(2R,2aR,7R,7aR,12S,12aS)-2,7,12-Tris(4-hydroxyphenyl)-2,2a,7,7a,12,12a-hexahydrobisbenzofuro[3',4':4,5,6;3'',4'':7,8,9]cyclonona[1,2,3-cd]benzofuran-4,9,14-triol/α-viniferin/(+)-α-Viniferin/alpha-Viniferin/(+)-alpha-viniferin/a-Viniferin/Bisbenzofuro[3',4':4,5,6;3'',4'':7,8,9]cyclonona[1,2,3-cd]benzofuran-4,9,14-triol, 2,2a,7,7a,12,12a-hexahydro-2,7,12-tris(4-hydroxyphenyl)-, (2R,2aR,7R,7aR,12S,12aS)-
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:62218-13-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Prostate cancer (PCa) is one of the most commonly diagnosed urological malignancies. However, there are limited therapies for PCa patients who develop biochemical recurrence after androgen deprivation therapy (ADT). In the present study, we investigated the therapeutic efficacy and mechanism of α-Viniferin (KCV), an oligostilbene of trimeric resveratrol, against human PCa cells and found that it markedly inhibited the proliferation of LNCaP, DU145, and PC-3 cancer cells in a time- and dose-dependent manner, and had a strong cytotoxicity in non-androgen-dependent PCa cells. In addition, KCV inhibited AR downstream expression in LNCaP cells, and inhibited activation of GR signaling pathway in DU145 and PC-3. Further investigation indicated that KCV could induce cancer cell apoptosis through AMPK-mediated activation of autophagy, and inhibited GR expression in castration-resistant prostate cancer(CRPC). These findings suggest that KCV may prove to be a novel and effective therapeutic agent for the treatment of CRPC.
AMPK; Autophagy; Glucocorticoid receptor; Prostate cancer; α-Viniferin
α-Viniferin activates autophagic apoptosis and cell death by reducing glucocorticoid receptor expression in castration-resistant prostate cancer cells.
Cheng K1, Liu X2,3, Chen L2, Lv JM2, Qu FJ3, Pan XW3, Li L3, Cui XG3, Gao Y4, Xu DF2.
2018 Jun 15;
α-Viniferin and caraphenol A, the two oligostilbenes, have the sole difference of the presence or absence of an exocyclic double bond at the π-π conjugative site. In this study, the antioxidant capacity and relevant mechanisms for α-viniferin and caraphenol A were comparatively explored using spectrophotometry, UV-visible spectral analysis, and electrospray ionization quadrupole time-of-flight tandem mass spectrometry (UPLC-ESI-Q-TOF-MS/MS) analysis. The spectrophotometric results suggested that caraphenol A always gave lower IC50 values than α-viniferin in cupric ion-reducing antioxidant capacity assay, ferric-reducing antioxidant power assay, 1,1-diphenyl-2-picryl-hydrazl radical (DPPH?)-scavenging, and 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide radical-scavenging assays. In UV-visible spectra analysis, caraphenol A was observed to show enhanced peaks at 250-350 nm when mixed with Fe2+, but α-viniferin exhibited no similar effects. UPLC-ESI-Q-TOF-MS/MS analysis revealed that α-viniferin mixed with DPPH? produced radical adduct formation (RAF) peak (m/z = 1070-1072). We conclude that the antioxidant action of α-viniferin and caraphenol A may involve both redox-mediated mechanisms (especially electron transfer and H?-transfer) and non-redox-mediated mechanisms (including Fe2+-chelating or RAF). The π-π conjugation of the exocyclic double bond in caraphenol A can greatly enhance the redox-mediated antioxidant mechanisms and partially promote the Fe2+-chelating mechanism. This makes caraphenol A far superior to α-viniferin in total antioxidant levels.
antioxidant; caraphenol A; conjugative double bond; oligostilbene; stilbene trimer; α-viniferin
π-π Conjugation Enhances Oligostilbene's Antioxidant Capacity: Evidence from α-Viniferin and Caraphenol A.
Li X1,2, Xie Y3,4, Xie H5,6, Yang J7, Chen D8,9.
2018 Mar 19
Rationale: cAMP up-regulates microphthalmia-associated transcription factor subtype M (MITF-M) and tyrosinase (Tyro) in the generation of heavily pigmented melanosomes. Here, we communicate a therapeutic mechanism of hyperpigmented disorder by α-viniferin, an active constituent of Caragana sinica. Methods: We used cAMP-elevated melanocyte cultures or facial hyperpigmented patches for pigmentation assays, and applied immunoprecipitation, immunobloting, RT-PCR or reporter gene for elucidation of the antimelanogenic mechanism. Results:C. sinica or α-viniferin inhibited melanin production in α-melanocyte-stimulating hormone (α-MSH)-, histamine- or cell-permeable cAMP-activated melanocyte cultures. Moreover, topical application with C. sinica containing α-viniferin, a standard in quality control, decreased melanin index on facial melasma and freckles in patients. As a molecular basis, α-viniferin accelerated protein kinase A (PKA) inactivation via the reassociation between catalytic and regulatory subunits in cAMP-elevated melanocytes, a feedback loop in the melanogenic process. α-Viniferin resultantly inhibited cAMP/PKA-signaled phosphorylation of cAMP-responsive element-binding protein (CREB) coupled with dephosphorylation of cAMP-regulated transcriptional co-activator 1 (CRTC1), thus down-regulating expression of MITF-M or Tyro gene with decreased melanin pigmentation. Conclusion: This study assigned PKA inactivation, a feedback termination in cAMP-induced facultative melanogenesis, as a putative target of α-viniferin in the treatment of melanocyte-specific hyperpigmented disorder. Finally, C. sinica containing α-viniferin was approved as an antimelanogenic agent with topical application in skin hyperpigmentation.
Caragana sinica; PKA inactivation; feedback loop; melanogenesis; α-viniferin
α-Viniferin Improves Facial Hyperpigmentation via Accelerating Feedback Termination of cAMP/PKA-Signaled Phosphorylation Circuit in Facultative Melanogenesis.
Yun CY1, Mi Ko S1, Pyo Choi Y1, Kim BJ2, Lee J3, Mun Kim J3, Kim JY4, Song JY1, Kim SH1, Hwang BY1, Tae Hong J1, Han SB1, Kim Y1.
2018 Feb 16;