniformed Sanitationmen's Association Compensation Accrual
Fund purchased the publicly-traded securities of Pfizer securities in an open and efficient market
at prices artificially inflated by defendants' misrepresentations and omissions during the Class
Period and suffered damages thereby, as set forth in its certification previously filed with the
Court:
DATE NO. OF SHARES PRICE PER SHARE
8/2/2006 3,150 $ 26.22
8/9/2006 3,200 $ 26.23
9/27/2006 700 $ 28.23
10/13/2006 4,411 $ 27.54
24 Additional named plaintiff Teamsters Local 617 Welfare & Pension Funds
purchased the publicly traded securities of Pfizer securities in an open and efficient market at
prices that were artificially inflated by defendants' misrepresentations and omissions during the
Class Period and suffered damages thereby, as follows:
DATE NO . OF SHARES PRICE PER SHARE
7/20/2006 5,870 $ 23.74
7/20/2006 430 $ 23.77
7/26/2006 2,370 $ 25.23
7/26/2006 430 $ 25.23
7/31/2006 2,700 $ 26.26
8/16/2006 2,700 $ 26.66
9/6/2006 1,300 $ 27.74
9/6/2006 1,200 $ 27.74
9/25/2006 3,000 $ 28.45
10/19/2006 3,600 $ 27.96
10/27/2006 2,500 $27.38
11/15/2006 700 $ 26.61
11/30/2006 500 $ 27.68
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25. Defendant Pfizer is incorporated in Delaware and maintains its executive offices
at 235 East 42nd Street, New York, NY, 10017. Pfizer is a research-based global pharmaceutical
company. Pfizer discovers, develops, manufactures and markets leading prescription medicines
for humans and animals as well as consumer healthcare products. As of October 31, 2006, there
were 7,210,444,662 shares of Pfizer common stock outstanding. Its shares are traded on the
New York Stock Exchange ("NYSE"), an open and efficient market.
26. Defendant Henry A. McKinnell ("McKinnell") was, until July 28, 2006,
Chairman of Pfizer's Board of Directors during the Class Period, and Pfizer's Chief Executive
Officer ("CEO"). McKinnell agreed to continue to serve as Chairman of the Board of Directors
and as a Pfizer employee until February 28, 2007.
27. McKinnell, as Chairman and CEO, met regularly with defendant John LaMattina
("LaMattina") and was sufficiently well-versed to respond to questions posed by analysts in
connection with torcetrapib clinical trials and to discuss the results of torcetrapib epidemiological
and other studies, including results concerning heightened blood pressure. (¶¶ 125-26, 128).
28. On December 18, 2006, McKinnell resigned from his position as Chairman of the
Board of Directors. In connection with his departure from Pfizer, McKinnell was awarded a
severance package, which was dependent, in part, upon "Pfizer's actual [stock] performance
relative to the pharmaceutical peer group ." As set forth in Pfizer's Form 8 -K filed with the SEC
on or about December 21, 2006, "[i]f target level performance is achieved with respect [to] these
outstanding awards, Dr. McKinnell would receive in settlement of such awards 719,533 shares of
Pfizer common stock with an aggregate value of $18,268,943, based on the closing price of
Pfizer common stock on December 13, 2006." As such, McKinnell was motivated to artificially
inflate Pfizer's common stock price - at least through the date of his departure from the
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Company (which was anticipated to be on February 28, 2007) - so that his severance
compensation would be maximized.
29. Defendant John LaMattina ("LaMattina") was, at all relevant times, President of
Pfizer Global Research & Development and had responsibility both for reviewing and
supervising the torcetrapib clinical trials and addressing investors about those trials. During
Pfizer conference calls with securities analysts and in other public statements, LaMattina was
presented as an expert in the pharmaceutical field, particularly in the development and testing of
torcetrapib. LaMattina made specific misrepresentations, inter alia, concerning torcetrapib's
potential for reducing artherosclerosis and minimizing torcetrapib's increased blood pressure
side effect (¶¶ 104, 132, 148). He also made materially false and misleading statements that
torcetrapib was the flagship of Pfizer's CETP " franchise ." (¶¶ 140).
30. Defendant Joseph Feczko ("Feczko") was at all relevant times Pfizer's Chief
Medical Officer. Like LaMattina, Feczko was presented as an expert in the pharmaceutical field,
particularly in the development and testing of torcetrapib, during Pfizer conference calls with
securities analysts and in other public statements. Feczko made specific misrepresentations inter
alia, concerning torcetrapib's potential for reducing arteriosclerosis and minimizing torcetrapib's
increased blood pressure side effect (¶¶ 104, 106, 108, 115, 144).
31. Defendants McKinnell, LaMattina and Feczko are collectively referred to herein
as the "Individual Defendants." During the Class Period, each of the Individual Defendants, as a
senior executive officer of Pfizer, was privy to non-public information concerning Pfizer's
business, finances, products, markets and present and future business prospects via access to
internal corporate documents , conversations and connections with other corporate officers and
employees, attendance at management and Board of Directors meetings and committees thereof
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and via reports and other information provided to them in connection therewith. Because of their
possession of such information, the Individual Defendants knew or recklessly touted torcetrapib
and disregarded the fact that adverse facts specified herein had not been disclosed to, and were
being concealed from, the investing public.
32. The Individual Defendants are liable as direct participants in the wrongs
complained of herein. In addition, the Individual Defendants, by reason of their status as senior
executive officers, were "controlling persons" within the meaning of §20(a) of the Exchange Act
and had the power and influence to cause the Company to engage in the unlawful conduct
complained of herein. Because of their positions of control, the Individual Defendants were able
to and did, directly or indirectly, control the conduct of Pfizer's business.
33. The Individual Defendants, because of their positions with the Company,
controlled and/or possessed the authority to control the contents of its reports, press releases and
presentations to securities analysts and, through them, to the investing public. The Individual
Defendants were provided with copies of the Company's reports and press releases alleged
herein to be misleading or untrue, prior to or shortly after their issuance and had the ability and
opportunity to prevent their issuance or cause them to be corrected. Thus, the Individual
Defendants had the opportunity to commit the fraudulent acts alleged herein.
34. As senior executive officers and as controlling persons of a publicly-traded
company whose common stock was, and is, registered with the SEC pursuant to the Exchange
Act, and was, and is, traded on the NYSE and governed by the federal securities laws, the
Individual Defendants had a duty to disseminate promptly accurate and truthful information with
respect to Pfizer's financial condition and performance, growth, operations, financial statements,
business, products, markets, management, earnings and present and future business prospects,
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and to correct any previously issued statements that had become materially misleading or untrue,
so that the market price of Pfizer's securities would be based upon truthful and accurate
information. The Individual Defendants' misrepresentations and omissions during the Class
Period violated these specific requirements and obligations.
35. The Individual Defendants are liable as participants in a fraudulent scheme and
course of conduct that operated as a fraud or deceit on purchasers of Pfizer's publicly-traded
securities by disseminating materially false and misleading statements and/or concealing material
adverse facts. The scheme: (i) deceived the investing public regarding Pfizer's business,
operations and management and the intrinsic value of Pfizer securities; and (ii) caused Plaintiffs
and members of the Class to purchase Pfizer's publicly-traded securities at artificially inflated
prices.
PLAINTIFFS' CLASS ACTION ALLEGATIONS
36. Plaintiffs bring this action as a class action pursuant to Federal Rule of Civil
Procedure 23(a) and (b)(3) on behalf of a class consisting of all those who purchased the
publicly-traded securities of Pfizer between January 19, 2005 and December 2, 2006, inclusive,
(the "Class Period") and who were damaged thereby (the "Class"). Excluded from the Class are
defendants, the officers and directors of the Company, at all relevant times, members of their
immediate families and their legal representatives, heirs, successors or assigns and any entity in
which defendants have or had a controlling interest.
37. The members of the Class are so numerous that joinder of all members is
impracticable. Throughout the Class Period, Pfizer stock was actively traded on the NYSE.
While the exact number of Class members is unknown to Plaintiffs at this time and can only be
ascertained through appropriate discovery, Plaintiffs believe that there are hundreds or thousands
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of members in the proposed Class. Record owners and other members of the Class may be
identified from records maintained by Pfizer or its transfer agent and may be notified of the
pendency of this action by mail, using the form of notice similar to that customarily used in
securities class actions.
38. Plaintiffs' claims are typical of the claims of the members of the Class as all
members of the Class are similarly affected by defendants' wrongful conduct in violation of
federal securities laws complained of herein.
39. Plaintiffs will fairly and adequately protect the interests of the members of the
Class and have retained counsel competent and experienced in class and securities litigation.
40. Common questions of law and fact exist as to all members of the Class and
predominate over any questions solely affecting individual members of the Class. Among the
questions of law and fact common to the Class are:
(a) whether the federal securities laws were violated by defendants' acts as
alleged herein;
(b) whether statements made by defendants to the investing public during the
Class Period misrepresented material facts about the business and operations of Pfizer;
(c) whether the prices of Pfizer's publicly traded securities were artificially
inflated during the Class Period; and
(d) to what extent the members of the Class have sustained damages and the
proper measure of damages.
41. A class action is superior to all other available methods for the fair and efficient
adjudication of this controversy since joinder of all members is impracticable. Furthermore, as
the damages suffered by individual Class members may be relatively small, the expense and
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burden of individual litigation make it impossible for members of the Class to individually
redress the wrongs done to them. There will be no difficulty in the management of this action as
a class action.
SOURCES
42. The sources include numerous articles relating to research and clinical studies of
CETP inhibition and coronary heart disease published in recognized academic journals including
journals of the AHA such as Arteriosclerosis, Thrombosis and Vascular Biology (`ATVB"),
Circulation, and Hypertension as well as The New England Journal ofMedicine. (See ¶¶ 58-82,
91, 100-102, infra).
43. The sources also include disclosures made by a former Pfizer Vice-President and
Medical Therapeutic Head of Pfizer's Cardiovascular & Metabolic Group, who also acted as
medical director of Pfizer's Cardiovascular Risk Factors Group in the U. S. (the "Pfizer Medical
Director") during the relevant period . (See ¶ 44, infra). These disclosures, made on or about
December 8, 2006 on a weblog called "In the Pipeline," which specializes in the reporting and
discussion of news and issues relating to new drug development. The disclosures were made in
response to an article describing Pfizer's halting of the Phase III clinical trials due to deaths of
patients who were given torcetrapib.
44. The former Pfizer Medical Director disclosed, inter alia, that Pfizer had received
warnings early in the development of torecetrapib from Michael Brown, Chairman of its Science
and Technology Committee of its Board of Directors, that CETP inhibition was "likely to
accelerate atherosclerosis" [i.e., adverse coronary heart disease effects]; Pfizer believed that the
potential cause of the blood pressure side effect found in the Phase II trials related to
torcetrapib's inhibition of monoamine oxidase; and Pfizer knew all of its animal and human
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trials tended to show that CETP inhibition worsened RCT, as follows:
The BP elevating problems of torcetrapib surfaced in early Phase 2 . The current
wisdom of the time is that one of the metabolites inhibited mono amine oxidase.
The Groton teamfelt that it could be managed by lowering the dose and hoped
that atorvastatin would also lower BP.
Pfizer was running a big study called RESPOND which was evaluating BP
lowering effects of atorvastatin at the time.
All the studies are done on top of atorvastatin for two reasons. 1. It is impossible
to ethically study patients at risk today without allowing statins. 2. All the
financial modeling showed that Pfizer made more money if torcetrapib was not
available as a single entity because the real gain was through recapturing the
Lipitor business before the 2011 patent extension.
Torcetrapib failed because inhibiting CETP is a flawed strategy. It raises HDL
by interfering with its functionality. The majority of cholesterol return to the liver
is via ApoB particles and this requires functional transfer from HDL to LDL via
CETP. All the RCT studies done by Pfizer, in animals and humans, either
failed to show an increase or showed a trend towards worsening RCT and the
best they could claim out of them was that "RCT was not worsened." Not too
promising for an HDL elevating drug! When that fact came out, the
discussion morphed to the other effects of HDL (anti-oxidant, anti-
inflammatory , anti- coagulant) but this data was totally lacking for
torcetrapib.
Early in the program, people like Brian Brewer and Michael Brown warned
Pfizer that blocking CETP was likely to accelerate atherosclerosis. Over time,
everyone drank the Cool Aid but now the truth is out. It's not the BP, it's the
mechanism. While BP is a potent risk factor, the BP elevation with torcetrapib
does not explain the magnitude of the disaster. Particularly ifyou feel that there
is a balancing benefitfrom CETPi.
Future HDL approaches will have to focus on functionality rather than levels
of HDL. The next successful drug will likely lower HDL while improving it's
functionality and will work via SRB1!
(Emphasis supplied).
SUBSTANTIVE ALLEGATIONS
A. Torcetrapib Emerges Amid Pfizer ' s Financial Dependence
On Liyitor And On Other Soon To Be Off Patent Drugs
45. During all relevant times, Pfizer was a multinational drug company that reported
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billions of dollars in annual revenue as a result of the development and manufacture of numerous
drugs. In recent years however, Pfizer's operating cost structure, reflected in its sales operations
and drug development costs, reflected steady growth while its sources of revenue became
focused on a number of drugs, most dramatically Lipitor, whose future financial strength was
limited by the fact that patent exclusivity was due to end by 2010. Lipitor had been developed
by Warner Lambert, which Pfizer had acquired in 2000. Lipitor reduces cholesterol synthesis
and LDL-c levels, which contribute to the formation of atherosclerotic plaque on arteries. Such
atherosclerotic plaque increases the likelihood of coronary heart disease.
