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WO1998025587A1 - Utilisation de composes antioxydants lipophiles pour empecher les reactions oxydatives induites par les retinoides et vehiculees par les uva - Google Patents

Utilisation de composes antioxydants lipophiles pour empecher les reactions oxydatives induites par les retinoides et vehiculees par les uva Download PDF

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Publication number
WO1998025587A1
WO1998025587A1 PCT/US1997/022441 US9722441W WO9825587A1 WO 1998025587 A1 WO1998025587 A1 WO 1998025587A1 US 9722441 W US9722441 W US 9722441W WO 9825587 A1 WO9825587 A1 WO 9825587A1
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WO
WIPO (PCT)
Prior art keywords
retinoid
lipid peroxidation
uva
induced
skin
Prior art date
Application number
PCT/US1997/022441
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English (en)
Inventor
Jeffrey C. Geesin
Original Assignee
Johnson & Johnson Consumer Products, Inc.
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Application filed by Johnson & Johnson Consumer Products, Inc. filed Critical Johnson & Johnson Consumer Products, Inc.
Priority to JP10526847A priority Critical patent/JP2000505816A/ja
Priority to BR9707630A priority patent/BR9707630A/pt
Priority to AU55188/98A priority patent/AU5518898A/en
Priority to EP97951582A priority patent/EP0914089A1/fr
Priority to IL12570097A priority patent/IL125700A0/xx
Publication of WO1998025587A1 publication Critical patent/WO1998025587A1/fr

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Classifications

    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61Q—SPECIFIC USE OF COSMETICS OR SIMILAR TOILETRY PREPARATIONS
    • A61Q19/00—Preparations for care of the skin
    • A61Q19/004—Aftersun preparations
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K8/00—Cosmetics or similar toiletry preparations
    • A61K8/18—Cosmetics or similar toiletry preparations characterised by the composition
    • A61K8/30—Cosmetics or similar toiletry preparations characterised by the composition containing organic compounds
    • A61K8/67—Vitamins
    • A61K8/671—Vitamin A; Derivatives thereof, e.g. ester of vitamin A acid, ester of retinol, retinol, retinal
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P17/00—Drugs for dermatological disorders
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61Q—SPECIFIC USE OF COSMETICS OR SIMILAR TOILETRY PREPARATIONS
    • A61Q17/00—Barrier preparations; Preparations brought into direct contact with the skin for affording protection against external influences, e.g. sunlight, X-rays or other harmful rays, corrosive materials, bacteria or insect stings
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61Q—SPECIFIC USE OF COSMETICS OR SIMILAR TOILETRY PREPARATIONS
    • A61Q17/00—Barrier preparations; Preparations brought into direct contact with the skin for affording protection against external influences, e.g. sunlight, X-rays or other harmful rays, corrosive materials, bacteria or insect stings
    • A61Q17/04—Topical preparations for affording protection against sunlight or other radiation; Topical sun tanning preparations
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K2800/00—Properties of cosmetic compositions or active ingredients thereof or formulation aids used therein and process related aspects
    • A61K2800/40—Chemical, physico-chemical or functional or structural properties of particular ingredients
    • A61K2800/52—Stabilizers
    • A61K2800/522—Antioxidants; Radical scavengers

