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     ANTI-AGE      exfoliating cream
          AHA’s and Vitamin C

 They are also named fruit acids.

 AHA’s are organic carboxylic acids having one hydroxyl group attached to the alpha position of
 the carboxylic carbon atom.

 Many AHA’s are naturally occurring, are present in body tissues, and can be considered non-

 A few commonly known ones are as follows :

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     glycolic acid is a constituent of sugar cane juice
     Lactic acid occurs in sour milk and tomato juice

     Malic acid occurs in apples
     Tartaric acid occurs in grapes and wine
 •   Citric acid occurs in citrus fruit and pineapples
 •   Gluconic acid is present in skin tissue

 Acid strength
     •   The relative strength of an acid is measured by its proton dissociation in solution and is
         expressed as the pKa of the acid.
     •   Since the pKa is a negative log ; an acid is stronger if its pKa number is lower.
     •   AHA’s remain moderate strength acids.

 Partial neutralization / buffered acid
     •   A formulation containing AHA without neutralization has a very acidic pH. Although pH
         varies with both concentration and the specific acid used, decreasing quantity does not
         raise pH significantly.
     •   Bear in mind that the normal skin surface has a pH of 4.2 to 5.6.
     •   Partial neutralization refers to an acid partly mixed with a base.
     •   Indeed there is no direct correlation between the pH of a product and the acid
         concentration of the product.

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                           Topical effects of AHA’s
 Effect on epidermis
     •   AHA’s have a strong effect on keratinization. They act on the lowest levels of the
         stratum corneum, and modulate its formation by diminishing cellular cohesion between
         corneocytes. (light exfoliation), leading to a decrease the stratum corneum’s thickness.
     •   Studies have shown that non AHA compounds do not have similar action.
     •   The elasticity of the stratum corneum depends of its water content and AHA’s can
         increase this capacity; thus improving epidermic hydration .
     •   AHA’s are cell stimulants (by accelerating cell division).

 Effect on dermis
     •   Some AHA’s, especially glycolic, lactic and citric acids, on topical application to photo-
         aged skin have been shown to produce increased amounts of mucopolysacharides
         (synthesis of glycosaminoglycanes) and collagen and increased skin thickness.
     •   Such an action comes from « boosting » the fibroblast activity, which helps stimulate
         synthesis of new collagen and mucopolysacharides.

                         Applications in dermatology
 Medical 3 days remove your acnes!
Only applications
     prevention and flattening of acne scars
 •   seborrheic keratosis
 •   keratosis follicularis
 •   acne vulgaris
 •   combined with antibiotics, fungicides, tretinoin, etc.

 Cosmetic applications
 •   Fine lines
 •   Impure skin (combined with vitamins)
 •   Pigmented marks (combined with skin discoloration fade cream
 •   Ingrowing hairs, etc…

                                      AHA’s and vitamin C

     New formulation facial skin cream containing AHA’s, 40 ml plastic tube

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     FLOXIA                                              and oily skin

  This skin disorder is caused both by hyperkeratinization
       of the sebaceous canal and by hyperseborrhea
  (overproduction of oil by the sebaceous glands that open
   into the hair follicle), which may lead to inflammation.

  Hyperseborrhea (primary condition : no acne without it)
 Increase in androgens (sex hormones that stimulate the oil glands and are produced in greater
 quantity in males than females).
 It has been explained above how androgenic hormones act.
 Sebaceous glands have special enzymatic " equipment " : 5 alpha reductase. (able to transform
 testosterone(T) into di-hydro-testosterone.(DHT), active hormone on lipogenesis by sebocyte.

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  The following will lead to aggravation of acne :
 * Hereditary factors

 * Medications (cortisone, barbiturates,bromides, ….)
 * Oil and grease from cosmetics
 * Menstruation preceded by changes in hormonal status
 * Emotional stress and tension

 Hyperkeratinization (second condition, hyperseborrhea without it leads to oily skin)
 Many of the desquamating cells, instead of being pushed out to the surface with the sebum,
 stick together and can block the canal around the infundibulum level.
 Such accumulation will end up blocking the canal. This is a microcokyste (closed comedon), or
 open comedon(black head).
 Such a change is mainly due to the qualitative modification of the composition of cutaneous
 lipids. A decrease in linoleic acid of the ceramides of the inter cell cement, especially at the acro
 infundibulum level is today considered to be responsible for keratinization disorder.
 Problems in keratinization (hyperkeratosis), responsible for sebum retention, and also related to
 irritant action of free fatty acids produced by lipase in P acne.

 Inflammation (pustules and papules) seen with acne may arise from :
 Proprioni bacterium (normally present in the skin), being aneorobic (develop without oxygen)
 these will easily develop inside the closed comedon.
 4 effects of P Acne :
     • Production of protease (downgrading the keratin)
     • Production of lipase (hydrolysing sebum is irritating : free fatty acids)
     • Cytoquines
     • Hyaluronidase downgrading intercell cement.

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 Comedogenesis ;
 This is an abnormality in the process of desquamation of follicular corneocytes in the sebaceous
 follicle duct.
 Most commons signs of acne are :
 Micro comedones: 1st stage, blockage of the folicular orifice by sloughing epithelium.
 Closed comedones (blackheads)
 Open comedones (microkyste or whiteheads)
 Papules or zits (inflammed firm lesions and pimples)
 Pustules (when sebum and bacteria spill onto the dermis (yellowish lesion), as white
 cells invade the area to attack bacteria.)
                                    Pathogenesis and treatment
 Results from 3 abnormalities :
 • Overproduction of sebum (hormonal dependent)
 • Keratinacious factor. Abnormal desquamation of corneocytes of the sebaceous follicle
 • Proliferation of P acne, which may generate inflammation.

  Local / topical treatments
 Anti bacterial (cream, gel, lotion, soap, …..)
 * Most commonly used acne medication is benzoyl peroxyde, anti inflammatory (first line mono
 therapy for mild acne). It is a potent anti bacterial oxidising agent, can decrease P acne and
 consequently the amount of free fatty acids. It is said that light exfoliant properties can also

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 unplug obstructed follicles…..(no real study). Side effects : irritation and photosensisitivity.
 * Erythromycin Antibiotic agent beware induced resistance. Side effects : resistance

 Keratolitic preparations :
 * Tretinoin cream, gel or liquid (Vit –A, retinoic acid).
 Trans retinoic acid is an effective topical comedolytic agent. Tretinoin decreases the
 cohesiveness of follicular epithelial cells, thus inhibiting the formation of microcomedones. Also
 decreases thickness of stratum corneum and improves penetration of topical agents. Tretinoin is
 available as retin-A cream, or liquid. Side effects are : irritative, drying skin, possible
 * Adapalene(said to be similar to Vit A, with better tolerance),
 * Azelaic acid (natural product , but showing poor results)
 * Topical anti-androgens (zinc sulphate)
 * AHA’s(glycolic, lactic, …) and BHA’s (salycilic acid) : for exfoliating action of corneocytes
 towards comedons
 Systemic / oral treatments
 * Antibiotics : Bacteriostatic action and anti inflammatory. tetracycline, minocycline, Main side
 effects : phototosensibility , pigmentation disorder, toxidermy, …
 * Hormonal treatments : estrogen, spironolactone.
 * Isotretinoin = 13 acid cis-retinoic = Roaccutane) : derivative from vitamin A ; the only systemic
 drug able to decrease sebum production and reverses the abnormal epithelial desquamation
 Action is atrophy of sebaceous gland, which obviously decreases sebum over production. Also
 decrease P acnes bacterias. Sebo regulator and thus anti inflammatory.
 Often side effects : dry skin, pruritus, photosensivity, cheilitis, teratogenous effects, ….
 * Zinc sulfate or gluconate. Mainly anti inflammatory agent.
 Cosmetic products
 Main products are creams and washing lathering gel

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 Creams may be used alone with acne prone skin, or in association with products mentioned above.
 Such products generally perform the following actions :
 Acne, whatever its severity, is a disease that requires dermatological care ; nevertheless added
 cosmetic products are considered to be more and more useful by physicians (help preventing
 disorder or complete efficiency of drug).
 Skin cleansing :For acne prone skin, it means removal from surface of debris and excess skin
 surface lipids, without irritating or drying the skin. Aggressive soap would remove too much
 lipidic skin film, and lead to a reactional hyperseborrhea. Purifying gels are increasingly
 recommended by doctors for daily use (pH close to skin).

