FIELD OF THE INVENTION
The present invention relates to a skin lightening composition comprising isoflavone actives. These actives are antagonist for eumelanin synthesis pathway and melanocyte dendricity for skin lightening.
BACKGROUND AND PRIOR ART OF THE INVENTION
Darker skin is predominant due to the increased level of eumelanin synthesis. Specific enzymes required for melanin synthesis is produced in melanosomes and transferred via dendrites to neighboring keratinocytes which determines skin color. The genes that control the enzymes for mainstream of melanin synthesis are tyrosinase, tyrosinase-related protein-1 (TRP-1), tyrosinase-related protein-2 (TRP-2) and associated transcription factors. Tyrosinase is required for both eumelanin and pheomelanin synthesis. TRP-1 and TRP-2 seem to be more crucial for eumelanin synthesis that is responsible for dark brown pigmentation in dark skin people. The identification of bioactives which antagonist TRP-1 and TRP-2 gene expression will help to reduce the eumelanin content in the dark skin people and will help to design product specifically targeting Indian population to achieve skin lightening.
Isoflavones may be known to inhibit tyrosinase and can be used as skin lightening agents. However, the present invention discloses a method of down regulating the mRNA expression of TRP-1 and TPR-2 genes using actives such as 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone that inhibits eumelanin synthesis.
Both isoflavones have been used as mushroom tyrosinase inhibitors; however, effect of isoflavones on human eumelanin synthesis and dendricity is currently not yet clearly defined.
Chang TS, et.al. (2005) disclose isoflavones that inhibit mushroom tyrosinase which involves In vitro enzyme kinetic assays whereas the present invention discloses a method of down regulating the mRNA expression of TRP-1 and TPR-2 genes using actives such as 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone that inhibits eumelanin synthesis in Indian human skin melanocytes.
The present invention is directed to the molecular mechanism involved in eumelanin synthesis mediated by TRP-1 /TRP-2 pathway by biotransformed isoflavones from soya.

Surprisingly, the present invention shows that the said isoflavones specifically antagonist the cAMP production, TRP-1 and TRP-2 mRNA expression, melanocyte dendricity and does not affect the tyrosinase and microphthalmia-associated transcription factor (MITF) mRNA expression.
OBJECTS OF THE INVENTION
The main objective of the present invention is to provide a skin lightening composition comprising actives such as 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone that down regulates TRP-1 and TRP-2 mRNA expression responsible for eumelanin synthesis.
Yet another objective of the present invention is to provide a skin lightening composition comprising actives such as 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone that can be used in human skin melanocytes especially in Indian human skin melanocytes.
SUMMARY OF THE INVENTION
According to one aspect there is provided an antagonist skin lightening composition for eumelanin synthesis pathway and melanocyte dendricity comprising atleast one active isoflavone within cosmetic acceptable vehicle wherein the isoflavones used are selected from the group comprising of 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone, or the like and mixtures thereof.
BRIEF DESCRIPTION OF THE ACCOMPANYING DRAWINGS:
Figure 1: A simplified schematic showing the features of key signaling pathways in melanin synthesis. Abbreviations: MITF, microphthalmia-associated transcription factor; TRP-1, tyrosinase related protein-1; TRP-2, tyrosinase related protein-2; PAX3, paired box 3 family of transcription factors; SOX 10, SRY-related HMG-box 10 family of transcription factors; cAMP, Cyclic adenosine monophosphate; CREB, cAMP response element-binding protein; MC1R, melanocortin 1 receptor; a-MSH, Melanocyte stimulating hormone; EDN, endothelin; EDNR, endothelin receptor; MAPK, mitogen activated protein kinase.
Figure.2: Dose dependent effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on cell viability.