Definitions

  • the present invention relates to the protection of skin from the oxidative effects of ultraviolet (UV) A radiation that are induced by retinoid use.
  • the present invention relates to means of topically applying a retinoid to skin that reduces or eliminates skin damage caused by retinoid induced, UVA- mediated oxidative effects.
  • Retinoids such as, retinoic acid (also known as vitamin A acid or tretinoin) , retinol, and retinol palmitate, are known to have beneficial effects on the skin. For example, they have been used both orally and topically to treat acne.
  • Retinoids have been shown to be able to act as antioxidants at high concentrations, protecting the skin from sunlight and preventing the induction of lipid peroxidation initiated by the use of ascorbic acid and iron [Das et al., J Neurochem (1989) 52:585-588; Khettab et al., Biochimie (1988) 70:1709-1713; and Geesin et al. Arch Biochem Biophys (1990) 278:350-355].
  • UV radiation from the sun produces its acute and chronic effects on skin involves the production of reactive oxygen species, which cause pathology by a number of different mechanisms including lipid peroxidation production [Shea et al . , "Nonionizing radiation and the skin.” In: Physiology, Biochemistry, and Molecular Biology of the Skin . 1991. LA Goldsmith, ed. Oxford University Press:New York. vol. 2, pp. 910-927]. Indeed, the production of free radicals and lipid peroxidation has been associated with characteristic changes associated with aging in many tissues including the skin [Machlin, et al., FASEB J (1987) 1:441-445; Emerit, I, "Free radicals and aging in skin.” In: Free Radicals and Aging.
  • retinoids have also been reported to produce undesirable side effects.
  • Retinoids have been reported to reduce the exposure time for individuals to produce UV-mediated erythema resulting in increased sensitivity to sunburn [Szaniawska et al., Neoplasm (1988) 35:191-195; Collins et al., J Am Acad Dermatol (1986) 14:274; Ferguson et al., Pharmac Ther (1989) 40:123-135; and Auffret et al . , J Am Acad Dermatol (1990) 23:321-322].
  • the present invention relates to a method of topically applying a retinoid to mammalian skin which reduces or eliminates retinoid induced, UVA-mediated oxidative damage to the skin.
  • the method comprises topically applying to the skin a composition comprising a safe and effective amount of a retinoid and a safe and effective amount of a lipophilic antioxidant.
  • Figure 1 shows the effect of different culture plates on the production of lipid peroxidation by human dermal fibroblasts exposed to solar simulated light.
  • Cells were exposed to solar simulated light through the covers on Corning 75 cm 2 flasks or through Costar 100 mm tissue culture dishes with or without the covers. Triplicate cultures were exposed to increasing numbers of MED using the solar simulator arrangement of lamps.
  • Figure 2 shows the spectral dose distribution of light sources with different culture materials.
  • the spectral dose distribution is presented for the three cell culture conditions identified in the lipid peroxidation measurements described previously (see Figure 1) using the solar simulator arrangement of lamps.
  • Figure 3 shows the spectral irradiance of F40 350BL lamps.
  • Figure 4 shows the absorbance spectra of Schott filters. The absorbance of various WG filters was determined and is shown.
  • Figure 5 shows the spectral dose distribution produced with the Schott Filters described in Figure 4.
  • Figure 6 show the difference spectra produced using the Sylvania F40 350BL fluorescent lamps in combination with the Schott Filters described in Figures 4 and 5. These spectra represent the differences in spectra produced when comparing one filter to the next in the series.
  • Figure 7 shows lipid peroxidation produced in human dermal fibroblasts (HSF) and Swiss 3T3 cells (S3T3) in the presence or absence of the Schott filters described in Figures 4-6.
  • Figure 8 shows lipid peroxidation action spectrum for human dermal fibroblasts (HSF) and Swiss 3T3 Mouse Fibroblasts (S3T3) . These action spectra were determined using the information from Figures 6 and 7.
  • Figure 9 shows difference spectra produced using the Sylvania F40 350BL fluorescent lamps as described in Figure 6. This presentation highlights selected wavelengths (290-310nm) from Figure 6.
  • Figure 10 shows the spectral irradiance of Westinghouse FS40 Sunlamps alone.
  • Figure 11 shows the effect of exposure to Westinghouse FS40 Sunlamps on the production of lipid peroxidation in human dermal fibroblasts. Triplicate cultures were exposed to increasing number of MED.
  • Figure 12 shows the effect of retinoids on UVA-induced lipid peroxidation.
  • Swiss 3T3 mouse fibroblasts (S3T3) (A) and human dermal fibroblasts (B) were exposed to 60 joules/cm 2 UVA using Sylvania F40 350BL lamps.
