Arvenin I
Based on 1 Customer Validation
Arvenin I is a natural cucurbitacin glucoside that activates T cells within the cancer-competitive environment. Arvenin I covalently reacts with and hyperactivates MKK3, thereby reviving the mitochondrial fitness of exhausted T cells through the activation of the p38MAPK pathway. Arvenin I exhibits broad-spectrum antiproliferative against cancer cells. Arvenin I enhances antitumor effects both as a monotherapy and in combination with immune checkpoint inhibitors in mice. Arvenin I can be used for cancer research, such as colon cancer, breast cancer, lung cancer, and ovarian cancer[1][2].
For research use only. We do not sell to patients.
- Purity : 89.41%
- CAS No.: 65247-27-0
- Formula: C38H56O13
- Molecular Weight:720.84
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Storage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Arvenin I (0.5-4 μM, 48 h) displays no detectable induction of IL-2 in Jurkat PD-1 cells in the absence of PHA and PMA (HY-18739) and exhibits no significant cytotoxicity in Jurkat PD-1 cells at 4 μM, suggesting that it does not independently activate T cells but rather augments the PHA/PMA-induced activation of T cells[1].
Arvenin I (0-30 μM, 24-48 h) forms a covalent bond with specific cysteine residues in AKT (Cys310) and MKK3 (Cys227) through its Michael acceptor moiety to activate the MKK3-p38MAPK signaling pathway, leading to increased IL-2 production[1].
Arvenin I (250 nM, 2 h) enhances the mitochondrial bioenergetics in primary CD8+ T cells by increasing basal and maximal respiration as well as spare respiratory capacity through the p38MAPK pathway[1].
Arvenin I (1-100 μM, 3 days) exhibits broad-spectrum antiproliferative activity against a panel of human cancer cell lines, with IC50 values of 17.0, 49.4, 14.7 and 42.8 μM in A-549, HT-29, OVCAR, and MCF-7 cells, respectively[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HEK293 and Jurkat PD-1 cells
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Concentration:0, 3, 10, and 30 μM for HEK293 cells; 0, 2, and 4 μM for Jurkat PD-1 cells
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Incubation Time:24 h
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Result:Caused slightly slower electrophoretic migration of the Western-blotted bands of Flag-AKT wt and Flag-MKK3 wt on SDS-PAGE gels at concentrations as low as 3 μM.
Failed to induce a band shift in mutants where each corresponding cysteine residue was substituted with a serine residue (Flag-AKT C310S and Flag-MKK3 C227S), even at a high concentration of 30 μM.
Markedly increased the phosphorylation of p38MAPK Thr180/Tyr182 in Jurkat hPD-1 cells either in the presence or absence of PHA and PMA.
Had no detectable effects on the phosphorylation of FOXO1 Ser256.
Increased the phosphorylation of MKK3 in Jurkat hPD-1 cells.
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Cell Line:Jurkat PD-1 cells
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Concentration:0.5, 1, 2, and 4 μM
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Incubation Time:48 h
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Result:Exhibited no significant cytotoxicity in Jurkat PD-1 cells at 4 μM.
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Cell Line:Jurkat PD-1, Jurkat MKK3 wild-type and C227S cells
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Concentration:4 μM
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Incubation Time:48 h
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Result:Its ability to restore IL-2 production (suppressed by MDA-MB-231 conditioned medium) was dose-dependently canceled by SB203580 (HY-10256).
Potentiated the augmentation of IL-2 production resulting from the overexpression of wild-type MKK3.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:WT C57BL/6N mice (6 weeks old) subcutaneously injected with MC38 colon cancer cells[1]
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Dosage:6 mg/kg
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Administration:i.p., every 3 days from day 10 to day 22
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Result:Caused a 40% inhibition of tumor growth in comparison to the control group, comparable to the efficacy of the PD-L1 antibody (30 μg every 6 day from day 10 to day 22).
Produced approximately 70% inhibition of tumor growth with a combination with PD-L1 antibody.
Did not lead to significant reductions in body weight or differences in liver toxicity markers, including AST, ALT, and LDH.
Significantly enhanced mitochondrial respiration and upregulated proliferation markers (Ki67) in DLN CD8+ T cells in combination with the PD-L1 antibody.
Increased TNF-α levels but reduced IFN-γ levels in combination with the PD-L1 antibody.
Showed a trend toward decreasing the population of terminally exhausted CD8+ T cells (PD1+ Tim3+) and increasing the proportion of less exhausted CD8+ T cells in the combination group.
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Animal Model:Rag2KO C57BL/6N mice (6 weeks old) subcutaneously injected with MC38 colon cancer cells[1]
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Dosage:6 mg/kg
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Administration:i.p., every 3 days from day 10 to day 22
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Result:Failed to suppress tumors in immunodeficient mice, thereby demonstrating that its antitumor efficacy is depends on the adaptive immune system.
Chemical Information
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CAS No. 65247-27-0
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Appearance Solid
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Molecular Weight 720.84
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Formula C38H56O13
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Color Off-white to light yellow
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SMILES
CC(OC(C)(/C=C/C([C@@]([C@H]1[C@H](O)C[C@]2(C)[C@]1(C)CC([C@]3(C)[C@H]2CC=C4[C@H]3C[C@H](O[C@H]5[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O5)C(C4(C)C)=O)=O)(O)C)=O)C)=O
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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
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Protocols
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (279 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Takemoto M, et al. Covalent Plant Natural Product that Potentiates Antitumor Immunity. J Am Chem Soc. 2025 Jan 22;147(3):2902-2912. [Content Brief]
[2]. Minh CV, et al. Chemical constituents of Trichosanthes kirilowii and their cytotoxic activities. Arch Pharm Res. 2015 Aug;38(8):1443-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Arvenin I Related Classifications
HY-N6579 Related Classifications
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