                “Les incontournables – the essentials” -                Cream : 40 ml plastic tube
 Double action on skin surface and deeper
         to regulate the production of sebum
   and restaure the natural aspect of the epidermis
 Medical treatments are mainly focusing on hyperkeratinization and inflamation, but less busy
 with sebum control. Therefore FLOXIA decided to help getting oil under control, on surface and
 in the epidermis;

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                                                double action

         On skin surface
 keratolytic with a mix of AHA’s
 Matting with titanium dioxyde
 Seboregulating: zinc gluconate, ceramides and latoferin-lacteine
 Soothing: calendula, bisabolol and tea tree oil

 NOURISH:                    Restore natural properties to epidermis with shea butter and beeswax

                                             Bibliography :
 Yamamoto A, Takenouchi, Ito. Impaired water barrier function in acne vulgaris Arch Dermato Res 1995 (287)
 Wertz, Miethke, Long, Strauss : Composition of the ceramides from human stratum / J Inv Dermatol 1985 (84)
 corneum and from comedons
 James Leyden New understanding of the pathogenesis of acne / J Am Acad Dermato 1995 (32)
 Downing, Stewart, Werth, Strauss : Essential fatty acids and acne / J Am Acad Dermatol 1986, (14)
 Stewart, Werth, Grahek, Downing : Relation ship between sebum secretion rates and Clin research 1985, (33)
 concentration of linoleate in sebum and epidermal lipids
 Thiboutot, Knacks, Gilliland : Activity of the type 5 & reductase is greater in Br J Dermatology , in press infudibulum
 than epidermis

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                 Skin discoloration fade cream
 FLOXIA : History
 During the last decade, treatment of hyperpigmented skin spots has been focusing on
 hydroquinone, due to its well-known depigmenting, and often associated with AHA’s
 (exfoliation of the stratum corneum, i.e. improve to eliminate the melanin contained in the
 keratynocytes moving upwards).
 A few years ago, various European experts discussed the possible toxicity of hydroquinone in
 topical application, and especially in vitro studies on a mutagenic point of view. This leaded to its
 banishment from cosmetic use in EEC and many countries around the world

 FLOXIA: composition and action.
 To find a substitute for hydroquinone, an already «advanced » ingredient was not an easy task.
 Indeed, only an association of active and synergistic ingredients could meet the necessary
 A long bibliographic overview, together with various studies and tests enabled FLOXIA to

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 complete its expertise in the area, and decide onn the following ingredients combination by
 selecting known depigmenting agents associated with ingredients for sun protection and
 epidermis nutriment and protection, and also limiting pH around 4.6 for stability and confort

 Still these ingredients had proven in vitro activity, but in vivo studies never show the same rate
 of sucess; which intend to show various origins for the hyperpigmentation, but also different
 grade of answer from every one epidermis. Therefore Floxia decided to go for an association of
 active ingredients, in order to cover most origins and generate an answer from a larger number
 of epidermis.
 The ingredients have been selected for their efficacy, confort and harmlessness; and are
 the following:

                         Depimenting agents
                                  Bearberry extracts, kojic acid,
                             licorice extract, ascorbic acid and AHA’s

                               Sun protection
                                      Cinnamate (4%): SPF 15

                 Nutriment and potection
                                 Shea butter, sodium hyaluronate
                                    apricot and grape seed oil

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                                 DEPIGMENTING AGENTS
 Rich in arbutin (glucoside flavonoide derivative, stable, natural and non aggressive). Arbutin
 competes with DOPA at its receptor site on tyrosinase and thus has 2 actions versus
 Able to chemically reduce melanin produced by melanocytis and leading to produice non coloured
 Furthermore, it shows a competitive inhibition of tyrosinase

 KOJIC ACID (0.5%): obtained from fermentation of aspergillus orizae, it has an inhibiting
 action on tyrosinase, by chelating its vital copper ion.
 Concentration has been purposely limited (for stability and harmlessness reason)

 ASCORBIC ACID (0.2%): Vitamin C has various properties with regards to cutaneous
 metabolism, and especially a depigmenting action due to its inactivating power of the tyrosinase
 by biotransformation of the dopaquinone into dopa at the level of the melanosomes, i.e. stopping
 the synthesis of melanin The inactivation of the copper ion, necessary for the effective
 functioning of tyrosinase, by the ascorbic acid, is also discussed to explain its action.

 It offers an excellent turosinase inhibition activity and also showing anti inflamatory properties

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 AHA (pH 4.7): The new formula of FLOXIA uses various AHA’s (citric and malic). With its

 progressive release, it results in better acceptance and less potential irritation, whilst still
 improving the bioavailibility of the depigmenting ingredients due to the exfoliating action.

                                    SUN PROTECTION
 Cinnamate with an SPF 15, for an immediate minimum sun protection

 Nourishing: shea butter
 Anti-oxydating: apricot oil (free radical scavenger)
 Scaring: grape seed oil
 Moisturizing: sodium hyaluronate

                     Skin depigmenting agents
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 Depigmenting agents commonly are prescribed to treat disorders of hyperpigmentation. In this
 article, a review is presented of several notable depigmenting agents reported in the literature.
 Although some of these topical agents are still available only in certain research institutions,
 others can be used by the interested and informed dermatologist as part of an armamentarium
 for treating disorders of hyperpigmentation.

 A basic understanding of the pigmentation pathway is helpful prior to a discussion of various
 skin-lightening agents and their known mechanisms of action. The type and amount of melanin
 synthesized by the melanocyte and its distribution pattern in the surrounding keratinocytes
 determines the actual color of the skin. Melanin forms through a series of oxidative reactions
 involving the amino acid tyrosine in the presence of the enzyme tyrosinase.

 The first step is the most critical because the remainder of the reaction sequence can proceed
 spontaneously at physiological pH. Here, tyrosinase converts tyrosine to dihydroxyphenylalanine
 (DOPA) and then to dopaquinone. Subsequently, dopaquinone is converted to dopachrome,
 through auto-oxidation, and finally to dihydroxyindole or dihydroxyindole-2-carboxylic acid
 (DHICA) to form eumelanin (brown-black pigment). The latter reaction occurs in the presence of
 dopachrome tautomerase and DHICA oxidase. In the presence of cysteine or glutathione,
 dopaquinone is converted to cysteinyl DOPA or glutathione DOPA. Subsequently, pheomelanin, a
 yellow-red pigment, is formed.

 Among skin-lightening agents, hydroquinone (HQ) is one of the most widely prescribed agents in
 the world. However, with reports of potential mutagenicity and epidemics of ochronosis in
 African nations, there has been increasing impetus to find alternative herbal and pharmaceutical

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 depigmenting agents. A review of the literature reveals that numerous other depigmenting or
 skin-lightening agents are in use or in investigational stages. Some of these, such as kojic and

 azelaic acid, are well known to most dermatologists. Others more recently have been discovered
 and reported in the literature.

 Melasma is a commonly acquired increase of pigmentation that occurs exclusively in sun-exposed
 areas. Brownish in color, it is exacerbated by sun exposure, pregnancy, oral contraceptives, and
 certain                                    anti-epilepsy                                  drugs.

 Melasma is reasonably common, especially in women of child-bearing age. However, up to 10% of
 cases have been reported in males. While all races are affected, there is a prominence among
 Latinos and Asians. Melasma is more apparent during and after periods of sun exposure and less
 obvoius in winter months, when sun exposure is lacking.

 Melasma presents itself in one of the three usually symetrical facial patterns. The most common
 is a centrofacial pattern involving the cheeks, forehead, upper lip, nose, and chin. Less common
 are the malar pattern, involving the cheeks and nose, and the mandibular pattern, involvong the
 ramus of the mandible (the side of the cheeks and jawline). Melasma also occurs on the
 forearms, but this is rare.

