Apoptosis Stem Cell/Wnt MAPK/ERK Pathway NF-κB Anti-infection Cytoskeleton Cell Cycle/DNA Damage Metabolic Enzyme/Protease Vitamin D Related/Nuclear Receptor Neuronal Signaling Immunology/Inflammation
Caspase ERK NF-κB Influenza Virus PAK LDLR PPAR PCSK9 Androgen Receptor Keap1-Nrf2 Monoamine Oxidase Cholinesterase (ChE) IKK Wnt β-catenin Reactive Oxygen Species (ROS) Apoptosis Cuproptosis
Vitisin A

Cat. No.: HY-142026

Vitisin A

(Synonyms: (+)-Vitisin A)

Customer Review

Based on 1 Customer Validation

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.

For research use only. We do not sell to patients.

Purity: 96%
CAS No.: 142449-89-6
Formula: C₅₆H₄₂O₁₂
Molecular Weight:906.93

Storage:

-20°C, protect from light

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

Vitisin A Chemical Structure

CAS No.: 142449-89-6

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[3]^[5]

Caspase 3

ERK1

ERK2

NF-κB

PPAR-γ

MAO-B

All Caspase Isoforms :

All ERK Isoforms :

All NF-κB Isoforms :

All PAK Isoforms :

All PPAR Isoforms :

All Monoamine Oxidase Isoforms :

MAO-A
MAO-B

All Cholinesterase (ChE) Isoforms :

AChE
BChE

All IKK Isoforms :

All Wnt Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	CC₅₀	22.4 μM Compound: (+)-Vitisin A	Cytotoxicity against human A549 cells assessed as reduction in cell viability by Alamar blue assay Cytotoxicity against human A549 cells assessed as reduction in cell viability by Alamar blue assay	[PMID: 32652408]
Huh-7.5	CC₅₀	>10 μM Compound: (+)-Vitisin A	Cytotoxicity against human Huh7.5 cells infected with Hepatitis C virus assessed as reduction in cell viability Cytotoxicity against human Huh7.5 cells infected with Hepatitis C virus assessed as reduction in cell viability	[PMID: 32652408]
Platelet	IC₅₀	10.3 μM Compound: (+)-vitisin A	Antiplatelet activity against citreated rabbit platelet assessed as arachidonic acid-induced platelet aggregation Antiplatelet activity against citreated rabbit platelet assessed as arachidonic acid-induced platelet aggregation	[PMID: 15730246]
Platelet	IC₅₀	13.3 μM Compound: (+)-vitisin A	Antiplatelet activity against citreated rabbit platelet assessed as inhibition of 9,11-dideoxy-11 alpha, 9 alpha epoxy-methanoprostaglandin F2alpha-induced platelet aggregation Antiplatelet activity against citreated rabbit platelet assessed as inhibition of 9,11-dideoxy-11 alpha, 9 alpha epoxy-methanoprostaglandin F2alpha-induced platelet aggregation	[PMID: 15730246]

In Vitro

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.

Cell Cytotoxicity Assay^[1]

Cell Line:

Human prostate cancer cell lines (PC-3, DU145, LNCaP)
Concentration:

4, 8 μM (combined with 20, 40 ng/mL TRAIL)
Incubation Time:

24 h
Result:

Enhanced cytotoxicity and sub-G1 accumulation in PC-3, DU145, and LNCaP cells with TRAIL, most potently in PC-3 cells.
Upregulated caspase 3, FADD, DR4, and DR5 expression when combined with TRAIL.
Downregulated pro-caspase 7/8, DcR1, Bcl-XL, and Bcl-2 expression with TRAIL combination.
Elevated DR5 promoter activity, cell-surface DR5, and ROS production with TRAIL.
Induced PARP cleavage when combined with TRAIL.

Cell Viability Assay^[2]

Cell Line:

TGF-β1-activated human hepatic stellate cell line LX-2
Concentration:

0, 2.5, 5.0, 7.5, 10 nM
Incubation Time:

0, 2, 4, 6, 8, 12, 24 h
Result:

Restored cell viability in a dose-dependent manner with increasing viability from 0 to 10 nM.
Restored cell viability in a time-dependent manner with increasing viability from 0 to 24 h incubation.