46. In 2003, Lipitor sales represented $9.23 billion, or 20.6 % of Pfizer's $44.7 billion
in total revenue; in 2004, Lipitor represented $10.86 billion, or 19.6% of Pfizer's $55.5 billion in
total revenue ; and in 2005 , Lipitor represented $12.187 billion or, 25.7 % of Pfizer's $47.40
billion in total revenue. In 2006, Pfizer's Lipitor revenue reached a record breaking $12.89
billion, or 26.6% of Pfizer's $48.37 billion in total revenue. Thus, Pfizer's dependence on Lipitor
grew substantially from 19.6% of revenue in 2004 to 23% of total revenue in 2005 and 26.6% in
2006.
47. Pfizer's financial dependence on Lipitor was problematic for a number of reasons.
First, Lipitor's future as a revenue producer was limited by the patent exclusivity period which
ended in 2010. However, even prior to that date, in 2006, Lipitor's principal competitor - Zocor,
manufactured by Merck - was losing its patent exclusivity. Thus, generic drug manufacturers
would begin to erode Lipitor revenue beginning as early as 2006 and then most definitively in
2010.
48. In addition, Pfizer's precarious financial condition was exacerbated by both the
fact that Pfizer had no drug that even approached the revenue generating capability of Lipitor -
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its next largest revenue generating drug Norvasc, which produced $4.7 billion in revenue - and
by the fact that a number of Pfizer's other drugs were also soon losing their patent exclusivity.
49. For example, Pfizer's patent on Zoloft, an antidepressant that generated $3.3
billion in sales in 2005, was to expire in 2006; and its patents on Norvasc, a blood pressure
medication that generated $4.7 billion in sales in 2005, and Zyrtec, an allergy drug that generated
$1.36 billion in revenue in 2005, were both to expire in 2007.
50. Pfizer's financial weakness was not lost on the financial markets. Pfizer's
development of torcetrapib and the pursuit of Phase III trials of torcetrapib in 2003 were very
much management's responses to the concerns of the financial markets that without a new
"blockbuster" multi-billion drug, Pfizer faced fundamental gaps in future revenue.
51. Torcetrapib was presented to analysts as both a stand-alone new drug that would
reduce coronary artery disease and as a drug to be taken with Lipitor that would enhance
Lipitor's LDL-c-reducing function . Pfizer noted that epidemiological studies, including the
authoritative studies of coronary heart disease in the Framingham, Massachusetts population
since 1948, showed that decreased coronary heart disease was correlated with low LDL-c and
high HDL-c levels. Further, these studies showed that only about 30% of the population
suffering from coronary heart disease could be treated successfully with Lipitor or other statins
lowering LDL-c levels. Thus, Pfizer suggested to analysts that torcetrapib, through its function
in increasing HDL-c, would provide a treatment to the remaining population of those suffering
from coronary heart disease.
52. The message of torcetrapib as the potential savior of Pfizer was not lost on the
financial markets. For example, a Bear Stearns & Co, Inc. January 20, 2004 analyst report
described the financial market ' s concern over generic competition for Lipitor:
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The statin market has become more competitive both on price and efficacy. But
we do not foresee increased price erosion in 2004 or 2005. Our pricing concerns
revolve around 2006 when 25% of the statin market becomes generic. Hopefully,
for PFE's sake, we'll have visibility on the next wave in cholesterol therapy,
their CETP/Lipitor combination that could conceivably become the gold
standarnL
... we do fear pricing pressure that will likely result when Merck's Zocor goes
off-patent in June of 2006.... This may be the force that forces Pfizer and
AstraZeneca to offer bigger and bigger discounts.
The one saving grace may be hidden in Pj'izer 's pipeline . mazer currently has a
compound in phase III that could be the next revolutionary step in the
treatment of cholesterol disorders . mazer is developing a drug called torcetrapib
(CETP).
(Emphasis supplied).
53. Similarly, Jon LeCroy of Natexis Bleichroeder Inc. wrote in an October 1, 2004
analyst report that " torcetrapib is the key to Pfizer's future ... and the main replacement for
patent losses. " (Emphasis supplied).
B. Lipitor Fights Heart Disease By Reducing
Low Density Lipoprotein ("LDL") Cholesterol
54. Generally, heart disease is caused by narrowing of the coronary arteries that feed
the heart. Like any muscle, the heart needs a constant supply of oxygen and nutrients, which are
carried to the heart by the blood in the coronary arteries. When the coronary arteries become
narrowed or clogged by cholesterol and fat deposits - a process called atherosclerosis - and
cannot supply enough blood to the heart, the result is coronary heart disease ("CHD," also
known as ischemic heart disease or "IHD"). If not enough oxygen-carrying blood reaches the
heart, one may experience chest pain called angina. If the blood supply to a portion of the heart
is completely cut off by total blockage of a coronary artery, the result is a heart attack. This is
usually due to a sudden closure from a blood clot forming on top of a previous narrowing.
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55. Cholesterol is a waxy, fat-like substance that occurs naturally in all parts of the
body and that the body needs to function normally. Most cholesterol is produced in the liver,
and is carried in the bloodstream to the body's cells by special proteins called lipoproteins. The
two major lipoproteins are LDL and HDL. The body uses cholesterol to produce many
hormones, vitamin D, and the bile acids that help to digest fat. The body only needs a small
amount of cholesterol in the blood to meet these needs. If there is too much cholesterol in the
bloodstream, the excess is deposited in the arteries, including the coronary arteries, where it
contributes to the narrowing and blockages that cause the signs and symptoms of heart disease.
56. Studies have established that high blood cholesterol is a risk factor for coronary
heart disease ("CHD"). While higher cholesterol levels increase the risk of CHD, CHD is
uncommon at total cholesterol levels below 150 milligrams per deciliter (mg/dL). Further,
studies have shown that lowering total and LDL-c levels significantly reduces the risk of CHD.
57. In the continuing efforts to treat CHD, one strategy is to lower overall cholesterol
and LDL-c through the use of drugs called statins, which help to lower LDL-c in the blood by
blocking synthesis of cholesterol. Lipitor is such a statin. A series of trials using statin drugs
have demonstrated conclusively that lowering total cholesterol and LDL-c reduces the chance of
having a heart attack, needing bypass surgery or angioplasty, and dying of CHD-related causes.
Pfizer stated that lowering LDL-c alone using only statins does not treat 60-65% of the
population suffering from coronary heart disease and thus led to its interest in targeting other
lipid-related risk factors which might have anti-atherogenic effects.4
4 Atherogenesis is the process of forming atheromas, plaques in the inner lining of arteries.
A compound that is anti-atherogenic stops the accumulation or formation of plaques in the blood
vessels; a compound is pro-atherogenic if it promotes such accumulation of plaques.
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C. HDL-c Levels Correlated With Anti-Atherogenic
Effects and HDL's Role In Removal Of Cholesterol
58. As early as the 1970s and 1980s, studies showed that there was an inverse
correlation between HDL-c levels and CHD. The Framingham Heart Study, which
authoritatively documented the risk factors for heart disease, noted that low LDL-c levels and
high HDL-c levels correlated with low incidence of CHD.
59. This correlation has been linked to HDL's role in the removal of cholesterol from
the arteries, and ultimately, the body. As noted, LDL-c accumulates along the walls of arteries,
forming hard, thick cholesterol plaques that clog blood vessels. This puts tremendous stress on
the heart, ultimately causing cardiovascular disease . In contrast to LDL, HDL acts as a
scavenger collecting cholesterol, removing it from artery walls, releasing the load in the liver for
disposal and then returning to the blood stream to repeat the process. Specifically, HDL removes
cholesterol from artery walls by attaching it to apolipoprotein A-I ("apoA-P"), the protein
contained in HDL particles which then transports the cholesterol to the liver which then excretes
the cholesterol from the body. In addition, CETP interacts with apolipoprotein B ("apoB"), the
major protein contained in LDL particles, which moves cholesterol to the liver for excretion as
well as back to other parts of the body. This clearly anti-atherogenic process of cholesterol
removal is called reverse cholesterol transport or RCT.
60. The importance of RCT in reducing atherogenic effects of cholesterol was noted
over twenty years ago in Limone, Italy, where scientists discovered that 44 descendants of
Cristoforo Pomaroli and Rosa Giovanni, who wed in 1760, carried a genetic mutation of apoA-I
that produced a super-charged HDL molecule. Scientists dubbed this protein "apoA-I Milano."
Scientists found that these descendants had very low levels of HDL-c, yet their heart and arteries
were clear of fat deposits . Scientists concluded that the Milano apoA-I mutation sends HDL's
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ability to get rid of LDL-c into hyperdrive, i.e., these HDL molecules are much more efficient in
latching on to cholesterol and sending it to the liver for excretion.
61. More recently, scientists attempted to create synthetic apoA-I Milano for injection
into humans. In late June 2003, a company called Esperion Therapeutics ("Esperion")
announced the results of a small placebo-controlled trial of 47 patients who had recently had
heart attacks or other serious coronary events. Those who received the synthetic form of apoA-I
Milano, called ETC-216, saw a marked decrease in plaque over the six-week duration of the trial.
On or about December 21, 2003, Pfizer agreed to acquire Esperion for $1.3 billion.
62. While increased HDL-c levels have been correlated with decreased CHD, and
while HDL's role in removing cholesterol from the body through RCT appears to be an
antiatherogenic process, a significant body of genetic studies reflect that the elevation of HDL-c
levels as a result of CETP deficiency due to genetic mutation was correlated with increased
coronary heart disease. Indeed, when the elevation of HDL-c levels has been achieved through
CETP-inhibition, a methodology that also partially impairs the RCT function, the benefits of
increased HDL-c levels are replaced with adverse effects . As set forth above, CETP transfers
cholesterol from its HDL carrier to LDL. However, CETP also participates in the RCT process
by transferring triglycerides and cholesterol esters between HDL and lipoproteins containing
apoB - which in turn transfers cholesterol to the liver for excretion. Thus, while a drug designed
to inhibit CETP would be expected to produce increased HDL-c levels and even do so
dramatically - since cholesterol would no longer be removed from HDL and transferred to LDL
via the CETP enzyme - the inhibition of CETP could also have adverse effects on the removal of
cholesterol through RCT.
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D. By 2003, Studies Indicated That While CETP Inhibition Resulted In Higher
HDL-c Levels, It Also Was Associated With Increased Coronary Heart Disease
1. 1996 Study Reflects That Men With CETP Deficiency Had Elevated
HDL-c Levels And Increased Coronary Heart Disease Risk
63. Dr. Alan Tall (Tall, JLipid Research, 34:1255, 1993) reported in June 1996 on a
clinical study of 3,469 men, including those with CETP gene mutations, conducted for the
purpose of "testing the hypothesis that genetic deficiency of CETP is associated with a decreased
prevalence of coronary heart disease (CHD)." The study found "this hypothesis was not
supported by the data" (Zhong et al ., J Clin. Inv. 97:2917, 1996). The prevalence of definite
CHD risk was 21% in men with mutations and 16% in men without mutations. The odds ratio
relating prevalence of CHD to CETP mutation was 1.43 (P<0.05). The study confirmed the
strong inverse relationship between plasma HDL-c and coronary heart disease but also concluded
that "genetic CETP deficiency was associated with increased CHD prevalence and was a
significant, independent risk factor for CHD." (Emphasis supplied).
64. The study concluded that genetic CETP deficiency appears to be an independent
risk factor for CHD and that there is a "strong inverse relationship between plasma HDL
cholesterol concentration and coronary heart disease. " (Emphasis supplied).
65. The study posited that "[t]he most likely explanation for the excess CHD
associated with genetic CETP deficiency is related to the role of CETP in reverse cholesterol
transport." The study noted that these findings are consistent with prior transgenic mouse and
human studies.
2. 1997 Study Reflects That CETP Inhibition Was Higher
In Patients With Coronary Heart Disease
66. An epidemiological study was carried out in a Japanese population with high
prevalence of CETP gene mutations (Hirano, ATVB, 15:1849, 1995 ; Hirano, ATVB, 17:1053,
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1997). The study found that atherosclerotic cardiovascular disease was highly prevalent in men
with mutations conferring low CETP activity. Such naturally occurring reduced CETP activity
through genetic diversity is used to predict the effects of pharmacological CETP.
3. 1999 Study Reflects Increased Heart Disease Risk With CETP Inhibition
67. Researchers in Copenhagen confronted the apparent paradox that CETP inhibition
is correlated with increased cardiovascular risk, but that CETP inhibition causes an increase in
HDL-c, which in normal populations is correlated with decreased cardiovascular risk (Agerholm-
Larsen, Circulation 101:1907, 2000). The researchers tested 9,168 white men and women from
the general population and 946 white men and women with ischemic heart disease to test
whether a particular genetic mutation that caused CETP deficiency affected the subjects' HDL-c
levels and the risk of heart disease . The study found that for those women with CETP
deficiency, the consequent increased HDL-c was a positive risk factor, that is, higher HDL-c
was correlated with greater ischemic heart disease.
68. These results suggest that although higher levels of HDL-c may be beneficial for
cardiovascular health, if those higher levels of HDL-c are achieved through CETP inhibition, the
effect is deleterious. The explanation offered was that this way of increasing HDL-c disrupted
cholesterol removal through RCT:
Although CETP deficiency might be an antiatherogenic state, due to HDL
cholesterol elevation, the role of CETP in reverse cholesterol transport [RCT]
suggests the opposite.
69. The study concluded that increased HDL-c resulting from CETP inhibition in fact
may increase risk of ischemic heart disease ("IHD") and may be misleading as a risk indicator:
"our data suggest that increased HDL-c levels caused by mutations in CETP may be associated
with an increased risk of IHD in white women and that the clinical use of the ratio of total to
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HDL-c as a risk indicator may be misleading in persons with CETP mutations." (Emphasis
supplied).
4. 2002 Studies Show Increased HDL-c Through
CETP Inhibition May Not Lower Risk of Heart Disease
70. In October 2002, a study of 9,121 subjects in Copenhagen, including 1,377 who
suffered from IHD, was accepted for publication by the Journal of the American College of
Cardiology (Andersen, I Am Coll Cardiol. 41:1972, 2003). This study similarly found that
common mutations to the proteins that influence RCT may increase HDL-c but, again
paradoxically, increase the risk of IHD. The scientists concluded that increased HDL-c levels in
certain circumstances may not be protective but rather may be pro-atherogenic, requiring that
"some patients with high HDL cholesterol levels, particularly those with manifest IHD, need
both aggressive lipid-lowering medication and other preventive measures against atherosclerosis
and MD."