 What is the Difference between Dermal and Epidermal Melasma? Every case of melasma starts
 off in the epidermis, where melanocytes are actively producing pigment. A normal case of
 melasma can turn into dermal melasma if skin becomes over-irritated and inflamed. When this
 happens, it causes a temporary split between the dermis and epidermis. During this time,
 hyperpigmented cells can drop from the epidermis into the dermis. Once in the dermis, these
 cells become very resistant to topical treatment. This is one reason why it is so important to
 avoid aggressiveness in the treatment of melasma.

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 What are the Causes of Melasma?Melasma has been considered to arise from pregnancy, oral
 contraceptives, endocrine dysfunction, genetic factors, medications, nutitional deficiency,
 hepatic dysfunction, and other factors. The majority of cases appear to be related to pregancy
 or oral contraceptives. The infrequency of melasma in postmenopausal women on estrogen
 replacement suggests that estrogen alone is not the cause. In more recent experience,
 combination treatment using estrogen plus progestational agents is being used in postmenopausal
 women, and melasma is being observed in some of these older women who did not have melasma
 during their pregnancies. Sun exposure would appear to be a stimulating factor in predisposed
 individuals. Although a few cases within families have been describe, melasma should not be
 considered a heriditary disorder.

                          List of depigmenting agents

 An important industrial chemical, HQ is also a ubiquitous chemical readily available in cosmetic
 and nonprescription forms for skin lightening. It is considered one of the most effective
 inhibitors of melanogenesis in vitro and in vivo. HQ causes reversible inhibition of cellular
 metabolism by affecting both DNA and RNA synthesis. The cytotoxic effects of HQ are not
 limited to melanocytes, although the dose required to inhibit cellular metabolism is much higher
 for nonmelanotic cells than for melanocytes. Thus, HQ can be considered a potent melanocyte
 cytotoxic agent with relatively high melanocyte-specific cytotoxicity. HQ is also a poor

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 substrate of tyrosinase, thereby competing for tyrosine oxidation in active melanocytes.

 The 2% HQ is readily available over-the-counter in various cosmetic preparations. However, for
 better efficacy, it often is compounded into various mixtures for treatment of
 hyperpigmentation. The original Kligman formula involves compounding 5% HQ with 0.1% retinoic
 acid and 0.1% dexamethasone in a hydrophilic ointment base. Concentrations as high as 10% can
 be compounded extemporaneously for refractory cases. Evidence of improvement with HQ
 (monotherapy) usually is observed at 4-6 weeks, with improvement appearing to plateau at about
 4 months.

 Despite its remarkable overall safety, the physician ought to bear in mind the potential adverse
 effects. Contact dermatitis occurs in a small number of patients and responds promptly to
 topical steroids. An uncommon, yet important, adverse effect of HQ is exogenous ochronosis.
 This disorder is characterized by progressive darkening of the area to which the cream
 containing HQ is applied. Histologically, degeneration of collagen and elastic fibers occurs. This
 degeneration is followed by the appearance of characteristic ochronotic deposits consisting of
 crescent-shaped, ochre-colored fibers in the dermis.

 Exogenous ochronosis generally has been observed in black patients and after use of high
 concentrations of HQ for many years. However, cases occurring after the use of 2% HQ also
 have been reported. A South African epidemic of exogenous ochronosis due to HQ has been
 reported. For this reason, it generally is agreed that the use of HQ should be discontinued if no
 improvement occurs within 4-6 months. HQ-induced ochronosis often responds to topical
 steroids and chemical peeling.

 Lastly, HQ has been reported to induce mutations in Salmonella and at the hart locus of Chinese
 hamster V79 cells. Because of its potential mutagenic properties, HQ currently is banned in
 Europe for use as a depigmenting agent.

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 As indicated above, tretinoin has been used to enhance the efficacy of HQ. In a large-scale,
 double-blind, placebo-controlled study, 0.05% tretinoin caused a decrease in melanin content at
 6 months. Two known inhibitors of glutathione, cystamine and buthionine sulfoximine, also have
 been reported for their enhancement of the inhibitory effect of HQ on pigmentation. The
 authors of the study reported a synergistic decrease in hair pigmentation when a combination of
 HQ (2% or 4%) and buthionine sulfoximine (5%) was applied to the dorsal skin of mice.

 Azelaic acid

 A naturally occurring, saturated dicarboxylic acid originally isolated from Pityrosporum ovale,
 azelaic acid is a rather weak competitive inhibitor of tyrosinase in vitro. In addition, azelaic acid
 has an antiproliferative and cytotoxic effect on melanocytes. The latter effect is because of a
 rather potent inhibition of thioredoxin reductase, an enzyme involved in mitochondrial
 oxidoreductase activation and DNA synthesis.

 Azelaic acid is prescribed topically as a 20% cream and has been combined with glycolic acid
 (15% and 20%), and its efficacy has been compared with HQ 4% in the treatment of facial
 hyperpigmentation in dark-skinned patients. It has been reported that the combination formula
 was as effective as HQ 4% cream, although with a slightly higher rate of local irritation.

 Kojic acid (5-hydoxy-4-pyran-4-one-2-methyl)

 A fungal metabolic product, kojic acid inhibits the catecholase activity of tyrosinase, which is
 the rate-limiting, essential enzyme in the biosynthesis of the skin pigment melanin. Kojic acid

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 also is consumed widely in the Japanese diet with the belief that it is of benefit to health.
 Indeed, it has been shown to significantly enhance neutrophil phagocytosis and lymphocyte
 proliferation stimulated by phytohemagglutinin. Melanocytes treated with kojic acid become

 nondendritic with a decreased melanin content. Additionally, it scavenges reactive oxygen
 species that are released excessively from cells or generated in tissue or blood.

 Kojic acid is used in concentrations ranging from 1-4%. Although effective as a skin-lightening
 gel, it has been reported to have high-sensitizing potential and cause irritant contact dermatitis.
 In a study comparing glycolic acid/kojic acid combination with glycolic acid/HQ, no statistical
 difference in efficacy existed between kojic acid and HQ. However, the kojic acid preparation
 was reported to be more irritating.


 Arbutin (hydroquinone-beta-D-glucopyranoside)

 A glycosylated HQ found at high concentrations in certain plants and capable of surviving
 extreme and sustained dehydration, arbutin has been shown to inhibit melanin synthesis by
 inhibition of tyrosinase activity. This appears to be because of the inhibition of melanosomal
 tyrosinase activity, rather than the suppression of the synthesis and expression of this enzyme.
 Because arbutin does not hydrolyze to liberate HQ, the latter agent is not responsible for the
 inhibitory effect of arbutin on melanogenesis. Inhibition of melanin synthesis (about 39%)
 occurs at a concentration of 5 X 10-5 mol/L. And many manufacturers are marketing arbutin as a
 depigmenting agent. When contacted, these manufacturers report arbutin as an effective
 depigmenting agent at a concentration of 1%.

 Paper mulberry

 This tyrosinase inhibitor was isolated from a plant herbal extract. The plant roots from which
 paper mulberry was isolated were collected in Korea. The authors compared the tyrosinase

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   inhibition of paper mulberry to kojic acid and HQ. IC50, the concentration causing 50% inhibition
   of the activity of tyrosinase, was reported to be 0.396% compared to 5.5% for HQ and 10.0%
   for kojic acid. The authors also performed a patch test using 1% paper mulberry extract and
   found no significant irritation at either 24 hours or 28 hours.

   Glabridin (licorice)

   Glabridin is the main ingredient in licorice extract. The authors investigated glabridin for its
   inhibitory effect on pigmentation and reported that glabridin inhibited tyrosinase activity of
   melanocytes without any cytotoxicity. They further showed that UV-B–induced pigmentation and
   erythema was inhibited by topical application of 0.5% glabridin. The anti-inflammatory
   properties of glabridin were attributed to inhibition of superoxide anion production and
   cyclooxygenase activity.

   Arctostaphylos patula and Arctostaphylos viscida

   The leaves of these 2 Arctostaphylos plants have been reported to be potent inhibitors of
   tyrosinase. These 2 extracts not only inhibited the production of melanin from dopachrome but
   also exhibited superoxide dismutaselike activity. The effective topical concentration of these 2
   plants in disorders of hyperpigmentation currently is not known.