  • Figure 13 shows dose and wavelength dependence for the effect of retinoic acid on UV-induced lipid peroxidation. Triplicate cultures were irradiated for the indicated number of MED using the solar simulator arrangement of lamps or for the indicated levels of joules/cm 2 UVA in the presence of 100 mM retinoic acid.
  • Figure 14 shows the effect of retinoids on the levels of lipid peroxidation produced in the presence or absence of the Schott filters.
  • Figure 15 shows the effect of retinoids on background levels of lipid peroxidation in Swiss 3T3 cells. Triplicate cultures were treated with the indicated concentrations and types of retinoids and maintained either under aluminum foil away from the lamps (NO UV) or under the lamps (FOIL) .
  • Figure 16 shows the lipid peroxidation action spectrum for Swiss 3T3 cells treated with retinoic acid.
  • Figure 17 shows the absorbance spectrum for a 50 ⁇ M solution of all-trans retinoic acid in methanol.
  • Figure 18 shows the effect of butylated hydroxyanisole, butylated hydroxytoluene, and ascorbic acid (asborbate) on the synergistic effect of retinoic acid and UVA on the production of lipid peroxidation in Swiss 3T3 cells.
  • the present invention is directed to methods of topically applying to the skin a retinoid while reducing or eliminating skin damage caused by retinoid induced,
  • UVA-mediated oxidative effects including UVA-induced lipid peroxidation and products produced by lipid peroxidation.
  • the present invention is also directed to retinoid compositions for topical application to skin of humans and like susceptible animals.
  • the present invention results from the surprising discovery that retinoids contribute to UVA-mediated oxidative damage but that their damaging effect can be reduced by topically applying the retinoids in combination with lipophilic antioxidants.
  • the skin receives the beneficial effects of retinoids while reducing and/or eliminating retinoid induced, UVA-mediated oxidative damage.
  • a composition that contains an effective amount of a retinoid and an effective amount of a lipophilic antioxidant that reduces and/or eliminates retinoid induced, UVA-mediated oxidative damage.
  • Retinoid induced UVA-mediated oxidative effects include, but are not limited to, lipid peroxidation and the products produced by lipid peroxidation such as cross-linking agents.
  • Lipophilic antioxidants have been found to be effective at preventing skin damage caused by retinoid induced, UVA-mediated oxidative effects.
  • Preferred lipophilic antioxidants include, but are not limited to, ascorbyl-6-palmitate, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) .
  • Ascorbyl palmitate has previously been shown to be ineffective at preventing UVB induced wrinkling in hairless mice [Bissett et al., Photodermatol Photoimmunol Photomed (1990) 7:56-62], however it has been shown to protect endothelial cells from the cytotoxic effects of products of lipid peroxidation [Kaneko et al., Arch Biochem Biophys (1993) 304:176-180]. No examination of the effect of ascorbyl-palmitate on UVA-mediated events has been reported. BHA has also been shown to be effective at preventing UVC-induced lipid peroxidation in liposomes [Pelle et al., Arch Biochem Biophys (1990) 283:234-240].
  • BHA has been found to be effective at preventing UVB- or PUVA-induced ornithine decarboxylase activity (associated with tumor formation) [Kono et al., J Dermatol (1992) 19:389-392; Black et al., Photochem Photobiol (1986) 43:403-408], however, BHA had no effect on UVB-induced photocarcinogenesis [Black et al., Photochem Photobiol (1986) 43:403-408]. No results concerning the effects of BHA on other UVA-mediated events have been reported.
  • BHT has been shown to be effective in preventing UVA- [Bose et al., Radiat Res (1993) 133:340-344] and UVC- [Pelle et al.. Arch Biochem Biophys (1990) 283:234-240] induced lipid peroxidation in liposomes. No evidence of activity of BHT against UVA-mediated oxidative effects in animals or cultured cells has been reported.
  • the retinoid composition containing a lipophilic antioxidant is applied topically to the skin to protect it from retinoid induced, UVA- mediated oxidative effects.
  • the amount of retinoid used in the topical compositions and methods of the present invention can vary within significant limits depending on the therapeutic use for which the retinoid composition will be applied to the skin.
  • the retinoid will be present from about 0.001 to about 3.0 percent by weight, more preferably from about 0.025 to about 0.5 percent by weight.
  • the amount of the lipophilic antioxidant present in the retinoid compositions and applied to the skin cells may vary so long as a sufficient amount of the antioxidant is present to reduce or eliminate retinoid induced, UVA- mediated oxidative damage, including lipid peroxidation, to the skin.