5. Other Research Noting Linkage Between CETP
Inhibition and Increased Coronary Disease
71. A July 2004 overview of the role of CETP in atherogenesis in the Journal ofLipid
Research further highlighted that studies could not clearly determine whether CETP inhibition
was anti-atherogenic. The review stated that research seemed to indicate that, far from being
able to treat large populations by inhibiting CETP, "the metabolic setting of the individual might,
at least in part, determine the ultimate effect of CETP on atherosclerosis[]" and "the role of
CETP in atherogenesis is likely dependent on the metabolic, genetic, and environmental
context."
72. A study first published online on May 9, 2006 by The Journal ofEndocrinology
& Metabolism studied the relationship between three different types of CETP mutations and
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CHD. The study found that such a mutation, "which beneficially contributes to higher HDL
cholesterol, is paradoxically associated with increased incidence of coronary disease in the
general population . Thus, CETP gene variation may affect coronary risk apart from the level of
HDL cholesterol." (Emphasis supplied).
73. Even animal studies indicated that CETP inhibition may not lead to a decrease in
atherosclerosis. For example, a study published in the October 1995 issue of the Journal of
Clinical Investigation found that CETP expression decreased early atherosclerotic lesions in
hypertriglyceridemic (i.e., high blood levels of triglycerides, the most abundant fatty molecule in
most organisms) mice . Further, a 1999 study published in the December issue of the Journal of
Biological Chemistry (Foger, J. Biol . Chem 274:36912. 1999) found that CETP corrects
dysfunctional HDL-c and reduces atherosclerosis in mice. This study provides "definitive in
vivo evidence supporting the theory that CETP has an antiatherogenic role in facilitating HDL-
mediated RCT" and " demonstrate [d] that CETP expression is beneficial in pro - atherogenic states
that result from impaired reverse cholesterol transport." Thus, based on animal models, in
persons who already suffer from atherosclerosis due to impaired RCT, CETP may act in an
anti-atherogenic way.
6. 2004 Study Shows Weak Correlation Between
CETP Inhibition and Positive Clinical Endpoints
74. One of the most direct tests of the promise of CETP inhibition was carried out by
Boekholdt, et al. (Circulation 110:1418,2004). In this investigation, CETP in blood was
measured directly - arguably a better measure than genotype and expected to correlate better
with coronary heart disease ("CHD") risk. The result was that there was no statistically
significant correlation between CETP and CHD risk across all patients. Only a subset of
patients, those with high triglyceride levels, showed the expected correlation, and even then the
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correlation was relatively weak (P=0.02), compared to other well-established variables, for
instance, diabetes (P<0.001), body mass index (P<0.001), or systolic blood pressure (P<0.001).
In the words of the authors: "Elevated CETP levels are associated with an increasing risk of
future CAD[coronary artery disease] in apparently healthy individuals, but only in those with
high triglyceride levels."
75. This finding restricts the population likely to benefit from CETP inhibition; and
even within that smaller population, one is far less confident about the likelihood of achieving
benefit from inhibiting CETP, compared to preventing diabetes, losing weight, or decreasing
blood pressure. This is based on the comparison of the P confidence indicators of P=0.02 for
CETP compared to > 50-fold higher confidence values for correlation between CAD and
diabetes, BMI, or systolic blood pressure.
76. Despite their findings supportive of CETP inhibition for at least some situations,
these investigators noted how unorthodox it is to be pursuing a pharmacotherapy based on CETP
inhibition without a more solid relationship between CETP activity and CAD risk:
However, it remains uncertain whether the increased HDL-C levels induced by
a pharmacological inhibition of CETP activity translate into a CAD risk
reduction... It is remarkable that despite the fact that pharmacological CETP
inhibition is already being assessed in human trials [i.e., toreetrapibl, no
epidemiological evidence exists to support a direct relationship between CETP
levels and CAD risk.
(Emphasis supplied).
E. Incremental Increases In Blood Pressure Have Been Found
To Be Significant By The Framingham Heart Study And By Pfizer Itself
77. The Framingham Heart Study originated in 1948 with the recruitment for medical
examination of 5,209 men and women between the ages of 30 and 62 from the town of
Framingham , Massachusetts . The first round of extensive physical examinations and lifestyle
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interviews that the study would later analyze for common patterns related to CHD development.
Since 1948, the subjects have continued to return to the study every two years for a detailed
medical history, physical examination, and laboratory tests, including a second-generation group
- 5,124 of the original participants ' adult children and their spouses.
78. In 1969, it was reported in the American College of Chest Physicians Journal
Chest (Kannel et al., Chest 1969:43, 1969), based on the study of the Framingham population,
that blood pressure was found to be strongly related to CHD. The study found:
Risk of every manifestation of CHD including angina, coronary insufficiency,
myocardial infarction and sudden death was distinctly and impressively related to
the antecedent level of both systolic and diastolic blood pressure. Risk was related
not solely to hypertension but was proportional to the level of the blood pressure-
even at non-hypertensive pressures-from the lowest to the highest recorded.
79. In 2000, a study again based on the Framingham database published in The
American Journal of Cardiology found that systolic blood pressure , as opposed to diastolic blood
pressure, to be "the prime causal factor of hypertension and its adverse cardiovascular sequelae."
80. In the 2003 AHA journal, Hypertension, it was found based on data from the
Framingham Study and other clinical studies that the effects of increased systolic blood pressure
were "graded." Specifically it was noted:
An even more definitive demonstration of the continuous, graded influence of BP
on CVD risk comes from a recent meta-analysis of data from 61 prospective
studies involving almost 1 million participants and 56 000 vascular deaths. This
Prospective Studies Collaboration found that BP is related to vascular mortality,
without any indication of a threshold down to 115/75 mm Hg. Persons aged 40 to
69 years had a doubling of risk of stroke or coronary mortality with every 20-mm
Hg increment in SBP (or 10-mm Hg higher DBP) throughout the entire range of
BP.
Furthermore, recent analysis of the relation of nonhypertensive BP to
development of CVD in the Framingham Study found a significant, graded
influence of BP from optimal (120/80 mm Hg) to normal (120 to 129/80 to 84
mm Hg) to high-normal (130 to 139/85 to 89 mm Hg) Joint National Committee
VI stages among untreated men and women (Table 4).
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81. As a result, it was emphasized that not even seemingly small or seemingly trivial
increases in blood pressure should be disregarded in terms of adverse impact on CVD:
There is overwhelming evidence of a continuous, graded influence of SBP on
CVD morbidity and mortality at all ages in both sexes. An optimal BP for
avoiding CVD is 140/ 90 mm Hg, and there is no clearly defined critical BP that
distinguishes normal from abnormal. It is the level of BP that kills, not arbitrarily
defined hypertension. Because the hazard of CVD increases in a continuous,
graded fashion in relation to BP, a population approach as advocated by Rose 19
must accompany efforts to detect and treat elevated values. The importance of
what appear to be trivial differences in BP, even within the high-normal BP
range, should not be underestimated,
(Emphasis supplied).
82. Thus, even supposedly small increases in blood pressure, such as the 3-4 mm/Hg
found in torcetrapib's Phase II study, are potentially deadly.
83. Pfizer was well aware of the critical and extremely dangerous nature of such an
increase in systolic blood pressure . As part of Pfizer' s October 17, 2001 announcement of its
third quarter full year 2001 results , the Company touted its pain medicine Celebrex in
comparison to Merck' s similar drug Vioxx when used with elderly patients, stressing that Vioxx
showed a 3mm/Hg increase in systolic blood pressure as compared to Celebrex:
We have conducted two large studies in almost 2,000 elderly patients who had
stable hypertension. We observed that significantly more patients on Vioxx as
compared to Celebrex had clinically significant increases in peripheral edema.
Additionally, significantly more patients in the Vioxx treatment group
demonstrated clinically significant increases in their systolic blood pressure.
Also, patients on Vioxx have an approximate 3 mm/Hg increase in systolic blood
pressure compared to Celebrex. Cardiologists have told us that a rise in the
mean systolic blood pressure ofas little as 3 mm/Hg, if sustained, could increase
the risk ofa person having a heart attack, stroke, or other cardiovascular events.
(Emphasis supplied).
84. Pfizer substantially repeated its knowledge of the deleterious effects of such small
increases in systolic blood pressure in its January 23, 2002 announcement of its fourth quarter
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and full year 2001 results:
We believe the data we have to date clearly support a cardiorenal safety
advantage for Celebrex compared to Vioxx in certain high-risk populations
(elderly hypertensive patients with osteoarthritis). These data were published in
the March 2001 issue of American Journal of Therapeutics, a peer review journal.
We have conducted two large studies in almost 2,000 elderly patients who had
stable hypertension. We observed that significantly more patients on Vioxx as
compared to Celebrex had clinically significant increases in peripheral edema.
Additionally, significantly more patients in the Vioxx treatment group (17.6% vs.
11%) demonstrated clinically significant increases in their systolic blood pressure.
Also, patients on Vioxx have an approximate 3 mmHg increase in systolic
blood pressure compared to Celebrex. According to leading cardiologists, a rise
in the mean systolic blood pressure of as little as 3 mmHg, if sustained, could
increase the risk of a person having a heart attack, stroke, or other
cardiovascular events.
(Emphasis supplied).
F. Pfizer Failed To Disclose That It Believed The Cause Of Increased Blood
Pressure Was Inhibition Of An Enzyme Vital To Controlling Blood Pressure
85. According to the Pfizer Medical Director, during the Phase II trials, Pfizer came
to believe that the increased blood pressure side effect was caused by one of torcetrapib's
metabolites (one of the compounds formed from torcetrapib by enzymes in the body of the
patient) inhibiting the MAO enzyme. Pfizer further believed that to avoid problems caused by
this MAO inhibitor, the dose of torcetrapib would need to be kept low.
86. MAO is an enzyme that is very widespread throughout the body that functions to
inactivate the many monamine neurotransmitters and hormones such as norepinephrine (a/k/a
noradrenaline) and epinephrine (adrenaline), which constrict the arteries and cause increased
blood pressure. Thus, the torcetrapib metabolite that inhibited MAO acted to increase
constriction of arteries, and consequently increased blood pressure and posed a potentially lethal
threat to patients who consumed foods containing monoamines that raise blood pressure (such as
cheese or wine).
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87. Thus, Pfizer knew, but failed to disclose, that increased blood pressure was
caused when a patient's body metabolized torcetrapib, creating an MAO inhibitor that could
potentially be deadly if the patient then consumed any common product that contains high levels
of monoamines.
G. Pfizer and Its Non-Independent DSMB Uses Statistical Measure - P Value -
To Delay Haltin2 Phase III Clinical Trials, Prolon2in2 Torcetrayib Hype
88. In order to ultimately have a new drug approved for sale to the public, a drug
maker must first successfully complete a series of trials that test the safety and efficacy of the
drug. As part of this process, the drug maker must file with the FDA an Investigational New
Drug Application (`IND")
89. The FDA's IND program is the means by which a pharmaceutical company
obtains permission to ship an experimental drug across state lines (usually to clinical
investigators) before a marketing application for the drug has been approved. The FDA reviews
the IND for safety to assure that research subjects will not be subjected to unreasonable risk.
90. In setting forth the requirements for an IND, the FDA also imposes on the sponsor
the obligation to obtain a commitment from the investigator that it will track and report to the
sponsor "adverse experiences that occur in the course of the investigation" that may reasonably
be regarded as caused by, or probably caused by, the drug being tested. Moreover, if the adverse
effect is "alarming," then the investigator is required to report the adverse effect immediately.
(See 21 C.F.R. §§ 212.53, 312.64).
91. An "investigator's principal ethical obligations are to design the study so as to
minimize risk, to ensure the adequate disclosure of the remaining risks to prospective subjects,
and to protect individual subjects enrolled in the study." "Data Safety Monitoring Boards," New
England Journal ofMedicine (Slutsky NEJM350:1143, 2004).
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92. A data safety monitoring board ("DSMB") is employed in double-blinded studies
for the purpose of having an independent body of researchers review adverse events and
beneficial results in the control versus blinded groups in order to ensure compliance with the
study guidelines and determine whether the trial should be halted either because the drug being
tested is causing harm or, conversely, exceptional benefit. The usual DSMB practice is to
demand less rigorous proof of harm to justify early termination as opposed to proof of benefit,
and not necessarily to be bound by preset measures for halting trials when faced with evidence of
such harm:
"Special circumstances may dictate the need for an interim analysis that was not
defined at the start of a trial ." Guidance for Industry: E9 Statistical Principles for
Clinical Trials; U. S. Department ofHealth and Human Services; Food and Drug
Administration , September 1998.
"It is well established that for ethical reasons statistical stopping rules are a
valuable aid in assessing whether interim data on treatment differences in a
clinical trial show sufficient evidence to necessitate termination of patient entry.
Although the deliberations of clinical trial data monitoring committees cannot be
trivialized by strict adherence to prespecified stopping boundaries, some
formalized procedures (e.g., group sequential designs) provide a valuable
guideline of objectivity." Pocock SJ, Hughes MD; Practical problems in interim
analyses, with particular regard to estimation. Control Clin Trials. 1989
Dec;10(4 Suppl):209S-221S.
If individuals given the investigational intervention are found to be at higher risk
for the outcome of interest (e.g., mortality, disease progression, loss of organ
function) sooner than those given the control, the DMC may consider
recommending early termination on safety grounds. Such assessments have
potential implications for falsely concluding that there is an adverse effect, just as
regular assessments of efficacy have the potential to lead to false positive
conclusions about benefit. Statistical considerations for early stopping when the
data are trending in the direction of harm are often different from the case of
trends in the direction of benefit, however. It is usually appropriate to demand
less rigorous proof of harm to justify early termination than would be
appropriate for a finding of benefit. Guidance for Clinical Trial Sponsors:
Establishment and Operation of Clinical Trial Data Monitoring Committees, U. S.