   Magnesium ascorbyl phosphate – Vitamin C derivative

   Magnesium-L-ascorbyl-2-phosphate (MAP) is a stable derivative of ascorbic acid. When used as a
   10% cream, MAP was shown to suppress melanin formation. A significant lightening effect was

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   seen clinically in 19 of 34 patients with melasma and solar lentigos. Furthermore, MAP has been
   shown to have a protective effect against skin damage induced by UV-B irradiation. The latter

   protective effect is because of the conversion of MAP to AS.

 Use of reconstituted tanned epidermis for in vitro testing &

     Whitening effect of              kojic acid on melanin production in reconstituted
   human tanned epidermis (type VI)

   1.2 l of 2 test products is deposited daily onto the surface of the stratum corneum of the
   epidermal tanned tissues of type VI (0.63 cm² surface) for 4 days. 48 hours later (at day 6),
   tissues are assessed for visual scoring and melanin content.
     Topical application of cream containing kojic acid

   Not treated   4 x 2 l 4 x 1.2 l    2 l    1.2 l
     Kojic acid solution added to the medium


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                                                                                 kojic acid
                                                                                 (250 M)


                       without KA              with KA
                       rep+m 1/10             rep+m 1/10

        Kojic acid (250 M) supplemented to the defined culture medium during tissue
   Description of the UV-induced melanogenesis

                                             After 3 consecutive UVA and
                                             UVB exposures, a faint

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                                             coloration of pigmented
                                             epidermis, resulting of the

                                             UVB-induced melanogenesis, can
                                             be observed.

                   -                +
               UVB: 50 mJ/cm² (x3)
                  UVA: 4J/cm² (x3)


  Arbutin is the active substance originated from natural plant which can whiten and lighten skin.
 It can infiltrate into the skin quickly without affecting the concentration of cell multiplication
 and effectively prevent activity of tyrosinase in the skin and the forming of melanin. By
 combined arbutin with tyrosinase, decomposition and drainage of melanin are accelerated, splash
 and fleck can be got ride of and no side effects are caused. It is one of the safest and most
 efficient whitening materials that are popular at present. It is also the most competitive
 whitening activity in the 21st century

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 [Inhibitory effect of arbutin on melanogenesis--biochemical study
 using         cultured        B16         melanoma          cells]
 Akiu        S,      Suzuki      Y,     Asahara        T,        Fujinuma     Y,     Fukuda     M.
 Basic            Research         Laboratories,            Shiseido        Research        Center.

 Inhibitory effect of arbutin (hydroquinone-beta-D-glucopyranoside) on the melanogenesis was
 studied biochemically using cultured B16 melanoma cells. The maximum arbutin concentration
 lacking an inhibitory effect on cell growth was 5 X 10(-5) M. At this concentration, melanin
 content per cell was decreased significantly to about 39%, compared with that of arbutin
 untreated cells. Also, tyrosinase activity of arbutin treated cells was decreased significantly.
 When arbutin was added to B16 melanoma cell suspension, arbutin was not hydrolyzed to liberate
 hydroquinone. Further, tyrosinase activity in crude preparations from B16 melanoma cells was
 inhibited by arbutin. From these results, it is suggested that arbutin can inhibit the
 melanogenesis by affecting not only the synthesis but also the activity of tyrosinase rather than
 by killing melanocytes B16 melanoma cells. Also, it is suggested that hydroquinone is not
 responsible for the inhibitory effect of arbutin on the melanogenesis.

 :   Arbutin: mechanism of its depigmenting action in human melanocyte culture.
 :   J Pharmacol Exp Ther; 276(2):765-9, 1996 Feb.

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 :   Arbutin, a naturally occurring beta-D-glucopyranoside of hydroquinone, is effective in the
     topical treatment of various cutaneous hyperpigmentations characterized by hyperactive
     melanocyte function. We examined the mechanism of its depigmenting action in human

     melanocyte cultures. Arbutin inhibited the tyrosinase activity of cultured human melanocytes
     at noncytotoxic concentrations. It did not affect the expression of tyrosinase mRNA. Melanin
     production was inhibited significantly by arbutin, as determined by measuring eumelanin
     radicals with an electron spin resonance spectrometer. The study of the kinetics and
     mechanism for inhibition of tyrosinase confirms the reversibility of arbutin as a competitive
     inhibitor of this enzyme. The utilization of L-tyrosine or L-dopa as the substrate suggests a
     mechanism involving competition with arbutin for the L-tyrosine binding site at the active site
     of tyrosinase. These results suggest that the depigmenting mechanism of arbutin in humans
     involves inhibition of melanosomal tyrosinase activity, rather than suppression of the
     expression and synthesis of tyrosinase.

                                       VITAMIN C

 Considered stable (low concentration) and is an effective antioxidant for skin. There is a study
 showing it to be effective for lightening skin by inhibiting melanin production (Source: Journal of
 the American Academy of Dermatology, January 1996, pages 29–33). The study concluded that a
 moisturizer with a certain concentration of magnesium ascorbyl phosphate "suppressed melanin
 formation… The lightening effect was significant in 19 of 34 patients with chloasma or senile
 freckles and in 3 of 25 patients with normal skin. This means some 1 to 2% pure vitamin C

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               Depigmenting activity of Vitamin C and its derivatives*
                                          P. MORGANTI1
   Pierfrancesco Morganti* President/Director, R. & D — Mavi Sud S.r.l., Viale dell’lndustria I,
 04011 Aprilia (IT), Italy; Dept. of Internal Medicine, Aesthetic Medicine Training School ,
 University of Rome “Tor Vergata”, Italy; Secretary General, International Society of Cosmetic

 The problem of the cutaneous hyperpigmentation is very common especially in East Asia where
 the concept of beauty is strictly linked to maintain the skin white. By the way
 hyperpigmentations represent a non-secondary problem also in the western world where has
 been recorded a remarkable increase due mostly to the increased usage of anticonceptional pills
 and perfumed products (
 As a matter of fact, both estrogens and fragrances cause the formation of hyperpigmentation
 of the skin usually exposed to the sunrays. For all these reasons, skin pigmentation represented
 by spots is one of the important targets in the cosmetic field. At this purpose, many compounds
 are frequently used as melanogenesis inhibitors such as hydroquinone, azelaic acid, kojic acid,
 arbutin, ellagic acid, rucinol, raspberry ketone glucoside, n-acetylsteine, vitamin C and its

 Furthermore, it has to be underlined the suppressing effect that vitamin C has on melanic
 pigmentation. Until now, because of its known inherent instability, it has not been used in
 cosmetic preparations. Recently, with the constant progress had in vehicles set up, this problem
 has been partly solved by including, for example, the unstable substances in peculiar

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 phospholipids, phosphatidylchiline-rich (PC), able to protect them against the oxidative
 processes even for a long period (

 For all these reasons, the use of vitamin C and its derivatives had a new impulse, and by means of
 the new technologies it has been possible to make vitamin C, which easily oxidizes in dehydro-
 ascorbic acid, more stable (Our work team was able to formulate a depigmenting and active
 cream based on the use of vitamin C and its hydrosoluble derivatives, l-ascorbyl-2-phosphate
 (VC-PMG) a liposoluble derivative, and hexyl-decanoyl-ascorbic acid (VC-IP) (), both already
 largely studied in vitro and in vivo by other authors (.

 Its interesting to underline that the combined activity of the two derivatives demonstrated to
 be strengthened by adding arbutin (which favors notably its depigmenting activity. Furthermore,
 it was possible to show how the sole vitamin C is able to penetrate quickly the skin to reach the
 melanocyte interfering with the melanogenetic process (The hydrosoluble derivative also acts as
 cutaneous depigmenting agent both on chloasma and on the ephelides showing to be as active as
 I-ascorbic acid (

 In fact, it is quickly hydrolyzed by the cutaneous enzymes. On the contrary, the liposoluble
 derivative, notwithstanding hydrolyzed to vitamin C, performs a slow but lasting activity. It is
 absorbed by the skin more rapidly than the hydrosoluble derivative but it’s hydrolyzed by the
 enzymes more slowly. Including in the same cosmetic product the hydrolsoluble vitamin C
 derivative (VC-PMG) with the liposoluble derivative (IP-VG), we obtain a rapid depigmenting
 activity, due to the fast hydrolyzation of the VC-PMG, which lasts thanks to the slow releasing
 of the vitamin C favored by the liposoluble derivative.