  • the antioxidant is present in the composition from about .0001 % to about 10 % (w/w) , more preferably from about .01 % to about 1 %, and more preferably still from about .1 % to about .5 %.
  • the retinoid compositions of the present invention may be made into a variety of product types.
  • the compositions can be in solid, liquid or aerosol form so long as they are suitable for topical administration.
  • the compositions can be formulated into a liposomal formulation, an emollient, a liquid, a cream, a gel, an ointment, a microemulsion, or a solution.
  • Other typical skin care agents and additives that assist in the purpose of the present invention or that are conventionally used in topical cosmetics or medical compositions may also be included in the retinoid compositions used in the present invention.
  • Various vitamins may also be included in the photoprotective compositions of the present invention. Examples of such vitamins include, but are not limited to. Vitamin A and derivatives thereof. Vitamin B 2 , biotin, pantothenic, Vitamin D, Vitamin E and combinations thereof.
  • S3T3 mouse Swiss 3T3
  • HSF human dermal fibroblasts
  • Example 1 Effect of culture materials on the production of lipid peroxidation
  • neonatal human dermal fibroblasts were irradiated using a combination of Sylvania F40 350BL lamps (98% UVA) and Westinghouse FS40 Sunlamps (approximately 50% UVA, 50% UVB) to simulate the normal solar spectrum.
  • Neonatal human dermal fibroblast cultures were grown as described above in Corning 75 cm 2 tissue culture flasks or in 100 mm Costar culture dishes. Cultures were then irradiated through the use of a solar simulator arrangement of bulbs with a 6:5 mix of Sylvania F40 350BL lamps and Westinghouse FS40 Sunlamps (50% UVA, 50% UVB) .
  • lipid peroxidation assay was conducted. Briefly, irradiated plates were scraped with a rubber policeman and cells and solution were homogenized on a dounce homogenizer. An aliquot of the protein extract was taken for Lowry determination of total protein [Lowry et al . , J Biol Chem (1951) 193:265-275]. The remainder of the extract was precipitated with trichloroacetic acid. The supernatant was assayed for malondialdehyde content in duplicate by combining it with 0.5% thiobarbituric acid solution before boiling for 30 minutes. Samples were measured for their absorbance at 532 nm. Malondialdehyde levels were determined using the reported extinction coefficient [Wilbur et al . , Arch Biochem Biophys (1949) 23:305-313].
  • the spectral power distribution of the Sylvania F40 350BL fluorescent lamps used to irradiate the cells was measured with an Optronics Model 742 Spectroradiometer at 2 nm intervals between 250 and 400 nm.
  • the irradiance was multiplied by the transmission of the Costar lid used to cover the cells at each wavelength to determine the irradiance of the source to the cells.
  • the irradiance at each wavelength was multiplied with a sealer value (representing time) such that the integral equaled 80 J/cm 2 .
  • Example 2 Determination of the action spectrum for the production of lipid peroxidation
  • Action spectra were determined by using a series of long pass filters to evaluate the differences in dose between two adjacent filters, and attributing the differences in the response being evaluated between the two filters to that waveband in proportion to the total energy difference between the two filters.
  • the spectral dose distributions of adjacent filters were subtracted from each other to determine the difference in spectral dose. This was done for each adjacent pair of filters. These difference dose distributions were integrated to determine the difference dose band (See Figure 6) .
  • the level of lipid peroxidation per unit protein content for each filter pair was determined as described above.
  • the differences in lipid peroxidation for each filter pair was determined by subtracting the levels for the adjacent pair.
  • the peroxidation differences for a filter pair were divided by the difference dose band to determine the level of peroxidation attributable to each unit dose of the difference band, indicating the absolute sensitivity of peroxidation to that wave band.
  • the absolute sensitivities of all wavebands were integrated and each of the individual sensitivities were divided by the sum to determine the percentage of sensitivity of each waveband.
  • the relative sensitivities were plotted as a function of the difference wavelength band to indicate which portion of the UV spectrum was most effective in causing lipid peroxidation.