Department ofHealth and Human Services Food and Drug Administration, OMB
Control No. 0910-0581, Expiration Date: 3/30/2009.
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(Emphasis supplied).
93. The Pfizer DSMB applied the most rigorous proof of harm prior to halting the
study: a P value of less than 0.01, requiring statistical certainty in excess of 99% that the deaths
of those patients taking torcetrapib were not due to chance.
H. P Value Is A Statistical Measure Designed To Minimize Random Results;
Not To Justify The Continuation Of Trials Where There Is A Risk Of Death To
A Healthy Patient Population
94. As set forth above, the P-value is a measure of probability indicative of the point
at which a difference or relationship in the results emerges that is unlikely to be due to chance,
and are deemed "significant." The appropriate statistical testing uses mathematical procedures to
examine particular differences between groups to see if it is likely that the observed difference
could have arisen by chance alone , based on the numbers of observations (the N), the size of the
difference, and the variation or scatter in the data. If it is unlikely that the difference would have
arisen by chance alone, the difference is "statistically significant."
95. More precisely, statistical testing works by assuming that the groups are actually
the same - that there is no difference - and then mathematically estimating the probability that
you would see a difference between groups at least as big as the one you actually saw just due to
chance. This probability is called "P" and is referred to as a "P-value." Mathematical
probabilities, like P values, range from 0 to 1 where 0 means no chance and 1 means certainty.
0.5 means a 50% chance and 0.05 means a 5% chance.
96. A P-value of 0.01 ("highly significant") means there is a one percent possibility
that particular results are the result of random chance and a 99% possibility that they are the
result of the circumstances being studied. A P-value of 0.05 ("significant") means there is a five
percent possibility that particular results are the result of random chance and a 95% possibility
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that they are the result of the circumstances being tested. A P-value of 0.05 or better (that is,
P<0.05) is the most common measure for accepting that a difference is statistically significant in
medical research.
97. In the context of comparing deaths or severe adverse events of two different drugs
(control and test), as Pfizer did in its Phase III trials of the torcetrapib/atorvastatin combination,
using a P-value of 0.05 is less demanding than one of 0.01 because it means that, when a
particular comparison is made of deaths and/or severe adverse events (`SAES") in the two
control groups, one would reach the conclusion that there is a 95% probability that the
deaths/SAEs are the result of the drug rather than mere happenstance (0.05) before reaching the
conclusion that there is a 99% probability that the deaths/SAEs are the result of the drug (0.01).
Other things being equal, it requires more observations (data on more patients) to achieve
statistical significance at P<0.01 than it does to achieve statistical significance at P<0.05. Since
observations from more patients are being added as time progresses in a clinical trial, one must
necessarily satisfy P<0.05 before one achieves P<0.01. Thus, if the protocol calls for a P-value of
0.05 (5% significance) in deaths to trigger the decision to stop a clinical trial, one would stop the
trial prior to reaching the P-value of 0.01 (1% significance).
98. Given what Pfizer management knew about the dangers of CETP inhibition, the
significant blood pressure side effects seen in Phase II and Phase III trials, the undisclosed
existence of a potentially toxic MAO-inhibiting metabolite of torcetrapib, the absence of
evidence of increased cholesterol removal and the clinical evdicen that CETP inhibition may
increase risk of coronary heart disease, Pfizer nevertheless continued to put these relatively
healthy people (only 20-50% had narrowing of the arteries; no requirement that subjects had
prior heart attack or stroke) at risk in order to satisfy the unnecessarily stringent statistical
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measure of 99% certainty (0.01 P-value) instead of a 95% certainty (0.05 P-value).
CHRONOLOGY OF FALSE AND MISLEADING STATEMENTS
A. January 2005: Pfizer Omits Adverse Human Trial Results
99. On January 19, 2005, Pfizer released its fourth quarter 2004 financial results.
Pfizer described the status of the Phase III clinical trials of torcetrapib, but cited only one
specific study as follows:
Q6) What is the status of the torcetrapib/Lipitor program?
A6) A combination product of torcetrapib, a cholesteryl ester transfer
protein (CETP) inhibitor, and Lipitor is now in global Phase III clinical trials for
dyslipidemia that include 12,000 patients and are enrolling 13,000 patients in
mortality and morbidity trials.
... Data from a study assessing torcetrapib 's impact on atherosclerosis in a
rabbit animal model, recently reported at the American Heart Association 2004
Scientific Session, supports its potential efficacy for patients. Torcetrapib was
found to inhibit CETP activity and raise HDL cholesterol, which strongly
correlated with reduction in atherosclerosis in this rabbit model.
(Emphasis added)
100. Pfizer's reference to this rabbit study alone was materially false and misleading
because, by October 2004 and in contrast to the rabbit study, a Pfizer-sponsored study received
by the AHA's journal ATVB October 1, 2004 and whose final version was accepted on February
23, 2005, showed that torcetrapib in humans did not increase the rate of cholesterol excretion
even though it increased HDL-c levels. In a study of 19 subjects, nine of whom took 20mg of
Lipitor followed by 120mg of torcetrapib for four weeks, the scientists studied the impact of
5
torcetrapib on RCT by analyzing the concentrations of sterols and bile acids6 in the feces of the
5 Sterols include any of a group of predominantly unsaturated solid alcohols of the steroid
group, such as cholesterol and ergosterol , present in the fatty tissues of plants and animals.
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patients since fecal excretion is the final step in the RCT pathway. If there was increased sterol
and/or bile acid concentrations in the subjects' feces, that would indicate an increase in RCT
activity, i.e., an increase in the excretion of cholesterol. However, the study found that
"Torcetrapib did not substantially alter concentrations of either fecal sterols or bile acids,
indicating that it did not influence fecal sterol excretion in these subjects." (Brousseau, ATT7B
25:1057, 2005).
101. In contrast to the Phase II trial's dose of 60 mg/day, subjects in the Brousseau
fecal sterol study received as high as 240 mg/day torcetrapib, 4 times the clinical dose, and still
could not detect even a hint of an effect in the desired direction. These results should have led to
the conclusion that the hope that this manner of raising HDL-c would lead to improved removal
of cholesterol from arteries was dashed.
102. Thus, Pfizer possessed data from experiments which they sponsored that
discredited the concept that torcetrapib might increase RCT, the proposed therapeutic
mechanism, leaving Pfizer only to hope that the empirical correlation of high HDL-c with
clinical endpoints might play out to its favor.
103. Pfizer's reference to the rabbit study alone was further materially false and
misleading because it omitted evidence that torcetrapib dangerously raised systolic blood
pressure (¶¶ 9, 44, 77- 87); there was conflicting evidence on whether CETP inhibition was pro-
or anti - atherogenic (¶¶ 63-76); Pfizer had been warned internally that CETP inhibition would not
work (¶¶ 44, 98, 100-02); and Pfizer believed, but did not disclose, that the metabolite(s) of
6 Bile is a complex fluid containing water, electrolytes and a battery of organic molecules
that flows through the biliary tract into the small intestine. Secretion into bile is a major route
for eliminating cholesterol. Free cholesterol is virtually insoluble in aqueous solutions, but in
bile, it is made soluble by bile acids and lipids. Bile acids are derivatives of cholesterol
synthesized in the hepatocyte that are ultimately secreted from the body.
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torcetrapib could inhibit MAO, thereby causing increased blood pressure and potential heart
attack and stroke. (¶¶ 44, 85-87).
B. April 2005: Pfizer Falsely Reassures Investors As To Adverse Blood
Pressure Side-Effect Found In Phase I Trials: "Not Really An Issue;"
Phase II Blood Pressure Increases "Evaporated"
104. During the same April 5, 2005 analyst conference call, in response to analysts'
questions regarding the resultant increase in blood pressure amongst the patients taking
torcetrapib, Pfizer falsely stated that "high blood pressure is really not an issue," as follows:
DAVE RISINGER, ANALYST, MERRILL LYNCH: Dave Risinger from
Merrill Lynch. My question is for John LaMattina. Could you comment on blood
pressure increases seen with torcetrapib in the clinical trials you have done to
date? And I guess specifically the number and magnitude of outliers because the
mean or median increase seems to be small and some people have written it off as
irrelevant. But if you could about the outliers that would be helpful?
JOHN LAMATTINA: So certainly in our Phase I studies at very high
doses, we did see elevations of blood pressure. But in our Phase IIprogram, we
had seen that pretty much evaporate. But you raised a good question about
outliers. And Joe, do you have any data on any outliers?
JOE FECZKO, CHIEF MEDICAL OFFICER, PFIZER: No.
HANK MCKINNELL: I'll it pass Joe Feczko, our Chief Medical Officer,
to comment on this.
JOE FECZKO: The high blood pressure is not really an issue. We're not
seeing significant outliers. Most of the studies are blinded, so of course going
forward - but what we found is, I think what has been exaggerated here is any
kind of development program. You study a significant dose range, and so some
of the early reports of some of the early studies is in doses we are not even
contemplating using or have any thought about using. So when we study a large
dose range in our trials, it is normal drug discovery and development. We find
the most effective dose that gives it the fewest side effects. And that is what we
take into the broader clinical trials. That is what we've done with torcetrapib, so
the high blood pressure should not be an issue.
(Emphasis supplied).
105. The statements in the preceding paragraph were materially false and misleading
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because, in fact, Pfizer failed to refer to outliers in the Phase II trials of 4% of torcetrapib patients
having increased blood pressure in excess of 15 mm/Hg. (¶¶ 9, 162). The statements were also
false and misleading because Pfizer knew, but failed to disclose, that a source of the increased
blood pressure was the inhibition of MAO by torcetrapib metabolites, a fact that could
potentially be lethal to certain patients. (¶¶ 44, 85-87).
C. November 15, 2005: Pfizer Misrepresents Phase II Clinical Trial Results
106. On November 15, 2005, Pfizer issued a press release presenting results from two
Phase -II studies for torcetrapib/atorvastatin. According to the press release, the first study
showed that torcetrapib combined with all doses of atorvastatin resulted in significant increases
in patients ' HDL-c levels while also significantly decreasing their LDL-c:
In a study of nearly 500 patients, those who received torcetrapib (60 mg) and
atorvastatin (10, 20, 40, 80 mg) had increases in HDL-cholesterol of 44% to 66%.
At the same time, their LDL-cholesterol dropped between 41% and 60%. "These
results demonstrate that torcetrapib/atorvastatin can dramatically raise HDL while
providing LDL-lowering benefits greater than Lipitor alone," said Dr. Joseph
Feczko, Pfizer's chief medical officer.
107. The statements set forth in the preceding paragraph were materially false and
misleading since Pfizer knew that although torcetrapib effectively increased HDL-c, this result
was not a beneficial clinical endpoint and was equally likely to be linked to adverse coronary
risks because it was achieved through CETP inhibition.
108. In the same November 15, 2005 press release, Pfizer suggested that the Phase II
results were "pivotal" in the decision to go forward with Phase III trial. Feczko stated:
These results were pivotal in our decision to move forward with a Phase 3
[clinical trial] program, the final stage in clinical development.
109. The statements set forth in the preceding paragraph were materially false and
misleading because there was no basis to go forward with Phase III trials where Phase II trials
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did not find any correlation between CETP inhibition and increased RCT and/or indication of
clinical efficacy for cardiovascular events.
110. The November 15, 2005 press release also sought to lead investors into believing
that torcetrapib, by raising HDL-c, would improve RCT cholesterol removal and also have
undefined "further benefits:"
One of the main effects attributed to HDL-cholesterol is the ability to carry
cholesterol away from cells (such as in the artery wall where it contributes to
heart disease) back to the liver. Researchers believe that raising HDL-cholesterol
may provide further benefits in the management of cardiovascular disease, which
may have the potential to further reduce cardiovascular risk for patients.
111. The statements set forth in the preceding paragraph were materially false and
misleading because Phase II trials did not find any correlation between CETP inhibition and
increased RCT removal of cholesterol. These statements further were false and misleading
because, in light of the increased blood pressure side effect believed by Pfizer to be caused by
torcetrapib metabolites inhibiting MAO, torcetrapib could not provide "benefits" sufficient to
reduce cardiovascular risk.
112. The November 15, 2005 press release also stated that the second Phase II study,
which was to determine if the HDL particles in patients taking torcetrapib could maintain the
ability to carry cholesterol away from the cells involving 40 patients, showed that patients who
received torcetrapib 120 mg had increases of 40 to 60 percent in their HDL-c levels compared to
patients who received a placebo. The press release further stated that "[a]dditionally, the raising
ofHDL cholesterol in torcetrapib treatedpatients showed an increased ability to transport
cholesterolfrom cells - an effect seen to befunctionally similar to patients with naturally
occurring high levels ofHDL-cholesterol." (Emphasis supplied).
113. The statements in the preceding paragraph were materially false and misleading
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because it omitted to state that the study merely concluded that torcetrapib did not worsen the
RCT process and potentially "may enhance" cholesterol efflux - an initial stage in the RCT
process. The abstract actually describing the study stated as follows: "These results demonstrate
that partial inhibition of CETP with T [torcetrapib] does not compromise, and may enhance, the
cholesterol efflux potential ofHDL, which is considered the first step in reverse cholesterol
transport." (Emphasis supplied). As a result, the Phase II trials demonstrated only that the
patients who took torcetrapib were no worse off than those who did not in terms of the
cholesterol removal RCT process. The statements in the preceding paragraph were also
materially false and misleading because, as set forth above, a Pfizer-sponsored study showed that
in humans and in vivo, RCT was not increased by torcetrapib. (¶¶ 98, 100-02).
