Taxifolin CAS NO.480-18-2

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition：Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Chemical Properties of Taxifolin

Cas No.	480-18-2
PubChem ID	439533	Appearance	White powder
Formula	C15H12O7	M.Wt	304.3
Type of Compound	Flavonoids	Storage	Desiccate at -20°C
Synonyms	Dihydroquercetin; Taxifoliol; (+)-Dihydroquercetin; (+)-Taxifolin
Solubility	DMSO : ≥ 100 mg/mL (328.68 mM) *"≥" means soluble, but saturation unknown.
Chemical Name	(2R,3R)-2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one
SMILES	C1=CC(=C(C=C1C2C(C(=O)C3=C(C=C(C=C3O2)O)O)O)O)O
Standard InChIKey	CXQWRCVTCMQVQX-LSDHHAIUSA-N
Standard InChI	InChI=1S/C15H12O7/c16-7-4-10(19)12-11(5-7)22-15(14(21)13(12)20)6-1-2-8(17)9(18)3-6/h1-5,14-19,21H/t14-,15+/m0/s1
General tips	For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging	1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment.
Shipping Condition	Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Taxifolin

1 Agrimonia sp. 2 Callitris sp. 3 Calluna sp. 4 Citrus sp. 5 Drimys sp. 6 Equisetum sp. 7 Fagus sp. 8 Inula sp. 9 Picea sp. 10 Pinus sp. 11 Pseudozuga sp. 12 Rhododendron sp. 13 Salix sp. 14 Silybum sp. 15 Thuja sp. 16 Thymus sp.

Biological Activity of Taxifolin

Description	Taxifolin exhibits important anti-tyrosinase activity, it also exhibits significant inhibitory activity against collagenase with an IC50 value of 193.3 μM.Taxifolin has anti-oxidant, anti-melanogenic, chemopreventive, anti-inflammatory, and cardioprotective effects. Taxifolin promotes osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, it also can enhance andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.
Targets	EGFR | PI3K | COX | PGE | Akt | NADPH-oxidase | ROS | Caspase | STAT | JAK | NOS | NO | NF-kB
In vitro	Taxifolin suppresses UV-induced skin carcinogenesis by targeting EGFR and PI3K.[Pubmed: 22805054 ] Cancer Prev Res (Phila). 2012 Sep;5(9):1103-14. Skin cancer is one of the most commonly diagnosed cancers in the United States. Taxifolin reportedly exerts multiple biologic effects, but the molecular mechanisms and direct target(s) of Taxifolin in skin cancer chemoprevention are still unknown. METHODS AND RESULTS: In silico computer screening and kinase profiling results suggest that the EGF receptor (EGFR), phosphoinositide 3-kinase (PI3K), and Src are potential targets for Taxifolin. Pull-down assay results showed that EGFR, PI3K, and Src directly interacted with Taxifolin in vitro, whereas Taxifolin bound to EGFR and PI3K, but not to Src in cells. ATP competition and in vitro kinase assay data revealed that Taxifolin interacted with EGFR and PI3K at the ATP-binding pocket and inhibited their kinase activities. Western blot analysis showed that Taxifolin suppressed UVB-induced phosphorylation of EGFR and Akt, and subsequently suppressed their signaling pathways in JB6 P+ mouse skin epidermal cells. Expression levels and promoter activity of COX-2 and prostaglandin E(2) (PGE(2)) generation induced by UVB were also attenuated by Taxifolin. The effect of Taxifolin on UVB-induced signaling pathways and PGE(2) generation was reduced in EGFR knockout murine embryonic fibroblasts (MEF) compared with EGFR wild-type MEFs. Taxifolin also inhibited EGF-induced cell transformation. Importantly, topical treatment of Taxifolin to the dorsal skin significantly suppressed tumor incidence, volume, and multiplicity in a solar UV (SUV)-induced skin carcinogenesis mouse model. Further analysis showed that the Taxifolin-treated group had a substantial reduction in SUV-induced phosphorylation of EGFR and Akt in mouse skin. CONCLUSIONS: These results suggest that Taxifolin exerts chemopreventive activity against UV-induced skin carcinogenesis by targeting EGFR and PI3K. Taxifolin enhances andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.[Pubmed: 23382917] PLoS One. 2013;8(1):e54577. Andrographolide (Andro) suppresses proliferation and triggers apoptosis in many types of cancer cells. Taxifolin (Taxi) has been proposed to prevent cancer development similar to other dietary flavonoids. METHODS AND RESULTS: In the present study, the cytotoxic and apoptotic effects of the addition of Andro alone and Andro and Taxi together on human prostate carcinoma DU145 cells were assessed. Andro inhibited prostate cancer cell proliferation by mitotic arrest and activation of the intrinsic apoptotic pathway. Although the effect of Taxi alone on DU145 cell proliferation was not significant, the combined use of Taxi with Andro significantly potentiated the anti-proliferative effect of increased mitotic arrest and apoptosis by enhancing the cleavage of poly(ADP-ribose) polymerase, and caspases-7 and -9. Andro together with Taxi enhanced microtubule polymerization in vitro, and they induced the formation of twisted and elongated spindles in the cancer cells, thus leading to mitotic arrest. In addition, we showed that depletion of MAD2, a component in the spindle assembly checkpoint (SAC), alleviated the mitotic block induced by the two compounds, suggesting that they trigger mitotic arrest by SAC activation. CONCLUSIONS: This study suggests that the anti-cancer activity of Andro can be significantly enhanced in combination with Taxi by disrupting microtubule dynamics and activating the SAC.
In vivo	Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.[Pubmed: 24269735] Food Chem Toxicol. 2014 Jan;63:221-32. Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. METHODS AND RESULTS: The objective of this study was to investigate the potential protective effects and mechanisms of Taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that Taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, Taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that Taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. CONCLUSIONS: In conclusion, Taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy. Flavonoids, taxifolin and luteolin attenuate cellular melanogenesis despite increasing tyrosinase protein levels.[Pubmed: 18729255 ] Phytother Res. 2008 Sep;22(9):1200-7. Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis. When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), Taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, Taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase. Therefore, the antimelanogenic effects of Taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.