  • Spectral absorbance of each of the Schott long pass filters used for the action spectra determination was measured using a Cary 2300 Spectrophotometer with diffuse reflectance accessory. Absorbances at wavelength between 250 and 400 nm in 2 nm intervals were converted to percent transmission. To determine the spectral dose distribution delivered to the filtered cells, the spectral dose distribution of the source with the Costar lid was multiplied at each wavelength with the transmission of the appropriate Schott filter. Each of these distributions was also integrated to determine the total energy delivered through the filter to the cells. The absorbance of these filters demonstrates the pattern of increased absorbance to higher wavelengths with successive filters. The resultant spectral dose distribution after subtracting the absorbance of each filter from the spectra produced by the lamps is shown in Figure 5. As shown, the use of the filters with increasing wavelength number shifts the absorbance maximum of the resulting spectra to higher wavelengths and eliminates the radiation at lower wavelengths.
  • the change in lipid peroxidation produced when the WG280 filter is used compared to no filter represents a region of the spectra which is important for the production of lipid peroxidation in human dermal fibroblasts and Swiss 3T3 cells.
  • the change from WG345 filter to the WG360 filter also represents a region which contributes significantly to this effect.
  • the difference spectra for each of these transitions produce a peak with absorbance maximum very close to 345 nm indicating that a chromophore exists which is important for the UV-dependent production of lipid peroxidation which has an absorbance maximum very close to 345 nm.
  • difference spectra with peaks closely adjacent to the two identified peaks are less sensitive and help to specifically identify the important wavelengths in the UVA region of the spectrum.
  • Human dermal fibroblasts also demonstrate another chromophore in the UVB region of the spectrum. This effect may be produced by the small peaks in the dose distribution of the lamp which correspond with 297 and 303 nm shown best in Figure 9. This effect of UVB on the production of lipid peroxidation in human dermal fibroblasts is further shown by the use of the Westinghouse FS40 Sunlamps (See Figure 10) for dose distribution produced with this lamp alone. Using the UVB dominant FS40 Sunlamps, lipid peroxidation can still be induced in human dermal fibroblasts in a dose dependent manner as shown in Figure 11.
  • retinoids To determine whether or not the antioxidant activities of retinoids would reduce UVA-induced lipid peroxidation, two different cell types were exposed to UVA in the presence or absence of various retinoids. Surprisingly, all three retinoids tested (all-trans retinoic acid, all-trans retinol and retinol acetate) stimulated lipid peroxidation.
  • Lipid peroxidation was increased between 2.5- and 4- fold by retinoid treatment in S3T3 cells (Figure 12A) .
  • Retinoic acid was the most active in these cells while retinol and retinol acetate required higher concentrations to achieve the same levels of lipid peroxidation.
  • retinoic acid did not stimulate greater amounts of lipid peroxidation than seen with retinol treatment ( Figure 12B) .
  • This effect of retinoids on UV-induced lipid peroxidation appears dose and wavelength dependent as shown in Figure 13.
  • retinoic acid treated cultures were irradiated with increasing amounts of UVA, a dose dependent increase in the levels of lipid peroxidation was seen.
  • the action spectra for the phenomenon was determined as described above. Briefly, using the Schott filters, the levels of lipid peroxidation were determined in Swiss 3T3 cells in the presence of retinoic acid, retinol or retinol acetate ( Figure 14) compared to UVA alone ( Figure 14 and Figure 7) . Treatment of S3T3 cells with retinoids produced a similar, but not identical, pattern for all the retinoids tested.
  • the loss in the production of lipid peroxidation with successive filters was quite different than the pattern produced by UVA alone.
  • the use of the WG 280 filter did not produce a decrease in the level of lipid peroxidation in retinoid treated cells. Instead, a consistently noted increase in lipid peroxidation was produced when the WG 280 filter was used, indicating that some wavelength or wavelengths (presumably found in the UVB region of the spectrum) is capable of inhibiting the ability of retinoids to induce the production of oxidative products in the presence of other portions of the emitted spectrum.
  • This effect of the WG280 filter was specific for retinoid treated cells since S3T3 cells in the absence of retinoids did not demonstrate the same increase in lipid peroxidation.
  • retinoic acid produces a very different action spectrum compared to that produced in untreated S3T3 cells.
  • the filters which block the UVB (WG280 and WG230) wavelengths inhibit the production of lipid peroxidation in these experiments.
  • the slow rise to a peak between 360-375 demonstrated by the greatest effect using the difference between the WG360 and the WG375 filters is similar to the absorbance spectra for retinoic acid (See Figure 17) .