Figure.3: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on TRP-2 mRNA expression in human melanocyte after 4, 8 and 16 hours treatment.
Figure.4: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on TRP-1 mRNA expression in human melanocyte after 4, 8 and 16 hours treatment.
Figure.5: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on tyrosinase mRNA expression in human melanocyte after 4, 8 and 16 hours treatment.
Figure.6: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on MITF mRNA expression in human melanocyte after 4, 8 and 16 hours treatment.
Figure.7: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on SOX10 mRNA expression in human melanocyte after 4, and 8 hours treatment.
Figure.8: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on PAX3 mRNA expression in human melanocyte after 4, and 8 hours treatment.
Figure.9: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on melanocyte dendricity in human melanocyte after 72 hours treatment.
Figure.10: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on melanocyte dendricity in human melanocyte after 72 hours treatment.
Figure.ll: Effect of 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on cAMP production in human melanocyte.
Figure.12: Synergistic effect of 1µM 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on TRP-2 mRNA expression.
Figure.13: Synergistic effect of luM 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone on dendrites formation.
DETAILED DESCRIPTION OF THE INVENTION
Accordingly, the present invention provides an antagonist skin lightening composition for human eumelanin synthesis pathway and melanocyte dendricity comprising atleast one active

isoflavone within cosmetic acceptable vehicle wherein the isoflavones used are selected from the group comprising of 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone, or the like and mixtures thereof.
The skin lightening composition provided by present invention for human eumelanin synthesis pathway and melanocyte dendricity is preferably a cream for skin lightening.
The isoflavones used are antagonist for eumelanin synthesis pathway and melanocyte dendricity for skin lightening as illustrated in figure 1. The present invention shows the effect of isoflavones on human eumelanin synthesis and dendricity.
The present invention also shows that the said isoflavones specifically antagonizes the cAMP production, TRP-1 and TRP-2 mRNA expression, melanocyte dendricity and does not affect the tyrosinase and microphthalmia-associated transcription factor (MITF) mRNA expression.
In the present invention, human melanocytes were treated with 20µM of 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone and Epigallocatechin gallate (EGCG), for 4, 8 and 16 hours. EGCG has been reported to reduce the protein levels of MITF and of tyrosinase, which is known to regulate the rate-limiting step of melanin synthesis therefore EGCG we selected as a positive control for pigmentation. The results showed down regulation of cAMP levels after 15 minutes for 7,8,4'-Trihydroxyisoflavone and 60 minutes for 6,7,4'-Trihydroxyisoflavone. TRP-1, TRP-2, SOX10 mRNA expression were down regulated upon treatment with 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone. In 6,7,4'-Trihydroxyisoflavone treated cells, 72% of cells exhibited less than three dendrites whereas the cells treated with 7,8,4'-Trihydroxyisoflavone did not shown any change in dendrites formation.
PAX3 did not show any change when treated with 7,8,4'-Trihydroxyisoflavone. On the other hand, 6,7,4 '-Trihydroxyisoflavone increased the levels of PAX3 mRNA.
Since, there was no significant change observed in 16 hours treatment on MITF, tyrosinase, TRP-1 and TRP-2, therefore further experiments were conducted for 4 and 8 hours for study. Treatment of 4 and 8 hrs 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone and EGCG significantly down regulated SOX10 mRNA expression (Fig 7). Both isoflavones

significantly reduced SOX 10 mRNA expression, which would result in defects in TRP-2 mRNA expression.
Deletion analysis of the TRP-2 promoter sequence reveals that TRP-2 contains a functional Pax3, Sox 10 and MITF responsive element. SOX 10 and PAX3 are an important transcription factor regulating the development of melanocytes and melanin synthesis. Therefore, further experiments were conducted and the results are shown in figures 7 and 8. The results indicated that 6,7,4'-Trihydroxyisoflavone significantly up regulated PAX3 expression and both isoflavones are down regulated SOX10 expression. Hence, 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone down regulated TRP-2 mRNA expression mediated by Sox 10 and PAX3 transcription factors.
Taken together all the results it is concluded that down regulation of TRP-1 and TRP-2 via PAX3 and SOX 10 transcription factors and reduction of cAMP level and melanocyte dendricity by bio-transformed isoflavones may lead to enhanced skin lightening.
The present invention relates to an antagonist composition for eumelanin synthesis pathway and melanocyte dendricity comprising atleast one active isoflavone within cosmetic acceptable vehicle.
In the present invention the isoflavones used are selected from the group comprising of 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone, or the like and mixtures thereof.
In another embodiment of the present invention where in the isoflavones used are in the range of 0.1-2% by weight.
The cosmetic acceptable vehicle comprises thickeners, chelating agents, emollients, emulsifiers, neutralizing agent, preservatives and fragrance.
The thickeners used are selected from the group comprising of acrylate polymer, xanthum gum, Hydroxyethyl Acrylate, Sodium Acryloyldimethyl Taurate Copolymer, Isohexadecane, Polysorbate 60 and mixtures thereof.
The chelating agent used is selected from the group comprising of disodium EDTA, tetrahydroxypropyl ethylenediamine, tetrapotassium etidronate, tetrasodium edta, tripotassium edta, trisodium edta, trisodium hedta, trisodium nta, tetrasodium etidronate etc.

