Vernodalin
Vernodalin is an orally active, cytotoxic sesquiterpene lactone with a Kd value of 9.55 μM for p38 MAPK. Vernodalin downregulates the expression of phosphorylated ERK, JNK, AKT, PI3K, mTOR, p38MAPK, FAK, MMP-2, MMP-9, and uPA, while upregulates the expression of TIMP-1 and TIMP-2. Vernodalin increases ROS production, upregulates the expression of Bax and caspase 3, downregulates the expression of Bcl-2, and induces apoptosis (apoptosis), oxidative stress response and cell cycle arrest. Vernodalin inhibits the proliferation, adhesion and metastasis of cancer cells. Vernodalin enhances the activity of VEGF-B, AMPK and eNOS signaling pathways. Vernodalin alleviates myocardial injury and restores hemodynamic parameters. Vernodalin inhibits the growth of Trypanosoma brucei rhodesiense. Vernodalin can be used in research related to various cancers including gastric cancer, colorectal cancer and lung cancer, as well as African human trypanosomiasis and myocardial infarction.
For research use only. We do not sell to patients.
- CAS No.: 21871-10-3
- Formula: C19H20O7
- Molecular Weight:360.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Vernodalin (5-40 μM; 24 h) inhibits the proliferation and induces apoptosis of SGC-7901 and AGS cells in a concentration-dependent manner, increases the levels of nuclear pyknosis and fragmentation, and induces a significant decrease in mitochondrial membrane potential[1].
Vernodalin (20 μM; 24 h pre-incubation, 60 and 100 min adhesion period) reduces the adhesion of SGC-7901 and AGS cells to extracellular matrix components at the 60 and 100 min time points[1].
Vernodalin (20 μM; 24 h) downregulates the protein expression of uPA, MMP-2 and MMP-9, while upregulates the protein expression of TIMP-1 and TIMP-2 in SGC-7901 and AGS cells. It inhibits the FAK/PI3K/AKT/mTOR signaling pathway by reducing the protein expression of FAK, p-PI3K, p-AKT, p-mTOR and RhoA in cells, and inhibits the MAPKs signaling pathway by reducing the protein expression of phosphorylated JNK, JUN, p38MAPK and ERK in cells[1].
Vernodalin (3.12-150 µM; 24 h) reduces the viability of HT-29 and HCT116 cells in a dose-dependent manner, with IC50 values of 7.17 µg/mL and 3.17 µg/mL, respectively[3].
Vernodalin (1-20 μM; 24-72 h) inhibits the proliferation of A549 lung cancer cells in a time-dependent manner, with IC50 values of 65.80 μM (24 h), 39.90 μM (48 h), and 25.85 μM (72 h), respectively[4].
Vernodalin (0.016-50 μg/mL; 48 h) potently inhibits the viability of a variety of human cancer cell lines (A549, HeLa, HuCCA-1, HepG2, H69AR, T47-D, MDA-MB-231, S102, HL-60, MOLT-3), with IC50 values ranging from 2.28 μM to 21.47 μM, and exhibits selective cytotoxicity toward cancer cells compared to normal MRC-5 fibroblasts[6].
Vernodalin (3-12 h) induces time-dependent oxidative stress in HT-29 and HCT116 cells by increasing ROS production, which is associated with cell necrosis and apoptosis[3].
Vernodalin (5-15 µg/mL for HT-29, 2.5-10 µg/mL for HCT116; 24 h) induces apoptosis in HT-29 and HCT116 cells in a dose-dependent manner, upregulates the expression of Bax and caspase 3, downregulates the expression of Bcl-2, and thereby increases the Bax/Bcl-2 ratio[3].
Vernodalin (10 μM; 48 h) [missing action in source text], accompanied by observable morphological changes in cells[6].
Vernodalin (5-20 µg/mL; 1.5-24 h) activates the JNK, ERK and p38 MAPK pathways in HT-29 and HCT116 cells in a time- and dose-dependent manner[3].
Vernodalin (26 μM; 72 h) induces excessive ROS production in A549 lung cancer cells[4].
Vernodalin (26 μM; 72 h) enhances oxidative stress in A549 lung cancer cells by increasing MDA levels and reducing the antioxidant defense capacities of SOD, CAT, GPX and GSH. It also impairs the endogenous antioxidant defense system by decreasing the mRNA expression levels of Nrf2 and HO-1, as well as the enzymatic activity of HO-1[4].