 Both derivatives show a further remarkable stability in the vehicle used. It was used as a
 phospholipidic vehicle able to encapsulate in its liposomes the vitamin C derivatives. That allowed
 obtaining also an emulsion similar to the cellular membranes and able to penetrate the cutaneous
 layers without damaging the skin biological structures

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 Its important to underline also that vitamin C derivatives can be used in combination with other
 compounds, such as arbutin, which seems to strengthen also the depigmenting activity

 Also different authors obtained analogous results, both in vivo and in vitro, with other
 compounds, such as 2-O--d-glucopyramosyl-l-ascorbic acid

 These derivatives also demonstrated to be stable in the cosmetic emulsions and easily
 hydrolyzed to vitamin C, when coming into contact with the skin enzymes. This way it
 demonstrated the possibility to use vitamin C and its derivatives not only as anti ROS (Radical
 Oxygen Species) but also as skin depigmenting agents able to solve the difficult problem of the
 black spots.

 Finally, it is interesting to observe the complete absence of side effect during their usage. By
 the way, its necessary to use correct vehicles which allow a rapid penetration through the
 cutaneous layers and which are able to protect these abilities against the oxidative processes
 such as lamellar phospholipid structure. Phospholipids seem to be the key to this riddle.


    1.   Mishima Y., Shibata K., Seto H. et al. (1994), Inhibitory action of kojic acid on
         melanogenesis and its therapeutic effect for various human hyperpigmentation disorders.
         Skin Research., 36, 134-150

    2. Maeda K., Fukuda M. (1996), Arbutin: mechanism of its depigmenting action in human
       melanocyte culture. J.Pharmacol. Exp. Therap., 276, 765-69

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    3. Okubo T., Oyobikawa M., Futaki H. et al. (1995). The inhibitory effects of 4-N-

       butyl-resorcinol on melanogenesis. J. Dermatological Science,1 0, 88

    4. Shinomiya T. Yakota T. and Hikima T. (1997), Function and application of vitamin C for
       cosmetics. Fragrance J., 1997-3: 80-89

    5. Morganti P., Fabrizi C., Morganti G and Guarneri F, (1999), A new cosmeceutical with
       a skin lightening activity: note II. The combining whitening activity of an hydrosoluble
       and a liposoluble vitamin C derivative, In print on SOFW Journal

    6. Moro O., (1999), Biological Activities of a stable ascorbic acid derivative, 2-0-a-D-
       glucopyranosyl-I-ascorbic acid (AA-2G) in Cosmetics, J. AppI. Cosmetol., 17, 154-163

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                                Anti redness

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 Skin regenerating cream
 Anti redness & scaring/                                     Background:
 Redness cover various origins: going from rosacea, to red spots, bruising, seborrhoea, spider
 veins, burns, various dermatitis and skin irritations, and after laser or surgical operations skin

 or INDUCED REDNESS (laser, operations, scars, etc…)
 and often associated with a demand for SCARING .

                                    INDUCED REDNESS
 LASER (light amplification by stimulated emission of radiation). It is a stimulated light energy
 which has certain properties that differs from other natural lights (ex sunlight)
 IPL (Intense pulse light). It goes beyond laser and emit a fixed coherent wavelength
 Both systems are efficient, but may generates redness which are cared with cosmetic cream
 such as Floxia
 SURGICAL OPERATION: scar is a physical aggression to epidermis
 It also generates redness and such cream is able to decrease redness and accelerates scaring.

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  A BRUISE is a common skin injury that results in a discoloration of the skin . Bloods from
  damaged vessels deep beneath the skin collects near the surface of the skin resulting in what we
  think of as a black or blue mark.

                   We are therefore focusing on the efficacy of 2 selected active ingredients:

         FLOXIA                          Regenerating cream
  40 ml, plastic tube

  This cream is to be used from 1 to twice a day on concerned areas. For scars & wounds, wait till
  wound is completely closed and epidermis already reconstructed.
  Use during minimum 2 to 3 months and renew when necessary
  For security purpose, Floxia is only using proven harmless ingredients.
  And looking for double range action

  Anti inflammatory     GLYCYRRHETINIC ACID, St John worth and camomile extract
  Lighten redness: repair broken micro blood vessels    VITAMIN K
  Scaring:    glyccyrrhetininc acid and jojoba oil
  Meanwhile there is and hydrating action due to jojoba oil and nutrient & anti oxidant action:
  Vitamin E, shea butter and avocado unsaponifiable

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 Blood vascular repairing, reduces bruising
  Vitamin K originates from the German term koajulation. It is also known as antihemorrhagic
  factor, is one of the four fat-soluble vitamins necessary for good health. The primary and best-
  known purpose of vitamin K is support of the process of blood clotting. It also plays a role in
  bone health, and may help to prevent osteoporosis. Appropriate growth and development are
  supported by adequate vitamin K.

  Now more and more widely used topically in cosmetics: to prevent and help reduce redness and
  bruising. There are several forms of the vitamin:

     •   K1 or phyiloguinone also known as phytonadione

     •   K2, a family of substances called menaquinones

     •   K3 or menadione, a synthetic substance
        Able to repair cutaneous broken micro blood vessels. Specific extern action on the sides of
   cutaneous micro blood vessels. Lighten redness from broken capillaries and treat skin irritations
  Vitamin K1 (phytonadione) nature nutrient found in green leafy vegetables.
  The effects of topical vitamin K on bruising after laser treatment.

  Shah NS, Lazarus MC, Bugdodel R, Hsia SL, He J, Duncan R, Baumann L.
  Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, FL
  33125,                                                                                USA.

  BACKGROUND: Pulsed dye laser treatment and other cosmetic procedures result in significant
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 bruising. Claims have been made regarding the efficacy of topical vitamin K in both preventing
 and speeding the clearing of bruising; however, well-controlled studies are lacking. OBJECTIVE:
 The purpose of this study is to evaluate the effects of topical vitamin K versus placebo in the
 prevention and clearing of laser-induced purpura. METHODS: A total of 22 patients were
 enrolled in this double-blind randomized placebo-controlled study. The patients were divided into
 pretreatment and posttreatment groups; the 11 patients in the former group applied vitamin K
 cream to half of their face and vehicle alone to the other half of their face twice daily for 2
 weeks before laser treatment. The latter group followed the same procedure for 2 weeks after
 laser treatment. On day 0, all subjects underwent laser treatment for facial telangiectases using
 a 585-nm pulsed dye laser. Bruising was rated by the both the patient and physician by means of
 a visual analogue scale on days 0, 3, 7, 10, 14, and 17. RESULTS: The side of the face treated
 with topical vitamin K before laser therapy showed no significant difference in bruising as
 compared to placebo. However, the side of the face treated with vitamin K cream after laser
 treatment had significantly lower scores of bruising severity when compared with the side
 treated with placebo. CONCLUSION: Although pretreatment with vitamin K did not prevent
 bruising after laser treatment, use of vitamin K cream after laser treatment did reduce the
 severity of bruising, particularly in the initial days of application.

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 Effects of topical vitamin K and retinol on laser-induced purpura on
 nonlesional                                                     skin.
 Lou      WW,    Quintana            AT,   Geronemus RG,   Grossman                       MC.
 Laser    and Skin Surgery           Center of New York, New York,                       USA.