Protocol of Taxifolin

Kinase Assay	Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation.[Pubmed: 16283433 ] J Biomed Sci. 2006 Jan;13(1):127-41. Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis. METHODS AND RESULTS: When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), Taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, Taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase. CONCLUSIONS: Therefore, the antimelanogenic effects of Taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.
Cell Research	Quercitrin and taxifolin stimulate osteoblast differentiation in MC3T3-E1 cells and inhibit osteoclastogenesis in RAW 264.7 cells.[Pubmed: 24060614] Biochem Pharmacol. 2013 Nov 15;86(10):1476-86. Flavonoids are natural antioxidants that positively influence bone metabolism. METHODS AND RESULTS: The present study screened among different flavonoids to identify biomolecules for potential use in bone regeneration. For this purpose, we used MC3T3-E1 and RAW264.7 cells to evaluate their effect on cell viability and cell differentiation. First, different doses of chrysin, diosmetin, galangin, quercitrin and Taxifolin were analyzed to determine the optimum concentration to induce osteoblast differentiation. After 48h of treatment, doses ≥100μM of diosmetin and galangin and also 500μM Taxifolin revealed a toxic effect on cells. The same effect was observed in cells treated with doses ≥100μM of chrysin after 14 days of treatment. However, the safe doses of quercitrin (200 and 500μM) and Taxifolin (100 and 200μM) induced bone sialoprotein and osteocalcin mRNA expression. Also higher osteocalcin secreted levels were determined in 100μM Taxifolin osteoblast treated samples when compared with the control ones. On the other hand, quercitrin and Taxifolin decreased Rankl gene expression in osteoblasts, suggesting an inhibition of osteoclast formation. Indeed, osteoclastogenesis suppression by quercitrin and Taxifolin treatment was observed in RAW264.7 cells. CONCLUSIONS: Based on these findings, the present study demonstrates that quercitrin and Taxifolin promote osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, showing a positive effect of these flavonoids on bone metabolism.
Animal Research	Modulation of hepatic lipoprotein synthesis and secretion by taxifolin, a plant flavonoid.[Pubmed: 11108730] J Lipid Res. 2000 Dec;41(12):1969-79. METHODS AND RESULTS: Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether Taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 microg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/-7% and 62%+/-6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappaB) that in turn signaled up-regulation of inflammatory proteins. NF-kappaB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by Taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by Taxifolin. CONCLUSIONS: These data suggest that amelioration of CI/R injury by Taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappaB activation that mediates CI/R injury.