Vernodalin (26 μM; 72 h) activates the pro-apoptotic signaling pathway in A549 lung cancer cells by upregulating the mRNA expression of p38 MAPK, caspase-3, caspase-9 and Bax, downregulating the mRNA expression of Bcl-2, and increasing the activities of caspase-3 and caspase-9[4].
Vernodalin potently inhibits the growth of bloodstream-form trypomastigotes of *Trypanosoma brucei rhodesiense* (strain STIB 900), with an IC50 value of 0.16 µM[5].
Vernodalin (10 μM; 48 h) induces apoptosis in 10.9% of HepG2 cells, triggers G2/M phase cell cycle arrest, and reduces the proportions of cells in the G0/G1 and S phases[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SGC-7901 and AGS cells
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Concentration:5, 10, 20, 30, 40 μM
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Incubation Time:24 h
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Result:Exerted concentration-dependent cytotoxic and anti-proliferative effects on both SGC-7901 and AGS cells.
Showed the strongest inhibition of cell proliferation at the highest tested concentration (40 μM).
Determined an IC50 corresponding to the 20 μM concentration selected for subsequent experiments.
Caused statistically significant reductions in cell viability at all tested concentrations compared to untreated controls.
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Cell Line:human gastric cancer SGC-7901 and AGS cells
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Concentration:20 μM
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Incubation Time:24 h
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Result:Induced apoptosis in SGC-7901 and AGS cells, as evidenced by a significant increase in cells with bright nuclear condensation or fragmented nuclei compared to untreated controls.
Caused statistically significant increases in apoptosis rate, with apoptosis rates rising to ~60% in SGC-7901 cells and ~60% in AGS cells.
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Cell Line:human gastric cancer SGC-7901 and AGS cells
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Concentration:20 μM
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Incubation Time:24 h
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Result:Down-regulated protein expression of uPA, MMP-2, and MMP-9 in both SGC-7901 and AGS cells.
Up-regulated protein expression of TIMP-1 and TIMP-2 in both SGC-7901 and AGS cells.
Caused statistically significant changes in fold expression compared to untreated controls.\nReduced protein expression of FAK, p-PI3K, p-AKT, p-mTOR, and RhoA in both SGC-7901 and AGS cells compared to untreated controls.
Caused statistically significant reductions in fold expression.\nReduced protein expression of p-JNK, p-JUN, p-p38MAPK, and p-ERK in both SGC-7901 and AGS cells compared to untreated controls.
Caused statistically significant reductions in fold expression.
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Cell Line:A549 lung cancer cells
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Concentration:26 μM
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Incubation Time:72 h
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Result:Significantly reduced HO-1 mRNA expression, HO-1 enzyme activity, and Nrf2 mRNA expression in A549 cells compared to control.\nIncreased p38 MAPK, caspase-3, caspase-9, and Bax mRNA expression in A549 cells compared to control.
Decreased Bcl-2 mRNA expression in A549 cells compared to control.
Increased the Bax/Bcl-2 mRNA ratio in A549 cells compared to control.
Increased caspase-3 and caspase-9 activity in A549 cells compared to control.
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Cell Line:A549, HeLa, HuCCA-1, HepG2, H69AR, T47-D, MDA-MB-231, S102, HL-60, MOLT-3, MRC-5
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Concentration:50, 10, 2.0, 0.40, 0.08, and 0.016 μg/mL
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Incubation Time:48 h
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Result:Exhibited cytotoxic activity across all tested cancer cell lines with IC50 values: A549 (13.61 μM), HeLa (3.81 μM), HuCCA-1 (8.17 μM), HepG2 (15.47 μM), H69AR (21.47 μM), T47-D (6.86 μM), MDA-MB-231 (16.14 μM), S102 (21.47 μM), HL-60 (2.28 μM), MOLT-3 (3.92 μM).
Showed low toxicity to normal MRC-5 cells with an IC50 of 69.83 μM, resulting in selectivity index (SI) values ≥3.0 for all cancer cell lines (HeLa SI=18.3, H69AR SI=3.3).