114. Pfizer 's announcement regarding the second Phase II study was further materially
false and misleading because the study plainly did not support the conclusion that Pfizer claimed.
Pfizer wrongly implied that there was a beneficial (hence, net) removal of cholesterol from cells
belonging to the patients - when in fact the cells tested were not from the patients' bodies, and
were not naturally occurring or human cells. The Phase II study did not involve in vivo (in the
body) human testing, but instead a type of "ex vivo" testing that involved the use of transformed
animal cells and test tube experimentation. Specifically, blood was removed from Phase II
patients at various times after treatment with a placebo or torcetrapib. The blood was allowed to
coagulate, and HDL particles were purified and mixed together with mouse or rat cells, both
having been labeled with radioactive cholesterol previously since the radioactivity is easier to
measure than cholesterol. After allowing the particles to sit together in the test tube for four
hours, the amount of radioactive cholesterol removed from the mouse or rat cells was measured.
This removal was increased in patients treated with a high dose of torcetrapib (120 mg) alone for
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8 weeks (which is different from the envisaged actual torcetrapib treatment, which would use a
lower dose of torcetrapib). Being ex vivo and involving transformed animal cells, this cannot
possibly be considered a clinical result, and is far too contrived to allow interpretation about
what actually occurs in vivo.
115. In the same November 15, 2005 announcement, Feczko stated: "This [second]
study provides important information to support CETP inhibition with torcetrapib as an
efficacious way to raise HDL which could offer significant cardiovascular benefits for
patients [.]" (Emphasis supplied).
116. Feczko's statement set forth in the preceding paragraph was materially false and
misleading since a Pfizer- sponsored study showed that in humans, RCT was not increased by
torcetrapib(¶¶ 100-02); there was evidence that torcetrapib dangerously raised systolic blood
pressure , including in excess of 15 mm in 4% of torcetrapib patients (¶¶ 9, 44, 77-87, 162); there
was conflicting evidence on whether CETP inhibition was pro- or anti -atherogenic (¶¶ 63-76);
Pfizer had been warned internally that CETP inhibition would not work (¶¶ 44, 100-02); and
Pfizer believed, but did not disclose, that the metabolite(s) of torcetrapib could inhibit MAO,
thereby causing increased blood pressure and potential heart attack and stroke. (¶¶ 44, 85-87).
D. November 25, 2005: Pfizer Reiterates Misrepresentation of
Phase II Clinical Trial Results
117. On November 25, 2005, Pfizer reiterated further in a press release the results from
the two Phase II studies set forth in the November 15, 2005 press release . First, as on November
15, 2005, Pfizer sought to link the study results with generally accepted concepts regarding the
benefits of HDL:
The two Phase 2 studies involving torcetrapib/atorvastatin were designed to
determine whether this combination therapy can effectively raise HDL-C while
lowering LDL-C. HDL-C carries cholesterol away from cells and tissues
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preventing its build up and resulting in deposits which contribute to heart disease.
Researchers believe that raising HDL-C levels may provide further benefits in the
management of cardiovascular disease (CVD) potentially reducing patients' CV
risk.
118. The statements set forth in the preceding paragraph were materially false and
misleading because the Phase II trials did not find any correlation between CETP inhibition and
increased RCT removal of cholesterol. The statements were also materially false and misleading
because, in light of the increased blood pressure side effect, believed by Pfizer to be caused by
torcetrapib metabolites inhibiting MAO, torcetrapib could not provide "benefits" sufficient to
reduce cardiovascular risk.
119. The November 25, 2005, press release further repeated the results of the first
study cited on November 15, 2005:
In a study of nearly 500 patients, those who received torcetrapib (60 mg) and
atorvastatin (10, 20, 40, 80 mg) had increases in HDL-cholesterol of 44% to 66%.
At the same time, their LDL-cholesterol dropped between 41% and 60%.
120. The statements set forth in the preceding paragraph were materially false and
misleading since Pfizer knew that although torcetrapib effectively increased HDL-c, this result
was not a beneficial clinical endpoint and was equally likely to be linked to adverse coronary
risks because it was achieved through CETP inhibition.
121. The November 25, 2005 press release went even further than the November 15,
2005 release when it claimed that "this new approach could change the way physicians manage
cholesterol:"
This new approach could change the way physicians manage cholesterol and
further reduce the risk of atherosclerosis in their patients.
(Emphasis added).
122. The statement set forth in the preceding paragraph was materially false and
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misleading because Phase II trials did not find any correlation between CETP inhibition and
increased RCT removal of cholesterol. The statement was also materially false and misleading
because, in light of the increased blood pressure side effect, believed by Pfizer to be caused by
torcetrapib metabolites inhibiting MAO, torcetrapib could not change the way doctors treated
their patients and could not reduce the risk of CHD. Both of these facts meant that torcetrapib
could not represent "a new approach" to managing cholesterol or reducing the risk of CHD.
123. As did the November 15, 2005 press release, the November 25, 2005 release
touted a second study involving forty patients that purported to show that patients who received
torcetrapib 120 mg had increases of 40 to 60 percent in their HDL-c levels compared to patients
who received placebo . Pfizer stated the study showed that "raising HDL-C with torcetrapib
increased the transportation of cholesterolfrom cells - an effect seen to be functionally
similar to patients with naturally occurring high levels ofHDL-C." (Emphasis supplied).
124. The statement in the preceding paragraph was materially false and misleading
because it omitted to state that the actual abstract describing the second study recognized that the
most that could be said was that torcetrapib did not worsen or "compromise " the RCT process
and stated that it potentially "may enhance" cholesterol efflux - an initial stage in the RCT
process , as follows : "[t]hese results demonstrate that partial inhibition of CETP with T
[torcetrapib] does not compromise, and may enhance, the cholesterol efflux potential ofHDL,
which is considered the first step in reverse cholesterol transport." As a result, the Phase II trials
demonstrated only that the patients who took torcetrapib were no worse off than those who did
not in terms of the cholesterol removal RCT processes. The statement was also materially false
and misleading because, as set forth above, a Pfizer-sponsored study showed that in humans and
in vivo, RCT was not increased by torcetrapib. (¶¶ 100-02).
45
125. On January 4, 2006, during an analyst conference entitled "Pfizer at Morgan
Stanley - Pharmaceutical CEOs Unplugged Conference Presentation," Pfizer downplayed
reports of higher blood pressure as result of torcetrapib/atorvastatin. In response to questions
concerning findings of increased blood pressure in the Phase II studies, McKinnell stated that it
would ultimately "dose" the higher blood pressure to get it under control, or treat it with blood
pressure medication, but was not allowed to do so under the strictures of its Phase II study:
in the real world, in clinical practice, if you were treating a patient with any
medicine that had important benefits and you saw an increase of 1 to 2 mg in
blood pressure, probably the first thing you would do is ignore it, but ifyou felt it
needed to be treated, you would increase the blood pressure medication. But
that's not allowed in Phase II study. We also saw this effect atfairly high doses
of Torcetrapib, so part of the dose-finding studies we did in deciding the dose
for the Phase III specifically addressed the question of blood pressure elevation.
(Emphasis supplied).
126. During the same conference call, McKinnell stated:
We spend - on this this specific safety issue you've raised of blood pressure,
we've obviously spent a lot of time on that, and we wouldn 't have launched an
$800 million study withoutfeeling pretty confident that we have that issue well
analyzed and addressed, The concern camefrom the Phase II data, which are
fixed-dose studies, and they did show 1 to 2 mg increase in blood pressure.
Fortunately, there's not real outliers there, so it was kind of on average a pretty
tight distribution around 1 to 2. But in the real world, in clinical practice, if you
were treating a patient with any medicine that had important benefits and you saw
an increase of 1 to 2 mg in blood pressure, probably the first thing you would do
is ignore it, but if you felt it needed to be treated, you would increase the blood
pressure medication. But that's not allowed in Phase II study. We also saw this
effect at fairly high doses of Torcetrapib, so part of the dose-finding studies we
did in deciding the dose for the Phase III specifically addressed the question of
blood pressure elevation. We hope we dose under it but of course, we won't know
that until we see the results of the Phase III study. So I don't think the kind of
gating critical issue here is so much blood pressure. I think that we will be able to
deal with.
(Emphasis added).
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127. The statements set forth in the previous two paragraphs were materially false and
misleading because, in fact, the Phase II patients experienced a 2 to 3 millimeter increase in
blood pressure, and Pfizer knew that there were significant outliers in the Phase II trials of 4% of
patients having increased blood pressure in excess of 15 mm/Hg (¶¶ 9, 162). Moreover, the
increased blood pressure caused by torectrapib was a serious issue that threatened the efficacy
and approval of the therapy and, as set forth above, Pfizer believed, but did not disclose, that the
metabolite(s) of torcetrapib could inhibit MAO, thereby causing increased blood pressure and
potential heart attack and stroke. (¶¶ 44, 85-87).
128. During the same January 4, 2006 Morgan Stanley analyst conference, McKinnell
represented to investors that torcetrapib's value to the medical community was in "the hundreds
of billions of dollars:"
HANK MCKINNELL: Well, we've committed to $800 million in Phase
III clinical work to answer exactly those questions. It's well underway. All of the
programs are fully enrolled. We expect those imaging studies, the IVAS and other
data to be available late 2006 and following along two years or so later is the
morbidity/mortality data. Now, if this medicine does what we think it does, it's
going to have a profound effect on cardiovascular events. If you look at the
Framingham data, lowering LDL eliminates 35, 40% of cardiovascular events.
That depends on the patient and the drug and the population study, but it's on the
order of 35 to 40%. What that really means is there's 60 to 65% of patients who
still have very high cardiovascular risk.
If you look at the patients in the Framingham data base with high HDL,
they have essentially no cardiovascular risk. That's an exaggeration; it's maybe
5%, but it's very, very low. So it looks to us, from the epidemiological data, that
HDL could be a more profound reducer of cardiovascular risk than could LDL.
Now, what is that worth ? It's in the hundreds of billions of dollars. So the real
issue here is not so much can we file based on the IVAS data; it's really, can we
convince the FDA, physicians and the public of the benefits of elevating HDL?
(Emphasis supplied).
129. The above statement was materially false and misleading because it not only
assumed that merely increasing HDL-c would be beneficial but Pfizer failed to disclose any of
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the studies which suggested the mechanism torcetrapib used to increase HDL-c could well
increase coronary heart disease . (See, e.g., ¶¶ 12, 44, 54-87).
130. A January 16, 2006 news article published by Drug Store News, entitled
"Generics Likely To Beat Switches In Race Against Branded Statins ; Patent Protection"
reiterated McKinnell's representations the that Lipitor/Torcetrapib combination therapy will be
the "next $10 billion drug," as follows:
Pfizer is developing a combination product of its yet-to-be-approved
HDL-raising therapy torcetrapib with its statin Lipitor, a combination therapy that
Pfizer chief executive officer Hank McKinnell believes will be the next $10-
billion drug. The torcetrapib/Lipitor product is expected to hit the market before
2011, when Pfizer's patents protecting Lipitor are expected to expire.
(Emphasis supplied).
131. The above statement was materially false and misleading because it not only
assumed that merely increasing HDL-c would be beneficial but Pfizer failed to disclose any of
the studies which suggested the mechanism torcetrapib used to increase HDL-c could well
increase coronary heart disease . (See, e.g., ¶¶ 12, 44, 54-87).
F. February 2006: Pfizer Again Falsely Reassures Investors That
"2 Millimeter" Phase II Blood Pressure Side Effect Is "Easily
Monitored and Managed"
132. On February 10, 2006, during an analyst conference call headlined "Pfizer
Analyst Meeting," John LaMattina represented to investors that early Phase II clinical data
showed that torcetrapib/atorvastatin increased the systolic blood pressure in patients, on average,
by two millimeters of mercury. Additionally, LaMattina stated that Pfizer believed that the
"overall benefit to patients cardiovascular health achieved through torcetrapib/atorvastatin
treatment will greatly outweigh the potential increased risk of this blood pressure elevation," as
follows:
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Early Phase II clinical data show that torcetrapib/atorvastatin increased HDL
by up to 65% and lowered LDL by up to 60%. There was, however, a rise in
blood pressure in patients receiving torcetrapib, the average effect being 2
millimeters of mercury systolic. If confirmed in Phase III, the blood pressure
effect is easily monitored and managed clinically. We believe the overall
potential benefit to patients' cardiovascular health achieved through
torcetrapib/atorvastatin treatment will greatly outweigh the potential increased
risk of this blood pressure elevation. Lipitor has become the standard by which
all lipid-modulating therapies are judged. We believe that the
torcetrapib/atorvastatin combination will become an even more important
medicine for those at risk of heart attack and stroke, a medicine that truly offers
the potential to reverse atherosclerosis.
(Emphasis supplied).
133. The statements in the preceding paragraph were materially false and misleading
because, in fact, the Phase II trial results showed increased blood pressure of between "2 to 3
millimeters" and not the "2 millimeters" referred to in the above paragraph. Further, Pfizer
failed to state that a significant portion of the torcetrapib patients experienced dramatic blood
pressure increases in excess of 15mm which severely undermined any justification for use of the
drug. Pfizer also failed to disclose that it believed the blood pressure increase was caused by a
metabolite (s) of torcetrapib inhibiting MAO which meant the blood pressure increase posed a
particularized threat of heart attack and stroke. (¶¶ 44, 85-87).
134. Additionally, during the February 10, 2006 analyst conference, Feczko stated that
unlike Lipitor which does not reduce plaque, torcetrapib - through its elevation of HDL-c -
would increase plaque regression:
JON LECROY, ANALYST, NATEXIS BLEICHROEDER: Jon LeCroy,
Natexis Bleichroeder. Can you talk about what difference in plaque reduction
your trials are powered to detect with torcetrapib, and then what your base case on
plaque reduction is for Lipitor?
HANK MCKINNELL: Joe?