 BACKGROUND: Pulsed dye laser treatments usually result in purpura. Any
 topical application that eliminates or shortens the duration of purpura would be
 extremely useful. OBJECTIVE: The purpose of this prospective study was to
 determine the safety and efficacy of topical vitamin K cream in shortening the
 duration of laser-induced purpura. METHODS: Twenty adult subjects were
 enrolled. Each subject had five 1.5 cm sites treated with a pulsed dye laser at
 585 nm, 450 nsec, 7 mm spot size at each subject's respective threshold
 fluence. Each subject had a control site where no topical application was used
 and four other sites where a different formulation was applied to each for 2
 weeks before and for 2 weeks after laser irradiation. Five vitamin K
 formulations with or without retinol were studied: 3% vitamin K in acrylates
 copolymer cream, 5% vitamin K in acrylates copolymer cream, 1% vitamin K and
 0.3% retinol in acrylates copolymer cream, 1% vitamin K and 0.15% retinol in
 acrylates copolymer cream, 1% free vitamin K cream. Purpuric discoloration at

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 each site was rated on days 0, 1, 3, 7, 10, and 14 after laser treatment on a
 quartile scale. Each site was assigned 100% discoloration on day 0 after laser

 irradiation. RESULTS: Laser-induced purpuric discoloration resolved faster with
 1% vitamin K and 0.3% retinol in acrylates copolymer cream than with no topical
 application. The difference is statistically significant from day 3 onward.
 CONCLUSION: A combination of 1% vitamin K and 0.3% retinol in acrylates
 copolymer cream hastened the resolution of laser-induced purpura
 Refined extract from the herb Licorice (Glycyrriza glabra): pentacyclic triterpenoid derivative
 of the Beta-amyrin type
 GA looks like cortisone, and to a degree acts like it, without, of course, the potential side
 effects of hydrocortisone. It is useful on inflammatory skin conditions or in the management of
 occasional mild inflammatory episodes

 Anti inflammatory and healing – scaring
 Glycyrrhetinic Acid (GA), the refined extract from the herb Licorice
 (Glycyrrhiza glabra), is now a well accepted topical agent in cream and ointment
 form for treating various skin conditions, Doctor F. Quentin Evans in his paper
 entitled "The Rational Use of Glycyrrhetinic Acid in Dermatology" gave the
 specific areas of use for GA as "sub-acute, chronic and intractable skin
 conditions" (1) where he concluded that "GA is more effective than
                            hydrocortisone". (2)

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 Study of tolerance and efficacy of cosmetic preparations with
 lenitive  action   in   atopic    dermatitis   in    children]

 GrassiA, Palermi G, Paradisi VII Divisione Dermatologia Pediatrica, Istituto Dermopatico
 dell'Immacolata               (I.D.I.)                 IRCCS,                  Roma,alia.

 PURPOSE: In AD (atopic dermatitis), the barrier function of skin is impaired, causing
 dryness and vulnerability: the first-end point to achieve is restoring skin's function to
 avoid relapses. Our aim was to assess tolerability and effecacy of two cosmetics with
 moisturizing and lenitive action in subjects affected by AD. PATIENTS AND
 METHODS: We used a topical preparation (product A) and a new formulation of it
 (product B) containing glycyrrhetinic acid, alpha-bisabolol, squalene, oryzanol and
 hohoba-oil. Product B was then compared with a third one (product C), also based on
 glycyrrhetinic acid and bisabolol. 30 subjects, aged between 4 months and 16 years,
 were included in the study (13 girls and 17 boys), suffered from mild-moderate AD, not
 treated with steroids. Patients were treated twice a day for 21 days, as follows: 12
 product A (Decortil lipocrema IDI Farmaceutici); 9 product B (Decortil crema, IDI
 Farmaceutici); 9 product B on the right and product C (Lichtena AI crema UCB Pharma)
 on the left. We also did: photografic documentation, SCORAD Index, evaluation of
 objective (erythema, exudation, excoriation, dryness) and subjective (itching and

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 burning) simptomatology (scoring 0-3) and physiopatological cutaneous tests as TEWL
 (Trans Epidermal Water Loss), corneometry and pHmetry at beginning and at end of

 treatment. RESULTS: All groups improved both clinically and instrumentally.
 Corneometry increased, TEWL lowed and pH turned to normality. CONCLUSIONS:
 Product A is better for restoring cutaneous physiology, B resulted more efficient in
 rehydration, in acute phase and as emollient agent, whereas C has more lenitive action.

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 All living things on planet earth need the sun; however over-
 exposure can be harmful: It is important therefore to be aware
 of the risks, especially for those who have a sensitive and/or
 photosensitive skin.

 Light or the sun’s energy is emitted in the form of radiation which is divided up into different
 types according to wavelength. There are: cosmic rays, gamma rays, X-rays, UV rays (A, B and
 C), visible light, invisible light, micro-waves and radio waves.
 The ozone layer filters the parts of this spectrum which are lethal.

    •   Ultraviolet C (UVC) - 100 –290nm

        These       wavelengths    are     the    shortest    ultraviolet rays,  extending
        from 100nm to 290nm, and are the most carcinogenic.                     While the
        sun generates ultraviolet C, the ozone layer of the atmosphere screens
        out virtually all UVC from reaching us. Ultraviolet C may become a
        problem for those living at high altitudes, and with the depletion of
        the ozone layer through pollution, may become a real problem. UVC
        is photo damaging to the skin, causing skin burn with exposure. Artificial
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        sources such as some mercury arc-welding units, and germicidal lamps
        emit ultraviolet C. These wavelengths can very efficiently kill germs,

        giving rise to their common name, “germicidal waves”.

        Ultraviolet B (UVB) – 290nm to 320nm

        These are the intermediate wavelength of Ultraviolet rays, and cause
        the initial appearance of redness, commonly called “sunburn”. UVB creates
        painful irritation, but is believed by many to be less damaging than tanning,
        the pigmentation changes caused by the UVA (320nm-400nm)

        UVB primarily damages the epidermis resulting in skin redness promoting a
        thickening of the outer most layer of skin, the stratum corneum (our body’s
        attempt to reduce UVB impact on the epidermis). UVB is a promoter of photo
        aging; this type of damage is cumulative, potentially resulting basal cell and squamous cell

    •   Ultraviolet A (UVA) – (320nanometers – 400nm)

        These longer UVA wavelengths, (near-UV) were once thought essentially harmless,
        contributing only to a “healthy tan”. Scientific evidence now indicates that this is
        not true. On skin, UVA induces cutaneous photo damage, dryness, uneven
        pigmentation, inflammation, skin darkening (tanning), photo aging skin cancer,
        and fine wrinkles. Even low dose UVA can reach to the underlying dermis, causing
        damage that results in wrinkles and sagging skin. UVA radiation penetrates deeply
        into our skin and is quite damaging. Furthermore, UVA adversely affects the deep
        dermis far more than the “sunburn” UVB rays, resulting in loss of the elastic it’s
        supportive collagen, and resulting in premature aging. Unlike the shorter UVB
        (290-320nm) wavelengths, UVA easily penetrates window glass. Interestingly,

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        the amount of UVA reaching the earth, unlike UVB retains essentially the same
        energy level every day of the year, morning,noon, and afternoon with 10 to
        12 times more UVA, then UVB reaching the earth’s surface at sea level.

        The most important aspect of UVA is the cumulative tissue damage that results
        from these deeply penetrating UV rays. Studies to date support the relationship
        of such UV exposure to the development of basal and squamous cell cancers, as
        well as pre-cancerous lesions. Recently, it has been reported that depletion
        of Vitamin A in the skin by UVA exposure may contribute to both photoaging and
        cancers of the skin.

    •   Visible Light (400nm – 760nm)

        Nearly 50% of the sun’s radiation, reaching us at sea level, is within the visible range.As
        the name describes, these are the wavelengths that humans can see (Violet – Blue –
        Yellow – Green – Orange, Red, etc.). Distributed from approximately 400nm to 760nm
        fortunately, its energy level is lower than that of ultraviolet rays.

        There have been a few published reports, regarding the research concerning
        photodamage caused by visible light. It has been reported in prestigious journals such as,
        the “Journal of Investigative Dermatology”, “Cancer Research”, and the “British Journal
        of Dermatology”, that visible light is capable of precipitating phototoxic reactions,
        promoting       DNA        cross-linking        and      enhancing      tumor     growth.
        This lower energy has the ability to penetrate the skin deeper than UVA, reaching down

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        within the dermis. Adverse skin reactions can occur within this visible light wavelength.
        It is a misconception to think visible light as being harmless to human skin.