The emollients used are selected from the group comprising of C12-15 alkyl benzoate, cetosteryl alcohol, Butyl isostearate, butyl myristate, butyl oleate, butyl stearate, butylene glycol dicaprylate / dicaprate, butylene glycol montanate, cl 1-15 pareth-12 stearate, cl1-15 pareth-3 stearate, cl2-13 alkyl lactate, cl2-13 alkyl octanoate, cl2-15 alkyl benzoate, cl2-15 alkyl lactate, cl2-15 alkyl octanoate, isocetyl myristate, isocetyl palmitate, isocetyl stearate, isodecyl citrate, isodecyl cocoate, isodecyl hydroxystearate, isodecyl laurate, isodecyl myristate, isodecyl neopentanoate, isodecyl octanoate, isodecyl oleate, isodecyl palmitate, isodecyl stearate, peg-5 tricetyl citrate, peg-5 tridecyl citrate, peg-5 trilauryl citrate, peg-5 trimyristyl citrate, peg-5 tristearyl citrate, peg-8 linoleate, peg-8 linolenate, propylene glycol behenate, propylene glycol capreth-4, propylene glycol caprylate, propylene glycol ceteth-3 acetate, propylene glycol ceteth-3 propionate, propylene glycol citrate, Propylene glycol cocoate, propylene glycol dicaprate, propylene glycol dicaproate, propylene glycol dicaprylate / dicaprate, propylene glycol diisostearate, propylene glycol dioctanoate and other emollients and others known in the art.
The emulsifiers used are selected from the group comprising Cetostearyl alcohol, Glyceryl Stearate, PEG-100 Stearate, capric acid, caproic acid, capryleth-4 carboxylic acid, capryleth-6 carboxylic acid, capryleth-9 carboxylic acid, caprylic / capric triglyceride peg-4 esters, caprylic acid, ceteareth-10, glycereth-20 stearate, glycereth-25 pea isostearate, glycereth-26 phosphate, glycereth-5 lactate, glycereth-7 benzoate, glycereth-7 diisononanoate, glycereth-8 hydroxystearate, glyceryl citrate / lactate / linoleate / oleate, glyceryl glycyrrhetinate, lyceryl isopalmitate, glyceryl isotridecanoate / stearate / adipate, glyceryl laurate, glyceryl montanate, glyceryl oleate, glyceryl palmitoleate, glyceryl stearate, glycol montanate, glycol octanoate, glycol palmitate, glycol stearate, hexacosyl glycol isostearate, hexyldeceth-2, hexyldeceth-20, hydrogenated laneth-20, hydrogenated laneth-25, hydrogenated laneth-5, hydrogenated lard glyceride, hydrogenated lard glycerides, hydrogenated lecithin, hydrogenated talloweth-12, hydrogenated talloweth-25, hydrogenated talloweth-60 myristyl glycol, hydrogenated vegetable glycerides citrate, hydroxycetyl isostearate, hydroxycetyl phosphate, hydroxylated lecithin, hydroxystearic acid, isoceteareth-8 stearate, isoceteth-10, isoceteth-10 stearate, isoceteth-20, isodeceth-4, isodeceth-5, isodeceth-6, isolaureth-10, isolaureth-3, isolaureth-6, isosorbide laurate, isosteareth-10, isosteareth-10 stearate, isosteareth-12, isosteareth-2,

