| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C20H23N3O2S |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Tenovin-1 is a p53 activator that protects p53 from MDM2-mediated degradation. It acts by inhibiting the protein-deacetylating activities of SirT1 and SirT2, and it also inhibits dihydroorotate dehydrogenase (DHODH)[1][2]. It is supplied as a white to off-white solid (C20H23N3O2S, MW 369.48) at 99.88% purity.
Physical & Chemical Properties
| CAS Number | 380315-80-0 |
|---|---|
| Molecular Formula | C20H23N3O2S |
| Molecular Weight | 369.48 g/mol |
| Purity | 99.88% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O=C(NC(NC1=CC=C(NC(C)=O)C=C1)=S)C2=CC=C(C(C)(C)C)C=C2 |
| Target | MDM-2/p53, DHODH, Sirtuin |
| Signaling Pathway | Apoptosis; Metabolic Enzyme/Protease; Cell Cycle/DNA Damage; Epigenetics; Autophagy |
| Solubility | In Vitro: DMSO: 100 mg/mL (270.65 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (270.65 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (6.77 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 2
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.77 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
Tenovin-1 prevents mdm2-mediated degradation of p53 and has little effect on p53 synthesis. Tenovin-1 acts on one or more factors upstream of p53 that modulate not only p53 function but also other cellular pathways. At 10 μM, Tenovin-1 inhibits SirT2 deacetylase activity[1]. In SK-N-MC cells, Tenovin-1 (1-10 μM) causes concentration-dependent cell death with a bell-shaped profile. Tenovin-1 changes gene and protein expression of Bcl-2 family members, although Tenovin-1 has a stronger effect on both mRNA and protein levels at the lower concentration than at the higher one. In p53 wild-type WE-68 cells, the cytotoxic effects of Tenovin-1 rely on caspases, whereas p53 null SK-N-MC cells show no such dependence. AIF is the main contributor to tenovin-1-induced death in p53 null SK-N-MC cells, which is not the case in p53 wild-type WE-68 cells. Reactive oxygen species also contribute to tenovin-1-mediated cell death in SK-N-MC cells. Tenovin-1 additionally causes DNA damage in SK-N-MC cells[3]. Tenovin-1 (5 μM) enlarges the nucleus in glioblastoma cells and rat primary astrocytes. Tenovin-1 induces cellular senescence, which does not appear to be linked to cell death[4]. Tenovin-1 (10 μM) lowers both proliferation and anchorage independent growth in NSCLC cells, and Tenovin-1 also inhibits growth of H358 lung cancer cells[5].
In Vivo
In SCID mice, Tenovin-1 (92 mg/kg, i.p.) reduces growth of tumors derived from BL2 cells or ARN8 cells[5].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[4]
Measure cell viability by thiazolyl blue tetrazolium bromide (MTT) assay. Seed cells in 96-well plates. Where indicated, treat with 10 μM Tenovin-1 (tnv-1) or transfect with siRNAs. After the specified period of time, add MTT solution (0.5 mg/mL). Dissolve the formazan crystals in an extraction buffer (50% dimethylformamide and 20% SDS, pH 4.7). Read absorbance (540/690 nm) in a SunRise plate reader[4].
Animal Administration[5]
Inject ARN8 melanoma or BL2 Burkitt’s lymphoma cells into the flank of SCID mice and allow tumors to develop until palpable. Administer Tenovin-1 (in 70% cyclodextrin) daily (14 days) by intraperitoneal injection at 92.5 mg/kg and measure tumor growth over a period of 18 days. Treat control animals with 70% cyclodextrin. BL2 experiment: n = 12 per treatment. ARN8 experiment: n = 14 controls and n = 16 tenovin-1 treated animals. Average growth measurements between groups and plot them[5].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Chin Herb Med. 2026 Mar 1.
P300/CBP inhibition sensitizes mantle cell lymphoma to PI3Kδ inhibitor idelalisib. Acta Pharmacol Sin 2022 Feb;43(2):457-469. PMID: 33850273
MGMT-activated DUB3 stabilizes MCL1 and drives chemoresistance in ovarian cancer. Proc Natl Acad Sci U S A 2019 Feb 19;116(8):2961-2966.
View. 2025 Oct 28.
Connexin 32 deficiency protects the liver against ischemia/reperfusion injury. Eur J Pharmacol 2020 Jun 5;876:173056.