    •   Infrared- “IR” (greater than 760nm to 1,000,000nm)

        Infrared goes from above 760nm to infinity (?), but most of the energy is from 760nm
        to about 1800nm, comprising more than 40% of the sun’s rays reaching us at sea level.
        These wavelengths warm us when we stand in the sun (perceived as deeply penetrating
        heat), and are emitted by stoves, furnaces, light bulbs, heat lamps, ovens, and space
        heaters. A number of studies have implicated Infra Red waves as photodamaging, and
        add to the UVB photodamage. Infrared has been known for centuries to cause cancers in
        some people. Cancers induced by such heat are referred to as; Kang Cancer in China,
        Kangri in Kashmir, Kairo in Japan, and Peat Fire Cancer in Ireland. Chronic exposure to
        infrared leads mottled pigmentation, loss of elastin elastosis, and the typical
        characteristics seen in photoaged skin. (wrinkling, sagging, leathery-feel).

 The effects of the sun
 Positive Effects     Activates the synthesis of Vitamin D (necessary for bones).
                      Maintains hormone levels, and contributes to circadian rhythms.

 Negative Effects     - UV rays cause sunburn, immune deficiency, problems with photo-sensitivity,
                      cancer and ageing skin.
                      - UVB: short-term exposure leads to redness, irritation, sun-burn and
                      tanning; long-term it causes irreversible damage to DNA structure leading to

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                        skin cancers.
                        - UVA: At first considered harmless, but in fact causes ageing and damage
                        to DNA by the formation of free radicals.
                        - Invisible : potential cause of cancer as carcinogenic in association with
                        other factors.

  Level of sun protection:

  The SPF coefficient indicates the level of protection against UVB rays. It is calculated
  according to the time it takes the skin to burn with and without a cream containing a given
  factor sun-screen.

  For example SPF 15 : if a person’s skin without sun-screen protection takes 10 minutes to burn in
  the sun at midday, this means that the same person with sun-screen will be able to stay 15 times
  longer in the same sun conditions without getting burnt (2½ hours).

  Sun-screen: application

  •   Sun-screen should be applied 20 minutes before exposure to sun (time it takes to be
      absorbed into the skin), and should be reapplied every following 2 hours (even if water-

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      A normal quantity is 2 mg for each cm2 of skin to be protected.
      Use of sun-screen does not interfere with the synthesis of Vitamin D.

       Specificity of Ingredients (chemical or mineral)

         Sunscreens: sunblocks (reflect sun rays) and are mineral origin. Powdered or micronized
         from oxides of metals (zinc, titanium or even iron). Wide spectrum and need specific
         texture to be water resistant

         Sunfilters: absorb UV rays and are chemical origin. Shorter spectrum covered, therefore
         needs a combination of several ones. Said to be potentially more allergizing than mineral
         ones. But nicer texture and better water resistant naturally, because entering the

  The best compromise is sought between effectiveness and cosmetic acceptability.
  PABA (para-amino benzoic acid)
  • Adheres well to cells (highly resistant to water and perspiration). However, greasy and has a
     narrow spectrum (UVB - 29 to 320 nM). PABA esters are used (less greasy). Possibility of
     contact allergies.
  •   Mostly screen UVA rays 320 to 400 nM, and to a lesser extent UVB rays. Oxy and
      dioxybenzone are used to the greatest extent (precipitate far fewer allergic reactions than
      PAB). However, being less resistant to water they require a thick base.

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    •    These products of cinnamome are excellent sun-screens. Possibility of allergic reactions.
         Non-greasy, but poor resistance to water, they need an appropriate base.
    •  Specific to UVB rays, they need to be combined with other ingredients to ensure complete
       sun protection.
    • The oldest form of UVA filter.
    Derivatives of dibenzolymethane
    • New UVA filters since 1979.
    Derivatives of camphor
    • Better known under their commercial name of mexoryl. Excellent UVA filters.

    Zinc or titanium oxide
    • These pigmented powders are often micro and sub-micronised to obtain transparency on the
        skin. Titanium acts on UVA and UVB whilst zinc is more UVA specific. Do not provoke
        allergic reactions.


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Infrared Light

Visible Light     500


                                                                      Mineral screens
                   Chemical               Chemical                       All radiation
                                                                      Titanium Dioxide
                    screens                screens                    Zinc Oxide


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            sun protection cream
                   SPF 70
                            (40 ml sealed plastic tube)

 has 3 special features:

 •     Protection against direct sun damages :very broad range of protection against the great
       proportion of existing rays, and not prone to causing allergic reactions)

    2 mineral screens

 Zinc oxide
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 Titanium dioxide

   2 chemical screens

 Octil methoxycinnamate
 Benzophenone 3
 •     Protection against sun inducted damages, especially towards DNA, with the recovering action

       of a special vegetal nucleotide contained in artemia salina, and   maintaining the
       DNA repair system.
 •     Nourishing and moisturizing to help epidermis to recover its natural protecting properties,
       with several vegetal extracts.

 •     Specific texture providing an excellent resistance to water

 Prevention of sunburn,

 Prevention of scaling and ageing,

 Prevention of photodermatoses (aftreatment with photosensitive drugs, or

 post surgery or laser treatment, ...)
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                                 DNA protection

                       Annual Cosmetic Conference - 2004
                                 South Africa

  Session 3 began with the presentation of Joel Mantelin of Vincience Research Centre France,
  discussing anti-stress “heat shock proteins” as a new generation of cosmetic active ingredients.
  UV radiation, heat and chemicals are stress factors and are the primary cause of actinic ageing.
  The stress results in a signal DNA to change the native protein into a newly formed protein,
  which is the heat stress protein, which will protect cell DNA against the damaging UV radiation.
  These newly formed proteins differ in molecular weight, the HSP 70 being the most needed.
  Artemia salina is marine plankton that has adaptive mechanisms as it lives in severe
  environmental conditions and has shown to compensate for the age related decrease of HSP 70
  in the skin.

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       The Fountain of Youth from the Sea

  The cosmetic active ingredient GP4G is obtained through biotechnology from the ocean
  plankton Artemia salina and is an uncommonly good energy deliverer for the skin.

  The ocean is the source of life and contains a multitude of different life forms, which in some
  cases survive in the most extreme conditions. To this particular sort belongs the ocean
  plankton Artemia salina. Under unfavourable environmental circumstances, Artemia salina
  synthesises a great amount of GP4G (Diguanosinetetraphosphate) and falls into a state of
  metabolic suspension, which can last many years. As soon as the external conditions improve,
  the organism awakens and the stored GP4G releases its energy to begin the process of life
  once again. For this the cell metabolism is excited.

  The energy that is required for metabolism is delivered from the nucleotides. Nucleotides
  such    as    ATP (Adenosinetriphosphate),     GTP      (Guanosinetriphosphate)   and    GP4G
  (Diguanosinetriphosphate) are able to liberate a high amount of energy, through hydrolysis of
  their phosphate bonds, that is directly bio-available. ATP and GTP are, however, very unstable
  and can therefore not be stored in the cell nor in cosmetics. In contrast to these, GP4G as a
  molecule is very stable.

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            Do you suffering on acnes? Romove it now!
           Do you suffering on acnes? Romove it now!

                                                Human skin has a very strong regenerative
                                                activity  and    undergoes    many    metabolic
                                                processes throughout life. This cell activity
                                                depends of course on the age of the cells and
                                                decreases steadily with age. The result of this
 ageing is a deficiency of energy of the visibly aged, stressed and tired skin. Signs of skin
 ageing are, for example, water depletion, reduced metabolism, defective mineralisation and
 loss of tissue elasticity. The active ingredient GP4G engages in countering exactly the
 described effects and keeps up the energy reserves of the cells. The particular properties of
 GP4G act exceedingly positively on the cell metabolism of the skin, help reactivate the self-
 repair mechanism of the cells and thereby produce the desired revitalising effect. Long lasting
 skin damage caused by temperature or environmental influences, dehydration and diverse signs
 of ageing can be avoided. The human cells can recognise GP4G, exploit it and store it. Studies
 show that GP4G stimulates a series of essential synthesis processes of the skin such as the

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 synthesis of keratin, filaggrin and fibronectin. GP4G acts as an energy push for stressed and
 tired skin.