Cell Differentiation Assay^[3]

Cell Line:

3T3-L1 preadipocytes
Concentration:

1, 5, 10 μM
Incubation Time:

8 days
Result:

Inhibited 3T3-L1 adipocyte differentiation in a dose-dependent manner.
Reduced relative lipid content to ~70% at 1 μM, ~35% at 5 μM, and nearly 0% at 10 μM relative to untreated control.
Almost completely suppressed differentiation at 10 μM.
Showed an IC₅₀ of 5.0 μM for adipocyte differentiation inhibition.

Western Blot Analysis^[3]

Cell Line:

differentiated 3T3-L1 cells
Concentration:

1, 5, 10 μM
Incubation Time:

8 days
Result:

Reduced the expression of PPARγ and C/EBPα, key adipogenic transcription factors.
Lowered protein levels of both factors at 1 μM.

Cell Proliferation Assay^[3]

Cell Line:

3T3-L1 preadipocytes
Concentration:

5, 10 μM
Incubation Time:

24, 48 hours
Result:

Significantly inhibited differentiation medium-induced mitosis of 3T3-L1 preadipocytes, reducing proliferation nearly to the level of normal growth-arrested cells.
Suppressed proliferation at both 5 and 10 μM, with no significant difference between the two concentrations at 24 and 48 hours.

Cell Cytotoxicity Assay^[3]

Cell Line:

3T3-L1 preadipocytes
Concentration:

1, 5, 10, 25, 50 μM
Incubation Time:

24 hours
Result:

Showed no cytotoxicity at concentrations up to 25 μM, as released LDH remained at control levels.
Increased released LDH to ~140% of the control at 50 μM, indicating cytotoxicity.

Cell Differentiation Assay^[3]

Cell Line:

3T3-L1 preadipocytes
Concentration:

10 μM
Incubation Time:

0-2 days, 2-5 days, 5-8 days, or 0-8 days
Result:

Reduced relative lipid content to 2.7% of the control when applied during days 0-2, nearly equivalent to the effect of continuous treatment over 8 days (1.6% of control).
Resulted in much weaker inhibition when applied from days 2-5 or 5-8, with relative lipid contents of 70.4% and 72.8% of the control, respectively.

Cell Cycle Analysis^[3]

Cell Line:

differentiation-induced 3T3-L1 preadipocytes
Concentration:

5, 10 μM
Incubation Time:

24 hours
Result:

Blocked differentiation medium-induced cell cycle progression at the G1-S transition.
Maintained 84.0% of cells in G0/G1 phase at 5 μM, with 7.7% in S phase and 7.9% in G2/M phase.
Maintained 89.6% of cells in G0/G1 phase at 10 μM, with 6.6% in S phase and 3.8% in G2/M phase.

Western Blot Analysis^[3]

Cell Line:

differentiation-induced 3T3-L1 preadipocytes
Concentration:

1, 5, 10 μM
Incubation Time:

6, 12, 18, 24 hours
Result:

Dose-dependently repressed the differentiation medium-induced increase in cyclin A and cyclin B expression.
Significantly reduced cyclin A and B levels at 10 μM starting at 12-18 hours post-induction.
Delayed CDK2 expression, while cyclin E expression was unaffected.

Western Blot Analysis^[3]

Cell Line:

differentiation-induced 3T3-L1 preadipocytes
Concentration:

1, 5, 10 μM
Incubation Time:

0.25, 0.5, 1, 2, 3 hours; 24 hours
Result:

Did not affect ERK or Akt phosphorylation at any tested time point.
Restored the differentiation-induced decrease in p21 expression in a dose-dependent manner.
Reduced differentiation-induced phosphorylation of retinoblastoma protein (Rb) at Ser780 in a dose-dependent manner.

