Vitisin A  (Synonyms: (+)-Vitisin A)

Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC₅₀ values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases^{[1][2][3][4][5]}.

Vitisin A exhibits antioxidant activity via free radical scavenging and iron reduction, with FRAP and DPPH values of 2.38 mM Trolox/g phenol and 1.24 mM Trolox/g phenol, respectively^[1].
Vitisin A is highly cytotoxic to human cancer cell lines, with an IC₅₀ of 1.11 μM against MES-SA cells, and induces apoptosis via sub-G1 cell cycle arrest^[1].
Vitisin A induces G2/M phase cell cycle arrest and apoptosis in HepG2 human hepatocellular carcinoma cells via increased ROS, caspase 3 activity, and modified Bax/Bcl-2 ratios, but has no effect on Hep3B cells^[1].
Vitisin A (4, 8 μM; 24 h) acts as a TRAIL sensitizer in PC-3, DU145, and LNCaP human prostate cancer cells by upregulating DR5 expression and inducing ROS generation, enhancing TRAIL-mediated apoptosis^[1].
Vitisin A inhibits influenza A virus-induced RANTES production in A549 human alveolar epithelial cells by modulating Akt and STAT1 phosphorylation^[1].
Vitisin A inhibits preadipocyte proliferation and differentiation by inducing G1 phase arrest and regulating p21, PPARγ, and C/EBPα expression, supporting anti-obesity activity^[1].
Vitisin A exerts hypocholesterolemic effects by regulating LDLR, HMG-CoA reductase, and PCSK9, and reduces triglyceride levels in HepG2 cells via modulation of lipogenesis and fatty acid oxidation pathways^[1].
Vitisin A inhibits osteoclast differentiation in RAW264.7 mouse macrophage cells and primary mouse bone marrow cells by targeting TRAF6-TAK1-NFATc1 signaling, supporting antiosteoporotic activity^[1].
Vitisin A enhances viability of H₂O₂-exposed SH-SY5Y human neuronal cells and provides partial protection against glutamate-induced neurotoxicity in primary rat cortical cells at 10 μM^[1].
Vitisin A inhibits androgen receptor activity and protects human dermal papilla cells from DHT-induced damage, supporting potential use in treating androgenetic alopecia^[1].
Vitisin A exhibits antifungal activity against Plasmopara viticola^[1].
Vitisin A (0-10 nM; 0-24 h) dose-dependently and time-dependently restores cell viability in TGF-β1-activated LX-2 cells^[2].
Vitisin A attenuates ES-Cu-induced cytotoxicity in TGF-β1-activated LX-2 cells^[2].
Vitisin A can inhibit fibrosis, copper death, lipid synthesis, and oxidative stress in TGF-β1-activated LX-2 cells in a dose-dependent manner by upregulating the Nrf2/HO-1 signaling pathway; and these effects can be eliminated by knocking down Nrf2 with siRNA, confirming that the Nrf2/HO-1 pathway is a key mediator^[2].
Vitisin A (1-10 μM; 8 days) potently inhibits 3T3-L1 preadipocyte differentiation with an IC₅₀ of 5.0 μM, reducing lipid accumulation in a dose-dependent manner^[3].
Vitisin A (1-10 μM; 8 days) dose-dependently reduces PPARγ and C/EBPα protein expression in differentiated 3T3-L1 cells^[3].
Vitisin A (1-10 μM; 24 h) weakly but significantly inhibits Rosiglitazone (HY-17386)-induced PPARγ transcriptional activity in transiently transfected COS-7 cells^[3].
Vitisin A (5-10 μM; 24-48 h) significantly inhibits differentiation medium-induced proliferation of 3T3-L1 preadipocytes, reducing proliferation to near growth-arrested levels^[3].
Vitisin A (1-50 μM; 24 h) is non-cytotoxic to 3T3-L1 preadipocytes at concentrations up to 25 μM, with cytotoxicity only detected at 50 μM^[3].
Vitisin A (10 μM; 0-2 days, 2-5 days, 5-8 days, or 0-8 days) primarily inhibits 3T3-L1 adipocyte differentiation by targeting the preadipocyte proliferation stage during the first 2 days of adipogenic induction, with minimal effect when administered after this period^[3].
Vitisin A (5-10 μM; 24 hours) blocks 3T3-L1 preadipocyte cell cycle progression at the G1-S transition, maintaining cells in the G0/G1 phase similar to non-differentiated growth-arrested cells^[3].
Vitisin A (1-10 μM; 6-24 hours) dose-dependently reduces cyclin A and cyclin B expression, delays CDK2 expression, and does not affect cyclin E expression in differentiation-induced 3T3-L1 preadipocytes, supporting G1 phase cell cycle arrest^[3].
Vitisin A (1-10 μM; 0.25-3 hours, 24 hours) modulates mitotic regulation in differentiation-induced 3T3-L1 preadipocytes by restoring p21 expression and reducing Rb phosphorylation^[3].
Vitisin A (1-10 μM; 24 h) dose-dependently inhibits LPS-induced NO production in RAW 264.7 macrophage cells^[4].
Vitisin A (1-10 μM; 8 h) dose-dependently inhibits LPS-induced iNOS expression in RAW 264.7 macrophage cells^[4].
Vitisin A (1-10 μM; 20 min) dose-dependently inhibits LPS-induced ERK1/2 and p38 phosphorylation in RAW 264.7 macrophage cells^[4].
Vitisin A (10 μM; 15 min) inhibits LPS-induced NF-κB activation in RAW 264.7 macrophage cells by suppressing IκB-α phosphorylation and degradation^[4].
Vitisin A potently inhibits recombinant human AChE with an IC₅₀ of 1.29 μM^[5].
Vitisin A potently inhibits recombinant human MAO-B with an IC₅₀ of 4.94 μM^[5].
Vitisin A (2.5-20 μM; 24 h pre-treatment) significantly protects human SH-SY5Y neuroblastoma cells against MGO-induced cell death^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Vitisin A (40 mg/kg; single administration) improves cognitive function in scopolamine-induced amnesiac mice by reducing oxidative stress, inhibiting acetylcholinesterase, and enhancing synaptic signaling^[1].
Vitisin A (central administration) restores cognitive function and hippocampal synaptic plasticity in scopolamine-treated C57BL/6 mice via activation of BDNF-CREB signaling^[1].
Vitisin A (topical application) protects against DHT-induced androgenetic alopecia in mice by preserving hair follicle structure and regulating Wnt/β-catenin signaling^[1].
Vitisin A (100 mg/kg; dietary intake) reduces body weight gain and plasma triglycerides in high-fat diet-fed mice by modulating hepatic lipid metabolism pathways^[1].
Vitisin A reduces body weight and improves plasma lipid profiles^[1].
Vitisin A (i.p.) dose-dependently inhibits liver fibrosis in CCl₄-induced mice by activating the Nrf2/HO-1 pathway and suppressing cuproptosis, lipid peroxidation, and hepatic stellate cell activation^[2].
Vitisin A (40 mg/kg; p.o.; daily; 13 days) significantly improves scopolamine-induced amnesia in male ICR mice, as shown by increased retention trial step-through latency, reduced brain AChE activity and oxidative stress, and restored BDNF/TrkB protein expression^[5].
Vitisin A (10 mg/kg; p.o.; single dose) significantly reduces systolic and diastolic blood pressure in spontaneously hypertensive rats, with peak effects observed at 8 hours post-treatment^[5].
Vitisin A (25 mg/kg; p.o.; daily; 36 days) reduces weight gain and improves obesity-related plasma lipid parameters in high-fat diet-fed C57BL/6 mice^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