isosteareth-20, isosteareth-22, isosteareth-3, isostearic / myristic glycerides, isostearoyl isostearyl stearate, laureth series, myristic acid, octyl linoleoyl stearate, octyldecyl oleate, octyldodeceth series, polyethylene glycol, steareth series, stearoyl lactylic acid, sucrose dilaurate, sucrose myristate, sucrose oleate, sucrose polylaurate, sucrose polylinoleate, sucrose polyoleate, sucrose polystearate, sucrose ricinoleate, sucrose stearate, sucrose tetrastearate triacetate, sucrose tribehenate, sucrose tristearate, tallowaminopropylamine, talloweth-6, trideceth series, undecanoic acid, undeceth-5, stearic acid and others known in the art.
The neutralizing agents used are selected from the group comprising Triethanolamine and others that are known in the art.
The preservatives used are selected from the group comprising Phenoxyethanol, Ethylhexyl Glycerin and other that are known in the art.
The composition of the present invention is water based composition.



Example 2
SYBR green based cell viability assay revealed that 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone were not cytotoxic to human melanocytes in the concentration range of l-20µM(Fig2).
Example 3
Treatment of 4 and 8 hrs 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone and EGCG significantly down regulated TRP-2 mRNA expression (Fig 3). Both isoflavones significantly reduced TRP-2 expression, which would result in defects in eumelanin biosynthesis.
Example 4
In this study, both isoflavones significantly down regulated TRP-1 mRNA expression after 4 and 8 hours (Fig 4).
Example 5
Isoflavones treated group results (Fig 5) revealed that there were no significant changes in Tyrosinase mRNA expression after 4, 8 and 16 hrs when compared with DMSO control. ECGC treated group showed the decreased level of tyrosinase mRNA expression after 4 hours treatment.
Example 6
MITF is one of the major transcriptional regulators of tyrosinase, and thus plays a critical role in melanin synthesis. Results from time course study (Fig 6) revealed that there was no significant change in MITF mRNA expression after 4, 8 and 16 hours isoflavones treated

groups, however our positive control EGCG treated group as expected down regulates MITF mRNA expression after 4hours when compared with DMSO control.
Example 7
MITF is a main regulator of melanin synthesis pathway which is regulates tyrosinase, TRP-1 and TRP-2 mRNA expression however our current study did not show any modulation in MITF mRNA expression after treated with isoflavones. Hence, to investigate understand the molecular mechanism involved in down regulation of TRP-1 and TRP-2, we analyzed two transcription factors namely SRY-related HMG-box (SOX 10) and Paired box 3 (PAX3) that directly regulate TRP-1 and TRP-2 expression. Previous studies have implicated SOX10 to play a major role in the establishment and normal function of the melanocyte and melanogenesis in adult. Moreover Sox 10 acts directly on the TRP-2 promoter to activate gene expression in neural-crest-derived melanocyte development. It is reported that over expression of Sox 10 increased TRP-2 expression, whereas inactivation of Sox 10 by Sox10del reduced TRP-2 expression in a dose-dependent manner.
Example 8
PAX3, another transcription factor also coordinates the development of the melanocytes and melanogenesis and overexpression of PAX3 was shown to repress the TRP-1 and TRP-2 expression. In our current study, we show that treatment of 6,7,4'-Trihydroxyisoflavone for 4 and 8 hours significantly up regulated PAX3 mRNA expression (Fig 8). Also, 6,7,4'-Trihydroxyisoflavone dramatically induced PAX3 mRNA expression, which would also result in down regulation of TRP-1 and TRP-2 mRNA expression.
Example 9
Movement of melanosomes along melanocyte dendrites is necessary for the transfer of melanin pigment from melanocytes to basal and suprabasal keratinocytes, an event critical to epidermal photoprotection and maintenance of normal skin color. Human melanocytes were cultured on tissue culture treated plates and drug treatment began 24 h after seeding. Cells were treated with DMSO, 20µM 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone, Forskolin and 100 nM a-MSH for 72 hours (Fig 9 and Fig 10). Cultures were washed with phosphate buffered saline and fixed using pre-cooled methanol for 1 hr at room temperature.