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Cell Line:HepG2
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Concentration:10 μM
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Incubation Time:48 h
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Result:Altered HepG2 cell cycle distribution: 47.9% of cells in G0/G1 phase, 10.3% in S phase, and 41.6% in G2/M phase, compared to control values of 49.8% (G0/G1), 11.6% (S), and 38.4% (G2/M).
Reduced G0/G1 and S phase populations and increased G2/M phase populations relative to controls.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar albino (male, 140-180 g, isoproterenol-induced myocardial infarction)[2]
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Dosage:10 mg/kg bw
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Administration:p.o.; daily; 30 days
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Result:Significantly reduced heart weight and heart weight/body weight index compared to isoproterenol-only rats.
Restored diastolic arterial pressure, systolic arterial pressure, mean arterial pressure, and heart rate to near-normal levels.
Significantly decreased serum levels of cardiotoxicity enzymes (AST, LDH, CK), cardiac biomarkers (H-FABP, MYO, CK-MB, GP-BBP, TGF-β, cTnI, BNP), and myocardial protein levels of inflammatory mediators (TNF-α, IL-6, NF-κB) compared to isoproterenol-only rats.
Significantly increased myocardial protein levels of VEGF-B, phosphorylated AMPK, and the phosphorylated eNOS/eNOS ratio compared to isoproterenol-only rats.
Reduced histopathological damage (necrosis, inflammatory cell infiltration, fragmented myofibrils) to near-normal levels, with a significantly lower histology damage score than isoproterenol-only rats.
Chemical Information
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CAS No. 21871-10-3
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Molecular Weight 360.36
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Formula C19H20O7
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SMILES
C(=C)[C@@]12[C@@]([C@@]3([C@@]([C@@H](OC(C(CO)=C)=O)C1)(C(=C)C(=O)O3)[H])[H])(C(=C)C(=O)OC2)[H]
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Luo Y, et al. Vernodalin Suppresses Tumor Proliferation and Increases Apoptosis of Gastric Cancer Cells Through Attenuation of FAK/PI3K/AKT/mTOR and MAPKs Signaling Pathways. Current pharmaceutical biotechnology. 2023;24(5):708-717. [Content Brief]
[2]. Tao T, et al. Vernodalin Alleviates Cardiotoxicity and Inflammation in Isoproterenol-Mediated Myocardial Infarction through NF-κB/AMPK Signaling Pathways in Rats. Comb Chem High Throughput Screen. 2025;28(9):1594-1603. [Content Brief]
[3]. Mohebali N, et al. Vernodalin induces apoptosis through the activation of ROS/JNK pathway in human colon cancer cells. Journal of biochemical and molecular toxicology. 2020 Dec;34(12):e22587. [Content Brief]
[4]. Zhou J, et al. Interaction of vernodalin with p38 mitogen-activated protein kinase (p38 MAPK) and subsequent effects in lung cancer cell model. International journal of biological macromolecules. 2025 Jun;311(Pt 1):143413. [Content Brief]
[5]. Kimani NM, et al. Sesquiterpene Lactones from Vernonia cinerascens Sch. Bip. and Their in Vitro Antitrypanosomal Activity. Molecules (Basel, Switzerland). 2018 Jan 27;23(2):248. [Content Brief]
[6]. Thongnest S, et al. Vernodalidimer L, a sesquiterpene lactone dimer from Vernonia extensa and anti-tumor effects of vernodalin, vernolepin, and vernolide on HepG2 liver cancer cells. Bioorganic chemistry. 2019 Nov;92:103197. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Vernodalin Related Classifications
HY-N19029 Related Classifications
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- Vernodalin
- 21871-10-3
- p38 MAPK
- PERK
- JNK
- Akt
- PI3K
- mTOR
- FAK
- MMP
- PAI-1
- Reactive Oxygen Species (ROS)
- Caspase
- Bcl-2 Family
- Apoptosis
- VEGFR
- AMPK
- Parasite
- human p38 MAPK
- human colon cancer HCT116 cells
- human colon cancer HT-29 cells
- colorectal cancer
- Trypanosoma brucei rhodesiense
- human gastric cancer AGS cells
- human gastric cancer SGC-7901 cells
- myocardial infarction
- gastric cancer
- lung cancer
- Inhibitor
- inhibitor
- inhibit