Preparing Stock Solutions of Taxifolin

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	3.2862 mL	16.4312 mL	32.8623 mL	65.7246 mL	82.1558 mL
5 mM	0.6572 mL	3.2862 mL	6.5725 mL	13.1449 mL	16.4312 mL
10 mM	0.3286 mL	1.6431 mL	3.2862 mL	6.5725 mL	8.2156 mL
50 mM	0.0657 mL	0.3286 mL	0.6572 mL	1.3145 mL	1.6431 mL
100 mM	0.0329 mL	0.1643 mL	0.3286 mL	0.6572 mL	0.8216 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

References on Taxifolin

Modulation of hepatic lipoprotein synthesis and secretion by taxifolin, a plant flavonoid.[Pubmed:11108730]

J Lipid Res. 2000 Dec;41(12):1969-79.

In the present study, the effects of Taxifolin, a plant flavonoid, on lipid, apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I) synthesis and secretion were determined in HepG2 cells. Pretreatment of cells with (+/-)-Taxifolin led to an inhibition of cholesterol synthesis in a dose- and time-dependent manner, with an 86 +/- 3% inhibition at 200 microM observed within 24 h. As to the mechanism underlying this inhibitory effect, Taxifolin was shown to inhibit the activity of HMG-CoA reductase by 47 +/- 7%. In addition, cellular cholesterol esterification, and triacylglycerol and phospholipid syntheses, were also significantly suppressed in the presence of Taxifolin. ApoA-I and apoB synthesis and secretion were then studied by pulse-chase experiments. ApoA-I secretion was found to increase by 36 +/- 10%. In contrast, an average reduction of 61 +/- 8% in labeled apoB in the medium was apparent with Taxifolin. This effect on secretion appeared not to be exerted at the transcriptional level. Rather, the effect on apoB secretion was found to be exerted in the early stages of apoB degradation and to be sensitive to dithiothreitol (DTT) and insensitive to N-acetyl-leucyl-leucyl-norleucinal, suggesting a proteolytic pathway involving a DTT-sensitive protease. Fractionation of secreted apoB revealed a slight shift in the distribution of secreted apoB-containing lipoproteins. Cholesteryl ester, rather than triacylglycerol, was shown to be the lipid that primarily regulated apoB secretion. In summary, our data suggest that Taxifolin decreases hepatic lipid synthesis with a concomitant decrease and increase in apoB and apoA-I secretion, respectively.

Quercitrin and taxifolin stimulate osteoblast differentiation in MC3T3-E1 cells and inhibit osteoclastogenesis in RAW 264.7 cells.[Pubmed:24060614]

Biochem Pharmacol. 2013 Nov 15;86(10):1476-86.

Flavonoids are natural antioxidants that positively influence bone metabolism. The present study screened among different flavonoids to identify biomolecules for potential use in bone regeneration. For this purpose, we used MC3T3-E1 and RAW264.7 cells to evaluate their effect on cell viability and cell differentiation. First, different doses of chrysin, diosmetin, galangin, quercitrin and Taxifolin were analyzed to determine the optimum concentration to induce osteoblast differentiation. After 48h of treatment, doses >/=100muM of diosmetin and galangin and also 500muM Taxifolin revealed a toxic effect on cells. The same effect was observed in cells treated with doses >/=100muM of chrysin after 14 days of treatment. However, the safe doses of quercitrin (200 and 500muM) and Taxifolin (100 and 200muM) induced bone sialoprotein and osteocalcin mRNA expression. Also higher osteocalcin secreted levels were determined in 100muM Taxifolin osteoblast treated samples when compared with the control ones. On the other hand, quercitrin and Taxifolin decreased Rankl gene expression in osteoblasts, suggesting an inhibition of osteoclast formation. Indeed, osteoclastogenesis suppression by quercitrin and Taxifolin treatment was observed in RAW264.7 cells. Based on these findings, the present study demonstrates that quercitrin and Taxifolin promote osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, showing a positive effect of these flavonoids on bone metabolism.

Flavonoids, taxifolin and luteolin attenuate cellular melanogenesis despite increasing tyrosinase protein levels.[Pubmed:18729255]

Phytother Res. 2008 Sep;22(9):1200-7.

Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis. When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), Taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, Taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase. Therefore, the antimelanogenic effects of Taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.

Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.[Pubmed:24269735]

Food Chem Toxicol. 2014 Jan;63:221-32.

Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential protective effects and mechanisms of Taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that Taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, Taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that Taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. In conclusion, Taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.

Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation.[Pubmed:16283433]

J Biomed Sci. 2006 Jan;13(1):127-41.

Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether Taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 microg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/-7% and 62%+/-6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappaB) that in turn signaled up-regulation of inflammatory proteins. NF-kappaB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by Taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by Taxifolin. These data suggest that amelioration of CI/R injury by Taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappaB activation that mediates CI/R injury.

Taxifolin enhances andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.[Pubmed:23382917]

PLoS One. 2013;8(1):e54577.

Andrographolide (Andro) suppresses proliferation and triggers apoptosis in many types of cancer cells. Taxifolin (Taxi) has been proposed to prevent cancer development similar to other dietary flavonoids. In the present study, the cytotoxic and apoptotic effects of the addition of Andro alone and Andro and Taxi together on human prostate carcinoma DU145 cells were assessed. Andro inhibited prostate cancer cell proliferation by mitotic arrest and activation of the intrinsic apoptotic pathway. Although the effect of Taxi alone on DU145 cell proliferation was not significant, the combined use of Taxi with Andro significantly potentiated the anti-proliferative effect of increased mitotic arrest and apoptosis by enhancing the cleavage of poly(ADP-ribose) polymerase, and caspases-7 and -9. Andro together with Taxi enhanced microtubule polymerization in vitro, and they induced the formation of twisted and elongated spindles in the cancer cells, thus leading to mitotic arrest. In addition, we showed that depletion of MAD2, a component in the spindle assembly checkpoint (SAC), alleviated the mitotic block induced by the two compounds, suggesting that they trigger mitotic arrest by SAC activation. This study suggests that the anti-cancer activity of Andro can be significantly enhanced in combination with Taxi by disrupting microtubule dynamics and activating the SAC.

Taxifolin suppresses UV-induced skin carcinogenesis by targeting EGFR and PI3K.[Pubmed:22805054]

Cancer Prev Res (Phila). 2012 Sep;5(9):1103-14.

Skin cancer is one of the most commonly diagnosed cancers in the United States. Taxifolin reportedly exerts multiple biologic effects, but the molecular mechanisms and direct target(s) of Taxifolin in skin cancer chemoprevention are still unknown. In silico computer screening and kinase profiling results suggest that the EGF receptor (EGFR), phosphoinositide 3-kinase (PI3K), and Src are potential targets for Taxifolin. Pull-down assay results showed that EGFR, PI3K, and Src directly interacted with Taxifolin in vitro, whereas Taxifolin bound to EGFR and PI3K, but not to Src in cells. ATP competition and in vitro kinase assay data revealed that Taxifolin interacted with EGFR and PI3K at the ATP-binding pocket and inhibited their kinase activities. Western blot analysis showed that Taxifolin suppressed UVB-induced phosphorylation of EGFR and Akt, and subsequently suppressed their signaling pathways in JB6 P+ mouse skin epidermal cells. Expression levels and promoter activity of COX-2 and prostaglandin E(2) (PGE(2)) generation induced by UVB were also attenuated by Taxifolin. The effect of Taxifolin on UVB-induced signaling pathways and PGE(2) generation was reduced in EGFR knockout murine embryonic fibroblasts (MEF) compared with EGFR wild-type MEFs. Taxifolin also inhibited EGF-induced cell transformation. Importantly, topical treatment of Taxifolin to the dorsal skin significantly suppressed tumor incidence, volume, and multiplicity in a solar UV (SUV)-induced skin carcinogenesis mouse model. Further analysis showed that the Taxifolin-treated group had a substantial reduction in SUV-induced phosphorylation of EGFR and Akt in mouse skin. These results suggest that Taxifolin exerts chemopreventive activity against UV-induced skin carcinogenesis by targeting EGFR and PI3K.

Description

Taxifolin ((+)-Dihydroquercetin) exhibits important anti-tyrosinase activity. Taxifolin exhibits significant inhibitory activity against collagenase with an IC50 value of 193.3 μM.

Keywords:

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