To examine dendrites formation in melanocytes, cells were analyzed under the microscope after Fontana Masson staining procedure.
In 6,7,4'-Trihydroxyisoflavone treated cells, 72% of cells exhibited less than three dendrites. In contrast, the number of dendrites projection was not changed in melanocyte treated with 7,8,4'-Trihydroxyisoflavone and positive controls (forskolin and a-MSH) are not changed in dendrites formation when compared with DMSO treated control. Reduced melanocyte dendricity by 6,7,4'-Trihydroxyisoflavone may decreases the melanosome transfer from melanocyte to keratinocytes, which would help skin lightening.
Example 10
cAMP is a critical factor, involved in the signal transduction pathways, that plays a role in the regulation of melanin synthesis. The mechanism by which cAMP regulates melanin synthesis involves activation of protein kinase A (PKA). The transcriptional activity is then regulated by PKA following phosphorylation of the cAMP responsible element binding protein (CREB) and CREB binding protein (CBP). Phosphorylated CREB then interacts with CBP to activate the expression of MITF. MITF is a key factor involved in regulation of major melanogenic proteins including tyrosinase, TRP-1 and TRP-2.
The present study, primary human melanocytes were treated with 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone and positive controls such as a-MSH and forskolin. Cellular levels of cAMP were greatly reduced by 15 min after treated with 7,8,4'-Trihydroxyisoflavone. Furthermore, 6,7,4'-Trihydroxyisoflavone significantly reduced cAMP level in 60 min. Positive control treatments steadily elevated cAMP levels. TRP-1 and TRP-2 promoter activities are also induced by cAMP, hence both isoflavones may also down regulate TRP-1 and TRP-2 mRNA expression via cAMP (Fig 11).
Example 11
The tyrosinase related protein-2 (TRP2) is specifically expressed in melanocytes, and it likewise contribute to the synthesis of eumelanin within the melanosomes. The present study, primary human melanocytes were treated with different ratios of 1µM 6,7,4'-THIF and lµM 7,8,4'-THIF such as 1:9 to 9:1 for 8 hours. Combination of 6,7,4'-THIF and 7,8,4'-THIF did

not down regulate expression of TRP-2 mRNA when compared with DMSO treated control (Fig 12).
Example 12
The number of dendrites projection was not changed in melanocyte treated with combination of lµM 6,7,4'-THIF and lµM 7,8,4'-THIF are not showed any synergistic effects in dendrites formation when compared with DMSO control (Fig 13). Hence, we conclude that combination of lµM 6,7,4'-THIF and lµM 7,8,4'-THIF ((other than 2µM to 20µM) did not show synergistic effects on eumelanin synthesis.

WE CLAIM:
1. An antagonist skin lightening composition for eumelanin synthesis pathway and melanocyte dendricity comprising at least one active isoflavone in cosmetic acceptable vehicle, wherein the isoflavones are selected from 6,7,4'-Trihydroxyisoflavone, 7,8,4'-Trihydroxyisoflavone, or the like and mixture thereof.
2. The composition as claimed in claim 1 where in the isoflavones used are in the range of 0.1-2.0% by weight.
3. The composition as claimed in claim 1 wherein the cosmetic acceptable vehicle comprises thickeners, chelating agents, emollients, emulsifiers, neutralizing agent, preservatives and fragrance.
4. The composition as claimed in claim 3 wherein the chelating agent used is selected from the group comprising disodium EDTA, tetrahydroxypropyl ethylenediamine, tetrapotassium etidronate, tetrasodium edta, tripotassium edta, trisodium edta, trisodium hedta, trisodium nta, tetrasodium etidronate.
5. The composition as claimed in claim 3 wherein the emollients used are selected from the group comprising C12-15 alkyl benzoate, cetosteryl alcohol, Butyl isostearate, butyl myristate, butyl oleate, butyl stearate, butylene glycol dicaprylate / dicaprate, butylene glycol montanate, cl 1-15 pareth-12 stearate, cll-15 pareth-3 stearate, cl2-13 alkyl lactate, cl2-13 alkyl octanoate, cl2-15 alkyl benzoate, cl2-15 alkyl lactate, cl2-15 alkyl octanoate, isocetyl myristate, isocetyl palmitate, isocetyl stearate, isodecyl citrate, isodecyl cocoate, isodecyl hydroxystearate, isodecyl laurate, isodecyl myristate, isodecyl neopentanoate, isodecyl octanoate, isodecyl oleate, isodecyl palmitate, isodecyl stearate, peg-5 tricetyl citrate, peg-5 tridecyl citrate, peg-5 trilauryl citrate, peg-5 trimyristyl citrate, peg-5 tristearyl citrate, peg-8 linoleate, peg-8 linolenate, propylene glycol behenate, propylene glycol capreth-4, propylene glycol caprylate, propylene glycol ceteth-3 acetate, propylene glycol ceteth-3 propionate, propylene glycol citrate, Propylene glycol cocoate, propylene glycol dicaprate,