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Abstract

Cette invention se rapporte à des moyens et à des procédés pour appliquer topiquement sur la peau d'un mammifère un rétinoïde qui réduit ou élimine les effets oxydatifs induits par les rétinoïdes et véhiculés par les ultra-violets A. Ce procédé consiste à appliquer topiquement sur la peau une composition de rétinoïde qui contient une quantité efficace de rétinoïde et une quantité efficace d'un antioxydant lipophile.
PCT/US1997/022441 1996-12-10 1997-12-08 Utilisation de composes antioxydants lipophiles pour empecher les reactions oxydatives induites par les retinoides et vehiculees par les uva WO1998025587A1 (fr)

Priority Applications (5)

Application Number Priority Date Filing Date Title
JP10526847A JP2000505816A (ja) 1996-12-10 1997-12-08 レチノイド誘発ｕｖａ媒介酸化反応を防止するための親脂性酸化防止剤化合物の使用
BR9707630A BR9707630A (pt) 1996-12-10 1997-12-08 Uso de compostos antioxidantes lipofílicos para prevenção de retinóides induzidos reações oxidantivas mediadas por ultravioleta do tipo a
AU55188/98A AU5518898A (en) 1996-12-10 1997-12-08 Use of lipophilic antioxidant compounds to prevent retinoid induced, UVA-mediat ed oxidative reactions
EP97951582A EP0914089A1 (fr) 1996-12-10 1997-12-08 Utilisation de composes antioxydants lipophiles pour empecher les reactions oxydatives induites par les retinoides et vehiculees par les uva
IL12570097A IL125700A0 (en) 1996-12-10 1997-12-08 Use of lipophilic antioxidant compounds to prevent retinoid induced uva-mediated oxidative reactions

Applications Claiming Priority (2)

Application Number Priority Date Filing Date Title
US76278496A 1996-12-10 1996-12-10
US08/762,784 1996-12-10

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WO1998025587A1 true WO1998025587A1 (fr) 1998-06-18

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EP (1) EP0914089A1 (fr)
JP (1) JP2000505816A (fr)
KR (1) KR19990082411A (fr)
CN (1) CN1215328A (fr)
AU (1) AU5518898A (fr)
BR (1) BR9707630A (fr)
CA (1) CA2246306A1 (fr)
ID (1) ID18520A (fr)
IL (1) IL125700A0 (fr)
IN (1) IN187969B (fr)
WO (1) WO1998025587A1 (fr)