906.93

C₅₆H₄₂O₁₂

142449-89-6

Solid

Brown to black

OC1=CC2=C(C3=C1)[C@]([C@@H](C(C=C4)=CC=C4O)O3)([H])C5=CC(O)=CC(O)=C5[C@H](C(C=C6)=CC=C6O)[C@H]2C7=CC(/C=C/C8=C9[C@H](C%10=CC(O)=CC(O)=C%10)[C@@H](C(C=C%11)=CC=C%11O)OC9=CC(O)=C8)=CC=C7O

Room temperature in continental US; may vary elsewhere.

-20°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

• [1]. Bakrim S., et al. Vitisin a and B: Natural sources, chemistry, metabolism, pharmacological properties, and health benefits – A comprehensive review. Journal of Functional Foods, 2025, 127: 106774.

  [2]. Ding S, et al. Vitisin A inhibits liver fibrosis by promoting Nrf2/HO-1 pathway and inhibiting Cuproptosis. Sci Rep. 2025;15(1):44186. Published 2025 Dec 19.

  [3]. Kim S.-h., et al. Vitisin A inhibits adipocyte differentiation through cell cycle arrest in 3T3-L1 cells. Biochemical and Biophysical Research Communications, 2008, 372(1): 108-113.

  [4]. Mi Jeong Sung, et al. Vitisin A suppresses LPS-induced NO production by inhibiting ERK, p38, and NF-kappaB activation in RAW 264.7 cells. Int Immunopharmacol. 2009;9(3):319-323.  [Content Brief]

  [5]. Chen LG, et al. Vitisin A, a Resveratrol Tetramer, Improves Scopolamine-Induced Impaired Learning and Memory Functions in Amnesiac ICR Mice. Biomedicines. 2022;10(2):273. Published 2022 Jan 26.