propylene glycol dicaproate, propylene glycol dicaprylate / dicaprate, propylene glycol diisostearate, propylene glycol dioctanoate and other emollients.
6. The composition as claimed in claim 3 wherein emulsifiers used are selected from the group comprising Cetostearyl alcohol, Glyceryl Stearate, PEG-100 Stearate, capric acid, caproic acid, capryleth-4 carboxylic acid, capryleth-6 carboxylic acid, capryleth-9 carboxylic acid, caprylic / capric triglyceride peg-4 esters, caprylic acid, ceteareth-10, glycereth-20 stearate, glycereth-25 pea isostearate, glycereth-26 phosphate, glycereth-5 lactate, glycereth-7 benzoate, glycereth-7 diisononanoate, glycereth-8 hydroxystearate, glyceryl citrate / lactate / linoleate / oleate, glyceryl glycyrrhetinate, lyceryl isopalmitate, glyceryl isotridecanoate / stearate / adipate, glyceryl laurate, glyceryl montanate, glyceryl oleate, glyceryl palmitoleate, glyceryl stearate, glycol montanate, glycol octanoate, glycol palmitate, glycol stearate, hexacosyl glycol isostearate, hexyldeceth-2, hexyldeceth-20, hydrogenated laneth-20, hydrogenated laneth-25, hydrogenated laneth-5, hydrogenated lard glyceride, hydrogenated lard glycerides, hydrogenated lecithin, hydrogenated talloweth-12, hydrogenated talloweth-25, hydrogenated talloweth-60 myristyl glycol, hydrogenated vegetable glycerides citrate, hydroxycetyl isostearate, hydroxycetyl phosphate, hydroxylated lecithin, hydroxystearic acid, isoceteareth-8 stearate, isoceteth-10, isoceteth-10 stearate, isoceteth-20, isodeceth-4, isodeceth-5, isodeceth-6, isolaureth-10, isolaureth-3, isolaureth-6, isosorbide laurate, isosteareth-10, isosteareth-10 stearate, isosteareth-12, isosteareth-2, isosteareth-20, isosteareth-22, isosteareth-3, isostearic / myristic glycerides, isostearoyl isostearyl stearate, laureth series, myristic acid, octyl linoleoyl stearate, octyldecyl oleate, octyldodeceth series, polyethylene glycol, steareth series, stearoyl lactylic acid, sucrose dilaurate, sucrose myristate, sucrose oleate, sucrose polylaurate, sucrose polylinoleate, sucrose polyoleate, sucrose polystearate, sucrose ricinoleate, sucrose stearate, sucrose tetrastearate triacetate, sucrose tribehenate, sucrose tristearate, tallowaminopropylamine, talloweth-6, trideceth series, undecanoic acid, undeceth-5, stearic acid.
7. The composition as claimed in claim 1 wherein the composition is water based composition.

8. The antagonist skin lightening composition for eumelanin synthesis pathway and melanocyte dendricity as described herein with reference to the examples and drawings.

ABSTRACT

The present invention discloses a skin lightening composition comprising isoflavones. The novelty of the invention lies in down regulation of TRP-1, TRP-2 gene expression, cAMP and melanocyte dendricity by isoflavones, specifically 6,7,4'-Trihydroxyisoflavone and 7,8,4'-Trihydroxyisoflavone in Indian skin melanocytes. The present invention does not show any significant change in tyrosinase and microphthalmia-associated transcription factor (MITF) mRNA expression.