Cited By (2)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2001039739A1 (fr) * 1999-12-03 2001-06-07 Pierre Fabre Dermo-Cosmetique Association retinal et aldehydes avec activite antifongique
WO2001068081A1 (fr) * 2000-03-13 2001-09-20 GSF-Forschungszentrum für Umwelt und Gesundheit GmbH Agent pour le traitement de maladies du tractus tracheobronchique, en particulier de la bronchopneumopathie chronique obstructive

Families Citing this family (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
JP5728152B2 (ja) * 2008-07-07 2015-06-03 株式会社ファンケル 乾燥リポソーム製剤

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EP0094771A2 (fr) * 1982-05-15 1983-11-23 Beecham Group Plc Composition pour le traitement de la peau
JPH0632716A (ja) * 1992-07-13 1994-02-08 Shiseido Co Ltd 皮膚外用剤
WO1995026709A1 (fr) * 1994-04-05 1995-10-12 Pierre Fabre Dermo-Cosmetique Composition topique a base de retinal
WO1997031620A2 (fr) * 1996-03-01 1997-09-04 Johnson & Johnson Consumer Products, Inc. Compositions a usage local contenant une emulsion aqueuse et un retinoide
WO1997047279A1 (fr) * 1996-06-12 1997-12-18 Johnson & Johnson Consumer Products, Inc. Composes photoprotecteurs a base d'antioxydant lipophile_0

Patent Citations (5)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
EP0094771A2 (fr) * 1982-05-15 1983-11-23 Beecham Group Plc Composition pour le traitement de la peau
JPH0632716A (ja) * 1992-07-13 1994-02-08 Shiseido Co Ltd 皮膚外用剤
WO1995026709A1 (fr) * 1994-04-05 1995-10-12 Pierre Fabre Dermo-Cosmetique Composition topique a base de retinal
WO1997031620A2 (fr) * 1996-03-01 1997-09-04 Johnson & Johnson Consumer Products, Inc. Compositions a usage local contenant une emulsion aqueuse et un retinoide
WO1997047279A1 (fr) * 1996-06-12 1997-12-18 Johnson & Johnson Consumer Products, Inc. Composes photoprotecteurs a base d'antioxydant lipophile_0

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Title
CHEMICAL ABSTRACTS, vol. 94, no. 12, 23 March 1981, Columbus, Ohio, US; abstract no. 90167c, SHI: "the degradation of tretinoin" XP002064774 *
PATENT ABSTRACTS OF JAPAN vol. 018, no. 251 (C - 1199) *
STN, File Supplier, Karlsruhe, DE, File *
T'AI-WAN YAO HSUEH TSA CHIH, vol. 31, no. 2, 1979, pages 131 - 136 *

Cited By (3)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2001039739A1 (fr) * 1999-12-03 2001-06-07 Pierre Fabre Dermo-Cosmetique Association retinal et aldehydes avec activite antifongique
FR2801790A1 (fr) * 1999-12-03 2001-06-08 Fabre Pierre Cosmetique Association retinal et aldehydes, composition cosmetique la contenant, a titre de medicament l'association retinal et aldehydes, et procede de preparation de cette association
WO2001068081A1 (fr) * 2000-03-13 2001-09-20 GSF-Forschungszentrum für Umwelt und Gesundheit GmbH Agent pour le traitement de maladies du tractus tracheobronchique, en particulier de la bronchopneumopathie chronique obstructive

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CA2246306A1 (fr) 1998-06-18
IN187969B (fr) 2002-08-03
EP0914089A1 (fr) 1999-05-12
JP2000505816A (ja) 2000-05-16
KR19990082411A (ko) 1999-11-25
ID18520A (id) 1998-04-16
AU5518898A (en) 1998-07-03
BR9707630A (pt) 1999-07-27
CN1215328A (zh) 1999-04-28

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