JOE FECZKO: There is no plaque reduction in Lipitor. We have seen
what the very aggressive Lipitor studies that have looked at plaque formation, but
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you see when it's been compared to Pravachol and others is that there is a small
but consistent increase in plaque growth on drugs like Pravachol when it was
studied head-to-head in a "Prove It" study, for instance. And there was a
stabilization of plaque over time on high dose Lipitor. That is why we think that
there is some room here.
The whole premise around HDL is elevated HDL molecules act as - I
think in a sense in a simplistic way to draw the LDL away from the plaque and,
therefore, shrink the plaque. It is the whole premise around what HDL does. So
we do anticipate it to be successful, that there would be extra plaque regression.
And because there is stabilization with Lipitor, which you don 't even see with
other statins, again, that we do think there is an opportunity.
(Emphasis supplied).
135. The statements in the preceding paragraph were materially are false and
misleading because a Pfizer- sponsored study showed: that in humans , RCT was not increased by
torcetrapib (¶¶ 100-02); conflicting evidence on whether CETP inhibition was pro- or anti-
atherogenic (¶¶ 63-76); and Pfizer had been warned internally that CETP inhibition would not
work. (¶¶ 44, 100-02).
G. March 2006 : Pfizer Announces Phase II Trial Results
136. On March 14, 2006, Pfizer issued a press release announcing the results of three
studies presented at the annual meeting of the American College of Cardiology ("ACC"), held on
March 11-14, 2006 in Atlanta, Georgia. The press release stated, inter alia, that:
Pfizer said today that new data, involving its medicine in development
torcetrapib/atorvastatin, provides important information on the benefit of
raising HDL, or "good " cholesterol, while simultaneously lowering LDL, or
"bad" cholesterol. These new findings may play a critical role in reducing the
burden of cardiovascular disease and potentially improving quality of life for
patients. Data from three separate studies were presented this week at the
American College of Cardiology meeting.
(Emphasis supplied). According to the press release , the first study showed that increased HDL-
c correlated to a decreased risk of heart attack or stroke; the second study showed that taking a
torcetrapib/atorvastatin combination in the morning was more effective than taking it in the
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evening ; and the third study of 493 patients showed that patients taking torcetrapib (30, 60 or 90
mg) and atorvastatin (10, 20, 40 or 80mg) together experienced a decrease in LDL-c and an
increase in HDL-c levels, as well as increases in the particle size of both HDL and LDL.
However, the increase in HDL-c was accompanied by "an increase in systolic blood pressure of
approximately 2 mm Hg, which will be further defined in ongoing phase 3 studies."
137. Pfizer' s statements set forth in the preceding paragraph were materially false and
misleading since Pfizer knew that, although torcetrapib effectively increased HDL-c, this result
was not a beneficial clinical endpoint and was equally likely to be linked to adverse coronary
risks because it was achieved through CETP inhibition. Also, Pfizer knew that, in fact, there
were important outliers in the Phase II trials of 4% of patients having increased blood pressure in
excess of 15 mm/Hg. (¶¶ 9, 162).
H. March 2006 : Pfizer Falsely Claims "Evidence" Drug Can "Reduce
Blockages " Sufficient So As "Not To Wait" To Go To The FDA
138. On March 21, 2006, a Bloomberg News article (which was reprinted in the
Ottawa Citizen), entitled "Pfizer Works to Offer Drug Ahead of Schedule; Cholesterol
Medication Called Crown Jewel of Research Program," reported on a March 13, 2006 interview
at the American College of Cardiology ("ACC") meeting in Atlanta with Tom Thuren, Pfizer's
senior director of clinical development. Thuren stated:
The plan, as it stands right now, is not to waitfor the later studies . Pfizer has
decided that evidence the drugs can reduce artery blockage, and possibly prevent
heart attacks and death, may be enough to persuade U.S. regulators to approve the
combination pill.
(Emphasis supplied).
139. The statements in the preceding paragraph were materially false and misleading
because they were unsupported by the reported results of the three studies Pfizer announced at
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the ACC annual meeting on March 14, 2006. Nowhere in these results was there "evidence" that
torcetrapib can reduce artery blockage. Pfizer omitted from its disclosure that no clinical trial
demonstrated an increase in RCT. Moreover, the Phase II studies showed enormous risk in use
of the drug since 4% of the torcetrapib patients experienced in excess of 15mm increase in blood
pressure not seen in the control group.
1. October 2006 : Pfizer Claims Torcetrapib Represents Tip Of "CETP Franchise"
140. On October 19, 2006, during an analyst conference call headlined "Q3 2006
Pfizer Earnings Conference Call," Jeff Kindler and John LaMattina deemphasized the individual
significance of torcetrapib, and rather falsely touted investors on Pfizer's "CETP franchise" and
other compound that Pfizer may begin testing:
JEFF KINDLER: Regarding torcetrapib, let me just make a comment, and
then I will turn it over to John. We're obviously very excited about the possibility
of torcetrapib, but I think what's really important to understand is that we think
of this as CETPfranchise, and we do have backup compounds and you will hear
a lot more about that at the November meeting. But I think the way we need to be
thinking about this, this is a franchise. We believe that this mechanism of action
makes a lot of sense and we're investing in it, and obviously others seem to
think so as well. And so, that's that I think the better way to look at the whole
question, but I will let John elaborate.
JOHN LAMATTINA: You have answered - you've taken the words out of
my mouth.
JEFF KINDLER: Sorry.
JOHN LAMATTINA: No, not a problem, so I think you answered it
correctly, and on November 30th, we'll talk about ourfranchise in regard to
torcetrapib, (indiscernible) in combination. Torcetrapib is a stand-alone agent
and the next-generation compound's in our pipeline.
(Emphasis supplied).
141. The statements in the preceding paragraph were materially false and misleading
because defendants knew that there was no way for torcetrapib to lead a "franchise" of CETP
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inhibitors since a Pfizer-sponsored study showed that in humans, RCT was not increased by
torcetrapib (¶¶ 100-02); there was evidence that torcetrapib dangerously raised systolic blood
pressure (¶¶ 9, 44, 77-87, 162); there was conflicting evidence on whether CETP inhibition was
pro- or anti-atherogenic (¶¶ 63-76); Pfizer had been warned internally that CETP inhibition
would not work (¶¶ 44, 100-02); and Pfizer believed, but did not disclose, that the metabolite(s)
of torcetrapib could inhibit MAO, thereby causing increased blood pressure and potential heart
attack and stroke. (¶¶ 44, 85-87).
J. October 31, 2006 : Pfizer Violates AHA Rules In Order to Misleadingly
Spin Phase II "2 to 3 mm " BP Increase and Phase III "3 to 4mm" BP
Increase : "Does Not Alter Favorable Clinical Profile"
142. The AHA has strict rules that preclude drug companies from " pre-announcing"
results of clinical trials to be presented at AHA proceedings. These rules are designed to prevent
companies from manipulating presentation of clinical trial data . The AHA so rigorously abides
by these rules that the AHA precludes companies which violate them from presenting at AHA
proceedings.
143. Pfizer was to present Phase III torcetrapib clinical trial results at a November 30,
2006 AHA conference. These results reflected further adverse blood pressure increases of, on
average, 4 mm/Hg for patients taking torcetrapib. In an effort to manipulate the release of this
information, Pfizer violated AHA rules and pre-released Phase III data.
144. In an October 31, 2006, press release appearing on PR Newswire, entitled "Pfizer
Updates Preliminary Results of Torcetrapib/Atorvastatin Clinical Trials as Abstract For Phase 3
Study Is Released," Pfizer released the Phase 3 results to date, which showed a greater increase
in systolic blood pressure than in Phase 2 clinical trials, stating as follows:
"We are pleased with the results of the HeFH study, and our overall lipid results
from all the trials completed are very positive, said Dr. Joseph Feczko, Pfizer's
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chief medical officer. "They generally show torcetrapib/atorvastatin significantly
increasing `good' cholesterol by 55 to 60 percent and additionally lowering `bad'
cholesterol by 10 to 15 percent over atorvastatin alone (leading to a combined
reduction in LDL of 50 to 60 percent), which supports ourfundamental premise:
this innovative medicine really can `do both' and manage cholesterol
successfully.
"Our overall Phase 3 results to date, which are incomplete and must be rigorously
analyzed when all the lipid and imaging trials are finished, also show an average
increase in systolic blood pressure of approximately one millimeter of mercury
above the two-to-three millimeter range that was observed in Phase 2 studies,
which we believe will not alter the favorable clinical profile of torcetrapib/
atorvastatin in the treatment of cardiovascular disease. "
(Emphasis supplied).
145. This press release was materially false and misleading since Pfizer is now for the
first time informing investors that the torcetrapib Phase II trials revealed blood pressure
increases in the " two to three millimeter range" as opposed to the " 2 millimeter" increase
disclosed for the Phase II trials in February 2006 (¶ 132); or the "1 to 2 milligram " [sic] increase
disclosed in January 2006 (¶ 125). The press release was also materially false and misleading
since there still was no disclosure that 4% of the patients in the Phase II trials had a blood
pressure increase in excess of 15mm, nor that 9% of the torcetrapib patients in the Phase III
trials had a blood pressure increase in excess than 15mm increase in blood pressure in the
Phase III trials; nor that Pfizer believed, but failed to disclose, that torcetrapib was an MAO-
inhibitor that could lead to increased risk of heart attack and stroke (¶¶ 44, 85-87), thereby giving
torcetrapib an extremely unfavorable clinical profile.
146. As a result of Pfizer's October 31, 2006 Phase III disclosures, the AHA banned
Pfizer's torcetrapib presentation at the November AHA conference. An AHA spokeswoman
stated, "Pfizer released the information early, and we need to uphold our policies."
147. On November 11, 2006, the Associated Press published a news article, entitled
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"Report: Pfizer Can't Give Cholesterol-Drug Data at AHA Conference." The article reported
that Pfizer would delay presenting its results on torcetrapib, as follows:
Pfizer Inc. scientists won't be allowed to present new data on its drug
called torcetrapib at the American Heart Association's annual scientific meeting
next week, according to a newspaper report.
A Pfizer spokesman said the company issued the press release last month
because of the high level of interest among doctors and investors in the
torcetrapib program. The results were to have been presented at the AHA meeting
in Chicago on Nov. 15.
(Emphasis supplied).
K. November 30, 2006: Pfizer Unequivocally Reaffirms Expectation of
Torcetrapib's "Unparalleled Efficacy" Describing It As the "Most Important
New Development in Cardiovascular Medicine in Years"
148. On November 30, 2006, Pfizer issued a press release on the PR Newswire entitled
"Pfizer Presents Robust and Diversified Product Pipeline Across 11 Therapeutic Areas; R&D
Briefing Highlights 30 Research Programs with More Than Half Discussed for the First Time;
Company Highlights Torcetrapib/Atorvastatin and Cholesteryl Ester Transfer Protein
Research as Most Important New Development in Cardiovascular Medicine in Years."
(Emphasis supplied). In the press release, LaMattina commented on Torcetrapib as follows:
Commenting on torcetrapib/atorvastatin (T/A), Dr. LaMattina said, "We
are first-in-class and we intend to remain best-in-class in a category that has the
potential to change the face of cardiovascular medicine . T/A raises HDL and
lowers LDL. We believe that the net benefits of the drug - characterized by
significant HDL elevation and LDL lowering vs. the small elevation in blood
pressure - will greatly benefit patients with CV risk.
" The development of T/A has required tremendous innovation on our part
from the earliest stages of discovery through one of the most cutting-edge
development programs ever carried out anywhere. At the end of this
comprehensive program, we expect to have a medicine with unparalleled
efficacy in raising HDL, lowering LDL and with an anti-atherosclerosis
indication.
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"We will learn of the top-line results of the three pivotal imaging trials
during the first quarter of 2007. During this same period, we will also receive the
results of some additional Phase III lipid studies. To obtain a reliable picture of
the overall safety and efficacy profile of T/A, the results of all these studies will
need to be analyzed and reviewed together, and this will happen in the context of
the American College of Cardiology Meeting in March, 2007."
149. The statements in the preceding paragraph were materially false and misleading
because not only was torcetrapib and CETP research not the "Most Important New Development
in Cardiovascular Medicine in Years," there was no way Pfizer could be "best in class"' in
connection with CETP inhibitors, nor would such drugs "greatly benefit patients with CV risk"
since a Pfizer-sponsored study showed that in humans, RCT was not increased by torcetrapib
(¶¶ 100-02); there was evidence that torcetrapib dangerously raised systolic blood pressure (¶¶ 9,
44, 77-87, 162); there was conflicting evidence on whether CETP inhibition was pro- or anti-
atherogenic (¶¶ 63-76); and Pfizer had been warned internally that CETP inhibition would not
work (¶¶ 44, 100-02). Moreover, the increased blood pressure was not small, but rather, could
lead to increased risk of heart attack and stroke because, as Pfizer believed, the composition of
torcetrapib could cause metabolites of the drug to inhibit MAO, thereby causing increased blood
pressure and potential heart attack and stroke . (Id.).
150. A December 1, 2006 Prudential Equity Group LLC analyst report commented on
the November 30, 2006 R&D Day update. The analyst report highlighted the "almost
orchestrated" nature of Pfizer's presentation:
... [Pfizer's] newfound (and almost orchestrated) optimism on lead pipeline drug
torcetrapib/atorvastatin, reversing the pessimistic tone that came out of Pfizer's
3Q conference call.
Whether PFE misspoke on torcetrapib/atorvastatin during 3Q results or not is
unclear. But now, we sense that PFE shares will drift up going into the March
release of pivotal data at the American College of Cardiology annual meeting,
given management's newfound optimism on the product. Consensus is likely to
56
L. The Truth Begins to Emerge: The Failure of Torcetrapib
151. A mere two days after further touting torcetrapib, on December 2, 2006, Pfizer
announced that it had halted development of torcetrapib after more patients than expected died
during a large clinical test:
NEW YORK, Dec. 2 / PR Newswire - FirstCall / - Pfizer Inc said that in
the interests ofpatient safety it is stopping all torcetrapib clinical trials and that
it has informed the Food and Drug Administration. The Company is in the
process of notifying all clinical investigators in the program as well as other
regulatory authorities.