Western Blot Analysis^[4]

Cell Line:

RAW 264.7 macrophage cells
Concentration:

1, 5, 10 μM (8 h incubation after LPS stimulation); 10 μM (non-LPS-treated cells)
Incubation Time:

8 h (after LPS stimulation); 30 min (pre-incubation with vitisin A prior to LPS treatment)
Result:

Dose-dependently inhibited LPS-induced iNOS expression, with significant suppression observed at all tested concentrations relative to LPS-only treated cells.

Western Blot Analysis^[4]

Cell Line:

RAW 264.7 macrophage cells
Concentration:

1, 5, 10 μM (20 min incubation after LPS stimulation); 10 μM (non-LPS-treated cells)
Incubation Time:

20 min (after LPS stimulation); 30 min (pre-incubation with vitisin A prior to LPS treatment)
Result:

Dose-dependently inhibited LPS-induced ERK1/2 and p38 phosphorylation.
Completely blocked LPS-induced ERK1/2 and p38 phosphorylation at 10 µM.

Western Blot Analysis^[4]

Cell Line:

RAW 264.7 macrophage cells
Concentration:

10 μM (15 min incubation after LPS stimulation); 10 μM (non-LPS-treated cells)
Incubation Time:

15 min (after LPS stimulation); 30 min (pre-incubation with vitisin A prior to LPS treatment)
Result:

Significantly suppressed LPS-induced IκB-α degradation and reduced LPS-induced IκB-α phosphorylation, relative to LPS-only treated cells.

Cell Viability Assay^[5]

Cell Line:

human SH-SY5Y neuroblastoma cells
Concentration:

2.5, 5, 10, 20 μM
Incubation Time:

24 h (pre-treatment)
Result:

Significantly elevated cell viability compared to the MGO-only control , showing robust neuroprotective effects.

In Vivo

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.

Animal Model:

ICR mice (scopolamine-induced amnesia)^[1]
Dosage:

40 mg/kg
Administration:

single administration
Result:

Significantly improved impaired learning behaviors in scopolamine-treated mice.
Decreased acetylcholinesterase activity and malondialdehyde levels in brain extracts.
Increased expression of brain-derived neurotrophic factor and its receptor tropomyosin receptor kinase B.
Enhanced expression of synaptic plasticity proteins synapsin I, calcium/calmodulin-dependent protein kinase II, and Akt.

Animal Model:

ICR (6-week-old male, scopolamine-induced amnesia)^[5]
Dosage:

40 mg/kg
Administration:

p.o.; daily; 13 days
Result:

Increased step-through latency in the retention trial of the passive avoidance test compared with scopolamine-treated control mice.
Reduced acetylcholinesterase (AChE) activity and malondialdehyde (MDA) levels in brain tissue extracts compared with the control group.
Restored protein expressions of brain-derived neurotrophic factor (BDNF; BDNF/β-actin = 1.25) and its receptor tropomyosin receptor kinase B (TrkB; TrkB/β-actin = 1.16) from scopolamine-induced decreases.

Animal Model:

C57BL/6 (high-fat diet-induced obesity)^[5]
Dosage:

25 mg/kg
Administration:

p.o.; daily; 36 days
Result:

Reduced weight gain in high-fat diet-fed mice.
Improved plasma cardiovascular risk parameters, including reduced total cholesterol, total triglycerides, low-density lipoproteins, and free fatty acids.

Chemical Information

CAS No. 142449-89-6
Appearance Solid
Molecular Weight 906.93
Formula C₅₆H₄₂O₁₂
Color Brown to black
SMILES

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
Synonyms

(+)-Vitisin A
Structure Classification
- Phenols
- Polyphenols
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, protect from light

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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (304 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[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. [Content Brief]

[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. [Content Brief]

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Vitisin A

All Caspase Isoforms

All ERK Isoforms

All NF-κB Isoforms

All PAK Isoforms

All PPAR Isoforms

All Monoamine Oxidase Isoforms

All Cholinesterase (ChE) Isoforms

All IKK Isoforms

All Wnt Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

Vitisin A Related Classifications

Cat. No.: HY-142026