 GP4G also shows astounding properties in the fight against fat deposition. G-proteins play an
 important role in slimming. Stimulated by GP4G, G proteins can initiate the conversion of ATP
 into AMPC. AMPC in turn dismantles lipids, reducing excess fat stored within the adipose cells.

 Marine biology is time and again good for surprises and in particular innovative active
 ingredients, which clarifies the inimitability of nature in application for cosmetics. The active
 ingredient obtained from Artemia salina, GP4G, is suited as an ingredient for products for
 which the goal is to revitalise the skin and acheive a younger effect. The use as a slimming
 agent also promises to have as great success.

 Prevention of allergies (see sun protectors with too much chemical filters)

 FUTURE of PROTECTION                                      RATING: SPF, IPF,

 Using sunscreens and/or sunfliters

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         Do you suffering on acnes? Romove it now!

 Sunscreens: sunblocks (reflect sun rays) and are mineral origin. Powdered or
 micronized from oxides of metals (zinc, titanium or even iron). Wide spectrum
 and need specific texture to be water resistant

 Sunfilters: absorb UV rays and are chemical origin. Shorter spectrum covered,
 therefore needs a combination of several ones. Said to be potentially more
 allergizing than mineral ones. But nicer texture and better water resistant
 naturally, because entering the epidermis

 Ozone layer naturally protects from UVC.        UVB enter the epidermis and
 generates redness, ageing and sun damage. Is stopped by glass and potency is
 variable according to season or time of the day. UVA are even longer rays and
 enter the dermis. Is not stopped by glass, and its potency has a consistent
 wavelength of penetration

 Today SPF is mainly a UVB rating protection: calculation of degree of erythema
 protection conferred by a particular sunscreen. Therefore claiming SPF 100,
 when meanwhile also recommending to renew application every 2/3 hours is very
 confusing .

  It is important to know that 90% of light is UVA, and that effect of UVB is
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 immediate, when UVA’s one is long term . SPF rating will likely change in the
 coming years, by maybe limiting the announced upper ratio, introducing a UVA-

 UVB protection ratio, and introducing integrity grade of the skin with an IPF
 ratio (Colipa suggest to adopt a SPF 50 upper limit)

 It is now recognized that sun exposure (especially UVA) results in suppression
 of skin ’immune function. Generally a good thing: failure can result in in
 photodermatoses such as chronic actinic dermatitis; but in case of pre-
 malignant and malignant lesion the immuno suppressant effect is deleterious,
 and besides also has a carcinogenic effect , fortunately animal studies suggest
 that this process can be reversed

 IPF is a useful tool to rate both UVA and UVB protection and also integrity
 information reflecting skin ability to repair DNA damage. Immuno suppressing
 UVA linked to oxidative stress. It has been shown that antioxidants are good
 useful: Langerhans cells remain higher level with anti oxidant protection.

 But today, there is absolutely no official and acceptable measurement of above

 When sun damages skin, it also impairs DNA. DNA repair system is needed to
 maintain genetic integrity of the epidermis; and defect in DNA repair system
 may result in skin cancer.

 Human body has 2 mechanisms to defend from UV damages:

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           Do you suffering on acnes? Romove it now!

 * Skin pigmentation (natural-constitutive or induced)

 * Repairing sun induced DNA damage, by removing the damaged bits of DNA.
 Knowing that such degree of protection varies from people to people, and may be
 improved by using adequate sun protection products.

 Oral (food additive) photoprotection is also becoming a focus and has been yield
 to a certain extent as photoprotection of the future.

 Coming years will draw the attention on UVA protection and DNA
  integrity measurement, and decreasing the upper limit of SPF
                            (maxi 50).

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                     Skin restructuring cream
                                 stretch marks

 STRIAE DISTENSAE is a common skin dermatosis that does not cause any significant medical
 problem; however, striae can be of significant stress to those afflicted.
 They represent linear dermal scars accompanied by epidermal atrophy

 Striae distensae affect skin that is subjected to continuous and progressive stretching
 (increased stress on the connective tissue due to increased size of the various portions of the
 body) such as the abdomen and breasts in pregnant women, shoulders in body builders,
 adolescents undergoing their growth spurt, and overweight individuals.
 Skin distension apparently leads to excessive mast cell degranulation with subsequent damage of
 collagen and elastin. Prolonged use of oral or topical corticosteroids or Cushing syndrome
 (increased adrenal cortical activity) will lead to development of these striae. Genetic factors
 could certainly play a role, although this is not fully understood.

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             Do you suffering on acnes? Romove it now!

       In the US: It is estimated that 90% of pregnant women, 70% of adolescent females,
          40% of adolescent males (many of whom participate in sports) suffer from stretch

 Striae distensae are usually a cosmetic problem; however, if extensive, they may tear and
 ulcerate when an accident or excessive stretching occurs.
 Race: Stretch marks affect all races.
 Sex: Striae affect women more commonly than men.
 Age: Stretch marks affect adolescents, pregnant females, and patients with excessive adrenal
 cortical activity.

 Early striae present as flattened, thinned skin with a pink hue that may occasionally be pruritic.
 Gradually, they enlarge in length and width and become reddish-purple in appearance (striae
 rubra). Their surface may be finely wrinkled. Mature striae assume white, depressed, irregularly
 shaped bands with their long axis parallel to the lines of skin tension. They are generally several
 centimeters long and 1-10 millimeters wide. Gradually, some striae may fade and become
 inconspicuous. The natural evolution of stretch marks is similar to that
 of scar formation or a healing wound.
 In pregnancy, striae usually affect the abdomen and the breasts.

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 The most common sites for adolescent striae are the outer aspects of the thighs and lumbo-
 sacral region in boys, and the thighs, buttocks and breasts in girls. There is considerable

 variation, and other sites, including the outer aspects of the upper arms, are occasionally

      Striae induced by prolonged systemic steroid use are usually larger and wider than
 other phenotypes of striae and involve widespread areas occasionally including the face.
      Striae secondary to topical steroid use are usually related to enhanced potency of
 the steroids when using occlusive plastic wraps. They usually affect the flexures and may
 become less visible if the offending treatment is withheld early enough.

          The factors that lead to the development of striae are poorly          understood. There is
 no general consensus as to what causes striae. It          has been suggested that they develop as a
 result of stress rupture of           the connective tissue framework. It has also been suggested
 that they           develop more easily in skin that has a high proportion of rigid cross-linked
 collagen, as occurs in early adult life. This is evident in striae due to pregnancy, lactation, weight
 lifting, and other stressful activities. Increased adrenal cortical activity has been implicated in
 the formation of striae, as in the case of Cushing syndrome.

 Scanning microscopy shows extensive tangles of fine curled elastic fibers; which is reverse to
 normal skin which has thick elastic fibers.

 Striae are usually of a cosmetic concern; however, if extensive, they         may rupture in an
 Treatments for rare but severe cases may go through cosmetic surgery, use of tretinoin, etc…
 Now, for most usual cases and as prevention, cosmetic appear to be of high useful importance/

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             Do you suffering on acnes? Romove it now!
            Do you suffering on acnes? Romove it now!

 Restructuring cream
 125 plastic tube

 This cream is to be used from month – 5 to month +3 or more (till striae fade away).

 For security purpose, Floxia is only using proven harmless ingredients.
 And looking for double action

 Restructuring & Toning: Improves skin colour & texture: firming and tensing action of fenugrek
 and wheat germ extracts
 Remodel collagen with sunflower oil
 Promote elastin synthesis by stimulating the skin with geranium, lavander and sunflower oils.
 When yeast and wheat germ extracts are toning.
 Improve blood circulation: with horse chesnut extract and vitamin PP-B3

 Meanwhile there is and hydrating action due to sunflower and palm kernel oil.

Only 3 days remove your acnes!

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            Do you suffering on acnes? Romove it now!

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