The Company was informed today that the independent Data Safety
Monitoring Board (DSMB) monitoring the ILLUMINATE morbidity and
mortality study for torcetrapib recommended terminating the study because of an
imbalance of mortality and cardiovascular events.
The Company has terminated ILLUMINATE and is in the process of
asking all clinical investigators conducting trials in this development program to
inform patient participants to stop taking the study medication immediately. The
Company has also ended the development program for this compound.
Dr. Philip Barter, Director of the Heart Research Institute in Australia and
Chairman of the Steering Committee overseeing the ILLUMINATE study, said,
"Based on all the evidence we have seen regarding torcetrapib and in light of prior
study results, we were very surprised by the information received from the
DSMB , the only body with access to the unblinded safety data . We believed that
the study was coming along as expected, and this new information was totally
unexpected and disappointing, given the potential benefits of this drug."
Pfizer's Chief Executive Officer Jeffrey B. Kindler said, "While the
DSMB information we received today was both surprising and disappointing, our
focus is on the best interests of patients and making sure all this information is
communicated to appropriate medical and regulatory authorities as quickly as
possible.
152. In fact, 82 patients taking the combined torcetrapib/Lipitor drug died during trials
as opposed to only 51 taking Lipitor alone. Moreover, patients taking torcetrapib also showed an
increase in angina, congestive heart failure and procedures to clear clogged arteries.
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153. Following this announcement of previously undisclosed information, shares of
Pfizer common stock declined by $2.96 per share (or almost 11%) from a closing price of $27.86
per share on December 1, 2006, to a closing price $24.90 per share on December 4, 2006, on
extraordinarily heavy trading volume of 289,209,504 - over seven times the previous trading
day's volume and more than nine times Pfizer's average daily volume for the previous year,
representing a market of loss of $855,984,640. The following day, December 5, 2006, Pfizer's
stock price further declined $0.08 per share, again on large volume of 118,558,300 shares traded,
contributing to a two- day market capitalization loss of $865 ,471,704
M. March 2007: Phase III Trial Results Confirm Even More Dramatic Blood
Pressure Side Effect And No Clinical Benefit of Plague Removal
154. On March 26, 2007, at the annual ACC conference, further disclosures were made
of the Phase III clinical trials that further demonstrated the severity of the blood pressure side
effect. The baseline, or average starting, blood pressure for the patients was 120/73
(systolic/diastolic). Patients taking the torcetrapib/atorvastatin therapy reported significantly
more high blood pressure adverse events than the control group (23.7% vs. 10.6%). Also,
9.3% of the patients taking torcetrapib experienced a sustained increase in blood pressure
in excess of 15 mm/Hg compared with 3.2% of the control group, and with 21.3% reporting
blood pressure in excess of 140/90 mm/Hg. In addition, there was an even further increase in
the average blood pressure increase of torcetrabip patients compared to the control group: the
average blood pressure of torcetrapib patients was 6 mm higher than the control patient blood
pressure, which was only 2 mm higher.
155. The study confirmed what should have been obvious to Pfizer from the start - that
Pfizer should have measured the appropriate clinical endpoint, rather than just HDL-c and LDL-c
levels:
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However, despite these favorable effects on lipoprotein levels, there was no
significant reduction in the progression of coronary artherosclerosis according to
percent atheroma [artery clogging] value, the primary efficacy measure.
(Emphasis supplied).
156. The ACC' s press release issued on March 26, 2007 in connection with the
torcetrapib results confirmed that plaque was not removed from patients' arteries and that there
was an even higher increase in blood pressure than was reported in either the Phase II trial or
previously for the Phase III trial:
The results of the [torcetrapib] study presented today at the American
College of Cardiology's 56th Annual Scientific Session are considered pivotal in
determining whether the failure of torcetrapib was the result of specific drug
toxicity or a failure of the entire approach as a means to raise HDL....
A total of 1,188 coronary artery disease patients were enrolled in a trial
called ILLUSTRATE (Investigation of Lipid L evel management using coronary
Ultra S ound T o assess Reduction of Atherosclerosis by CETP Inhibition and HDL
Elevation). All patients had a clinical indication for cardiac catheterization, had a
baseline intravascular ultrasound (IVUS), and received 10-80 gm of atorvastatin
adjusted during a two- to 10-week period until LDL levels reached national
guidelines. Patients were then randomized to receive either 60 mg of torcetrapib
or a matching placebo for two years. At the end of the treatment period, a second
IVUS was performed, examining the same coronary arteries. Researchers
measured the change in plaque volume in the artery, comparing the baseline to the
follow-up ultrasound, and measured patients' blood cholesterol levels and
biomarkers of inflammation at several points during the trial.
Patients in the torcetrapib/atorvastatin group experienced a 61 percent
relative increase in HDL cholesterol levels and a 20 percent relative decrease in
LDL levels, as compared with patients in the atorvastatin-only group. Despite
those results, there was no statistical difference between the two groups in
plaque volume changes. Plaque volume increased by 0.19 percent in the
atorvastatin-only patients and 0.12 percent in the combination group, p = 0.72.
Torcetrapib was associated with a substantial increase in blood pressure.
During the course of the study, the torcetrapib-treated patients had a systolic
BP that averaged 4.6 mm Hg greater than the atorvastatin-only patients.
Furthermore, torcetrapib patients were more than twice as likely to increase
systolic BP more than 15 mmHg compared with atorvastatin alone.
(Emphasis supplied).
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N. CETP Inhibition Researcher Reviewing Clinical Trial
Data Finds Blood Pressure Side Effect "Important"
157. Contrary to Pfizer's false statements during the Class Period that discounted the
importance of the increased systolic blood pressure side effect, a prominent researcher, Dr. Tall,
who examined the torcetrapib clinical trial results, deemed that side effect to be "important"
(noting the increases in the Phase I trial and the finding in the Phase II trial that 4% of the
torcetrapib population showed an increase in blood pressure in excess of 15mm Hg, even if that
side effect was not the cause of the Phase III deaths . In a study published in February 2007, Dr.
Tall stated as follows:
An important adverse side- effect of torcetrapib was the increase in blood
pressure (BP). In phase 2 trials, this appeared to be small in magnitude, perhaps
1 to 2 mm Hg in systolic BP. But from the early phase 3 experience, the increase
in BP was reportedly larger, on average 3 to 4 mm Hg. Moreover, about 4% of
subjects in phase 2 experienced BP elevations in excess of 15 mm Hg. The
hypertensive side-effect does not appear to be mechanism related, as genetic
CETP deficiency does not result in hypertension, and some other CETP inhibitors
with different chemical structures to torcetrapib do not elevate BP. A mean
increase of 3 to 4 mm of BP in itself seems unlikely to completely explain the
adverse outcome from ILLUMINATE, but there may have been a sizeable subset
of patients with larger BP increases. Moreover, the BP increase could be just a
sentinel of a more profound underlying adverse vascular effect of torcetrapib,
such as vasospasm or activation of the renin-angiotensin system.
(Emphasis supplied).
158. Significantly, Dr. Tall's recognition in February 2007 of the significance of the
blood pressure side effect was based on Pfizer's announcements during the Class Period
concerning blood pressure increases, rather than the March 26, 2007 announcement of even more
significant adverse blood pressure side effects noted above.
0. Torcetrapib's Failure Accelerates Pfizer Restructuring
159. In its December 2, 2007 press release, Pfizer also acknowledged the devastating
impact torcetrapib's failure would have on the Company:
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Pfizer's previously announced plan for transforming the company will now be
accelerated. Pfizer will focus on its core research and development,
manufacturing and commercial operations, as well as procurement and other
areas, to improve efficiency and lower its costs as expeditiously as possible.
160. Less than two months later, on January 22, 2007, Pfizer released its year-end
results for 2006. CEO Kindler acknowledged that torcetrapib's failure had caused the Company
to intensify its review of its restructuring plans:
Our decision to discontinue development of torcetrapib/atorvastatin in early
December 2006 was disappointing and brought into sharper focus the need to
transform Pfizer over time to succeed in a dynamic healthcare marketplace. We
are reviewing every aspect of our business ...
161. As reported by the Associated Press on January 22, 2007, Pfizer also announced
that it would cut 10,000 jobs and close five facilities after "[p]ressure on Pfizer ... intensified
since safety issues forced it to halt development of the star drug in its pipeline, which was slated
to replace Lipitor as it loses patent protection as early as 2010:"
PFIZER TO LAY OFF 10,000, CLOSE PLANTS IN COST-CUTTING MOVES
- Pfizer Inc., struggling with fierce competition from makers of generic drugs,
announced Monday it will cut 10, 000 jobs and close at least five facilities as part
of an effort to slash its annual costs by up to $2 billion by the end of next year
The latest cuts come on top of a previously announced plan to slash costs by $4
billion a year by 2008. On Monday, Pfizer said it would cut an additional $500
million to $1 billion in costs. However, it said some of the savings would be
redeployed into the company so the total savings would be between $1.5 billion
and $2 billion a year.
The 10,000 layoffs amount to about 10 percent of the company's global work
force and include the elimination of 2,200 jobs from the U.S. sales force, which
Pfizer announced late last year. The company said Monday it would cut 20
percent of its European sales force but didn't say how many jobs that will be.
Pfizer will close three research sites in Michigan and two manufacturing plants in
New York and Nebraska. It may also sell another manufacturing site in Germany
and close research sites in Japan and France.
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Aside from outlining cuts, Pfizer also detailed how it would restructure its
business in an effort to become more nimble and flexible. The U.S. commercial
business will be divided into five distinct units, each with a general manager
responsible for that group's performance. Two research areas are being
abandoned while other research and development efforts are being consolidated.
Pressure on Pfizer has intensified since safety issues forced it to halt
development of the star drug in its pipeline, which was slated to replace Lipitor
as it loses patent protection as early as 2010.
(Emphasis supplied).
ADDITIONAL SCIENTER ALLEGATIONS
162. As alleged herein, defendants acted with scienter in that defendants knew that the
public documents and statements issued or disseminated in the name of the Company were
materially false and misleading:
(a) Defendants' intentional conduct or severe recklessness is reflected in the
fact that many of their challenged statements were directly contradicted by actual study results,
for example, that HDL-c increases caused by torcetrapib 's CETP inhibition could increase RCT
and that increased blood pressure was "not an issue," and the increase in blood pressure did not
change the clinical efficacy of torcetrapib . (¶¶ 44, 77-87).
(b) Pfizer believed internally but failed to disclose that the increased blood
pressure side effect was due to one of torcetrapib ' s metabolites inhibiting MAO. (¶¶ 44, 85-87).
(c) Pfizer failed to disclose that it was warned early in the clinical trials that
the mechanism of CETP inhibition would " accelerate atherosclerosis ." (¶¶ 44, 63-76).
(d) Pfizer intentionally established endpoints for the Phase II trial of increased
HDL-c in order to ensure that the endpoints would be obtained, knowing full well that such
endpoints (given the mechanism by which torcetrapib leads to increased HDL) potentially were
associated with increased coronary heart risk. (¶¶ 100-102).
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(e) Pfizer intentionally violated AHA Rules in order to pre-announce its Phase
III clinical results in order to "spin" the adverse blood pressure side effect results found therein.
(¶¶ 142-44).
(f) Pfizer knowingly designed the torcetrapib Phase III trials to allow the trial
to continue until an unreasonably high statistical certainty was met to determine that deaths were
caused by torcetrapib and not chance. (¶¶ 88-98).
LOSS CAUSATION/ECONOMIC LOSS
163. During the Class Period, as detailed herein, defendants engaged in a scheme to
deceive the market and a course of conduct that artificially inflated the prices of Pfizer's
securities and operated as a fraud or deceit on Class Period purchasers of Pfizer's securities by
failing to disclose the truth about torcetrapib. Defendants' false and misleading statements had
the intended effect and caused Pfizer's common stock to trade at artificially inflated levels
throughout the Class Period, reaching as high as $28.59 per share on October 3, 2006. As a
direct result of defendants' disclosures on December 2, 2006, Pfizer's common stock price fell
precipitously. This price decline removed inflation from the price of Pfizer's securities, causing
real economic loss to investors who had purchased the Company's securities during the Class
Period. As a result of their purchases of Pfizer's securities during the Class Period, Plaintiffs and
the other Class members therefore suffered economic loss, i.e., damages under the federal
securities laws.
164. By failing to disclose the truth about torcetrapib, Defendants presented a
misleading picture of Pfizer's operations and financial performance. Thus, instead of disclosing
during the Class Period the truth about Pfizer's operations and financial performance,
Defendants concealed the truth.
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165. The approximate 11% decline in the price of Pfizer's common stock after these
disclosures came to light was a direct result of the nature and extent of defendants ' fraud finally
being revealed to investors and the market. The timing and magnitude of Pfizer's common stock
price declines negate any inference that the loss suffered by Plaintiffs and the other Class
members was caused by changed market conditions, macroeconomic or industry factors or
Company-specific facts unrelated to the defendants' fraudulent conduct. The economic loss, i.e.,
damages, suffered by Plaintiffs and the other Class members was a direct result of Defendants'
fraudulent scheme to artificially inflate the prices of Pfizer's securities and the subsequent
significant decline in the value of Pfizer's securities when Defendants' prior misrepresentations
and other fraudulent conduct were revealed.
APPLICABILITY OF PRESUMPTION OF RELIANCE:
FRAUD ON THE MARKET DOCTRINE
166. At all relevant times, the market for Pfizer's securities was an open and efficient
market for the following reasons , among others:
(a) Pfizer's securities met the requirements for listing, and was listed and
actively traded on the NYSE, a highly efficient and automated market;
(b) as a regulated issuer, Pfizer filed periodic public reports with the SEC and
the NYSE;
(c) Pfizer regularly communicated with public investors via established
market communication mechanisms, including through regular disseminations of press releases
on the national circuits of major newswire services and through other wide-ranging public
disclosures, such as communications with the financial press and other similar reporting services;
and
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(d) Pfizer was followed by several securities analysts employed by major
brokerage firms who wrote reports which were distributed to the sales force and certain
customers of their respective brokerage firms. Each of these reports was publicly available and
entered the public marketplace.
167. As a result of the foregoing, the markets for Pfizer's securities promptly digested
current information regarding Pfizer from all publicly available sources and reflected such
information in the prices of the securities. Under these circumstances, all purchasers of Pfizer's
securities during the Class Period suffered similar injury through their purchase of Pfizer's
securities at artificially inflated prices and a presumption of reliance applies.
NO SAFE HARBOR
168. The statutory safe harbor provided for forward-looking statements under certain
circumstances does not apply to any of the allegedly false statements pleaded in this complaint.
Many of the specific statements pleaded herein were not identified as "forward-looking
statements" when made. To the extent there were any forward-looking statements, there were no
meaningful cautionary statements identifying important factors that could cause actual results to
differ materially from those in the purportedly forward-looking statements . Alternatively, to the
extent that the statutory safe harbor does apply to any forward-looking statements pleaded
herein, defendants are liable for those false forward-looking statements because at the time each
of those forward-looking statements was made, the particular speaker knew that the particular
forward-looking statement was false, and/or the forward-looking statement was authorized
and/or approved by an executive officer of Pfizer who knew that those statements were false
when made.
65
169. Plaintiffs repeat and reallege each and every allegation contained above as if fully
set forth herein.
170. During the Class Period, defendants carried out a plan, scheme and course of
conduct which was intended to and, throughout the Class Period, did: (i) deceive the investing
public regarding Pfizer's business, operations, management and the intrinsic value of Pfizer
securities ; and (ii) cause Plaintiffs and other members of the Class to purchase Pfizer' s securities
at artificially inflated prices. In furtherance of this unlawful scheme, plan and course of conduct,
defendants, and each of them, took the actions set forth herein.
171. Defendants: (a) employed devices, schemes, and artifices to defraud; (b) made
untrue statements of material fact and/or omitted to state material facts necessary to make the
statements not misleading; and (c) engaged in acts, practices, and a course of business which
operated as a fraud and deceit upon the purchasers of the Company's securities in an effort to
maintain artificially high market prices for Pfizer's securities in violation of Section 10(b) of the
Exchange Act and Rule I Ob-5. All defendants are sued either as primary participants in the
wrongful and illegal conduct charged herein or as controlling persons as alleged below.
172. Defendants, individually and in concert, directly and indirectly, by the use, means
or instrumentalities of interstate commerce and/or of the mails, engaged and participated in a
continuous course of conduct to conceal adverse material information about the business,
operations and future prospects of Pfizer as specified herein.
173. Defendants employed devices, schemes and artifices to defraud, while in
possession of material adverse non-public information and engaged in acts, practices, and a
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course of conduct as alleged herein in an effort to assure investors of Pfizer's value and
performance and continued substantial growth, which included the making of, or the
participation in the making of, untrue statements of material facts and omitting to state material
facts necessary in order to make the statements made about Pfizer and its business operations and
future prospects in the light of the circumstances under which they were made, not misleading,
as set forth more particularly herein, and engaged in transactions, practices and a course of
business which operated as a fraud and deceit upon the purchasers of Pfizer's securities during
the Class Period.
174. Each of the Individual Defendants' primary liability, and controlling person
liability, arises from the following facts: (i) the Individual Defendants were high-level executives
and/or directors at the Company during the Class Period and members of the Company's
management team or had control thereof, (ii) each of these defendants, by virtue of his
responsibilities and activities as a senior officer and/or director of the Company was privy to and
participated in the creation, development and reporting of the Company's internal budgets, plans,
projections and/or reports; (iii) each of these defendants enjoyed significant personal contact and
familiarity with the other defendants and was advised of and had access to other members of the
Company's management team, internal reports and other data and information about the
Company's finances, operations, and sales at all relevant times; and (iv) each of these defendants
was aware of the Company's dissemination of information to the investing public which they
knew or recklessly disregarded was materially false and misleading.
175. Defendants had actual knowledge of the misrepresentations and omissions of
material facts set forth herein, or acted with reckless disregard for the truth in that they failed to
ascertain and to disclose such facts, even though such facts were available to them. Such
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material misrepresentations and/or omissions by defendants were done knowingly or recklessly
and for the purpose and effect of concealing Pfizer's operating condition and future business
prospects from the investing public and supporting the artificially inflated price of its securities.
As demonstrated by defendants' overstatements and misstatements of the Company's business,
operations and earnings throughout the Class Period, defendants, if they did not have actual
knowledge of the misrepresentations and omissions alleged, were reckless in failing to obtain
such knowledge by deliberately refraining from taking those steps necessary to discover whether
those statements were false or misleading.
176. As a result of the dissemination of the materially false and misleading information
and failure to disclose material facts, as set forth above, the market prices of Pfizer's securities
were artificially inflated during the Class Period. In ignorance of the fact that market prices of
Pfizer's publicly-traded securities were artificially inflated, and relying directly or indirectly on
the false and misleading statements made by defendants, or upon the integrity of the market in
which the securities trade, and/or on the absence of material adverse information that was known
to or recklessly disregarded by defendants but not disclosed in public statements by defendants
during the Class Period, Plaintiffs and the other members of the Class acquired Pfizer securities
during the Class Period at artificially high prices and were damaged thereby.
177. At the time of said misrepresentations and omissions , Plaintiffs and other
members of the Class were ignorant of their falsity, and believed them to be true. Had Plaintiffs
and the other members of the Class and the marketplace known the truth regarding Pfizer's
financial results, which were not disclosed by defendants, Plaintiffs and other members of the
Class would not have purchased or otherwise acquired their Pfizer securities, or, if they had
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acquired such securities during the Class Period, they would not have done so at the artificially
inflated prices which they paid.
178. By virtue of the foregoing, defendants have violated Section 10(b) of the
Exchange Act, and Rule 10b-5 promulgated thereunder.
179. As a direct and proximate result of defendants' wrongful conduct, Plaintiffs and
the other members of the Class suffered damages in connection with their respective purchases
and sales of the Company's securities during the Class Period.
COUNT II
Violation of Section 20(a) Of
The Exchange Act Against The Individual Defendants
180. Plaintiffs repeat and reallege each and every allegation contained above as if fully
set forth herein.
181. The Individual Defendants acted as controlling persons of Pfizer within the
meaning of Section 20(a) of the Exchange Act as alleged herein. By virtue of their high-level
positions, and their ownership and contractual rights, participation in and/or awareness of the
Company's operations and/or intimate knowledge of the false financial statements filed by the
Company with the SEC and disseminated to the investing public, the Individual Defendants had
the power to influence and control and did influence and control, directly or indirectly, the
decision-making of the Company, including the content and dissemination of the various
statements which plaintiff contends are false and misleading . The Individual Defendants were
provided with or had unlimited access to copies of the Company's reports, press releases, public
filings and other statements alleged by Plaintiffs to be misleading prior to and/or shortly after
these statements were issued and had the ability to prevent the issuance of the statements or
cause the statements to be corrected.
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182. In particular, each of these defendants had direct and supervisory involvement in
the day-to-day operations of the Company and, therefore, is presumed to have had the power to
control or influence the particular transactions giving rise to the securities violations as alleged
herein, and exercised the same.
183. As set forth above, Pfizer and the Individual Defendants each violated Section
10(b) and Rule lob-5 by their acts and omissions as alleged in this Complaint. By virtue of their
positions as controlling persons, the Individual Defendants are liable pursuant to Section 20(a) of
the Exchange Act. As a direct and proximate result of defendants' wrongful conduct, Plaintiffs
and other members of the Class suffered damages in connection with their purchases of the
Company's securities during the Class Period.
WHEREFORE , Plaintiffs pray for relief and judgment, as follows:
A. Determining that this action is a proper class action, designating Plaintiffs as Lead
Plaintiffs and certifying Plaintiffs as class representatives under Rule 23 of the Federal Rules of
Civil Procedure and Plaintiffs' counsel as Lead Counsel;
B. Awarding compensatory damages in favor of Plaintiffs and the other Class
members against all defendants, jointly and severally, for all damages sustained as a result of
defendants' wrongdoing, in an amount to be proven at trial, including interest thereon;
C. Awarding Plaintiffs and the Class their reasonable costs and expenses incurred in
this action, including counsel fees and expert fees; and
D. Such other and further relief as the Court may deem just and proper.
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JURY TRIAL DEMANDED
Plaintiffs hereby demand a trial by jury.
DATED: New York, New York
April 2, 2006
SCHOENGOLD SPORN LAITMAN &
LOMETTI, P.C.
/s/ Samuel P. S p orn
Samuel P. Sporn (SS-4444)
Joel P. Laitman (JL-8177)
Christopher Lometti (CL-9124)
Jay P. Saltzman (JS-7335)
Ashley Kim (AK-0105)
Frank R. Schirripa (FS-1960)
19 Fulton Street, Suite 406
New York, New York 10038
Telephone: (212) 964-0046
Facsimile (212) 267-8137
Attorneys for Plaintiffs
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GLOSSARY OF TERMS
AHA American Heart Association
apoA-1 apolipoprotein A-I, a lipoprotein which can attach lipids (or fatty
molecules). ApoA-1 is characteristically contained in HDL particles It
functions to collect cholesterol like a dump truck from the arterial wall;
and is involved in direct release of cholesterol into the liver.
apoB apolipoprotein B, a lipoprotein which can attach lipids (or fatty
molecules). ApoB is characteristically contained in LDL particles, and
is involved in the transfer of cholesterol from HDL particles to LDL
particles; and from LDL particles to the liver.
ATVB Arterial Thrombosis and Vascular Biology (medical research and
scientific journal)
BP blood pressure
CETP cholesteryl ester transfer protein; the enzyme which transfers a form of
cholesterol between LDL and HDL, among other functions; thought to
play a key role in reverse cholesterol transport
CETPi Inhibitor of cholesteryl ester transfer protein (CETP), for instance,
torcetrapib
CAD or CHD Coronary artery disease or coronary heart disease; narrowing of the
blood vessels that supply blood to the heart; synonymous with ischemic
heart disease (II-ID); typically caused in part by atherosclerosis
CVD cardiovascular disease; covers a wide array of disorders, including
diseases of the cardiac muscle, the vascular system supplying the heart,
brain, and
other vital organs; venous thromboses; stroke; etc.
DSMB data safety monitoring board: committee permitted to examine
unblinded data during a clinical trial for ethical and safety purposes
FDA Food and Drug Administration
HDL high density lipoprotein, characterized as the dump truck which
accumulates cholesterol from the arterial wall and sends it to the liver
HDL-c cholesterol attached to high density lipoprotein; the parameter which is
correlated with low cardiovascular risk in normal people; also known as
"good cholesterol"
Case 1-06-cv-14199-LAK Document 9 Filed 04/02/2007 Page 73 of 75
IHD ischemic heart disease, equivalent to ischemic cardiomyopathy: damage
to heart muscles caused by insufficient blood supply; typically caused in
part by atherosclerosis
LDL low density lipoprotein, best known for its role in transporting
cholesterol to the artery where it deposits cholesterol in a
proatherogenic role, LDL also plays a role in reverse cholesterol
transport, accepting cholesterol from HDL particles and carrying it to
the liver
LDL-c cholesterol attached to low density lipoprotein; the parameter which is
correlated with high cardiovascular risk in normal people; also known
as "bad cholesterol"
MAO monoamine oxidase , an enzyme that breaks down hormones like
adrenaline or drugs like dextromethorphan . Inhibition of MAO by drugs
is dangerous and can cause constriction of blood vessels, increased
blood pressure , and fatal strokes and heart attacks
NEJM New England Journal of Medicine, a medical research journal
Outlier For a set of numerical data, any value that is markedly smaller or larger
than other values.
P index of confidence in a result's statistical significance, i.e., not being
due to chance
Phase I clinical Experiment in humans intended to determine safety and examine
trial metabolism of drugs
Phase II clinical Experiment in humans intended to test efficacy in target population
trial
Phase III clinical Large scale, multicenter clinical trial intended to establish efficacy of
trial new drug, usually compared to reference drug
RCT reverse cholesterol transport; the combination of steps by which
cholesterol is moved from potential or actual atherosclerotic plaques to
the liver for excretion; an important pathway which scientists believe
will cause atherosclerotic plaques to regress
SAE serious adverse event - medical event that could be an adverse effect of
a drug that can alter quality of life; these must be reported promptly to
FDA and are important safety parameters in clinical trials
SBP systolic blood pressure; the higher of the two blood pressure readings,
which is more closely related to cardiovascular risk
2
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UNITED STATES DISTRICT COURT
SOUTHERN DISTRICT OF NEW YORK
IN RE PFIZER INC. : MASTER FILE No. 06-CV-14199
SECURITIES LITIGATION : AND RELATED CASES
-------------------------------------------------------------x
THIS DOCUMENT RELATES TO:
ALL CASES
CERTIFICATE OF SERVICE
I, FRANK R. SCHIRRIPA, one of the counsel for Lead Plaintiff, Uniformed
Sanitationmen's Association Compensation Accrual Fund and, Additional Named Plaintiff,
Teamsters Local 617 Welfare & Pension Funds, hereby certify that on April 2, 2007, I filed the
Amended Class Action Complaint with the Clerk of the Court, electronically mailed a copy to
the Clerk of the Court and served a copy of said document by hand on the following:
Dennis Block, Esq.
Martin L. Seidel, Esq.
Cadwalader, Wickersham & Taft LLP
One World Financial Center
New York, NY 10281
/s/ Frank R. Schirri
Frank R. Schirripa
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