Kevetrin
Based on 4 publication(s) in Google Scholar
Kevetrin (3-Cyanopropyl carbamimidothioate; 4-Isothioureidobutyronitrile) is an apoptosis inducer that exhibits p53-dependent and p53-independent antitumor activity. In TP53 wild-type models, Kevetrin activates and stabilizes the p53 protein by altering the processing of MDM2, thereby inducing cell cycle arrest and apoptosis. Kevetrin shows higher sensitivity in mutant models. Kevetrin is applicable for the research of various cancers including acute myeloid leukemia and breast cancer.
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- CAS. Nr.: 500863-50-3
- Formel: C5H9N3S
- Molecular Weight:143.21
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Publications Citing Use of MedChemExpress (MCE) Kevetrin
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Biologische Aktivität
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Cell Line
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Type | Value | Description | References |
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| Caco-2 | Inhibition |
-5.91 %
Compound: KEVETRIN (HYDROCHLORIDE)
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Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging
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10.21203/rs.3.rs-23951/v1 |
Kevetrin (85-340 μM; 6-72 h) does not reduce the viability of TP53 wild-type MOLM-13 acute myeloid leukemia (AML) cells, nor does it induce significant apoptosis in these cells[1].
Kevetrin (85-340 μM; 6-72 h) reduces cell viability and induces apoptosis in TP53-mutant KASUMI-1 acute myeloid leukemia (AML) cells in a dose- and time-dependent manner, with more significant efficacy after repeated administration cycles[1].
Kevetrin (340 μM; 6 h) alters the expression of MT family genes and several leukemia-related transcriptional regulators in TP53 wild-type MOLM-13 cells and TP53 mutant KASUMI-1 acute myeloid leukemia (AML) cells[1].
Kevetrin (85-340 μM; 48 h) reduces cell viability in both TP53 wild-type and TP53 mutant AML cell lines, with TP53 mutant cell lines exhibiting higher sensitivity[1].
Kevetrin (85-340 μM; 24-48 h) induces apoptosis in both TP53 wild-type and TP53 mutant acute myeloid leukemia (AML) cell lines, with TP53 mutant cell lines exhibiting a stronger, dose-dependent apoptotic response[1].
Kevetrin (85, 170, 340 μM; 24-48 h) induces G0/G1 cell cycle arrest in TP53 wild-type OCI-AML3 cells and TP53-mutant NOMO-1 acute myeloid leukemia (AML) cells, but does not alter the cell cycle progression of TP53 wild-type MOLM-13 cells or TP53-mutant KASUMI-1 AML cells[1].
Kevetrin (85-340 μM; 48 h) reduces the viability of primary AML cells and induces their apoptosis, exhibits selective cytotoxic activity against blasts, and shows higher sensitivity in primary samples with TP53 mutations[1].
Kevetrin (340 μM; 48 h) alters a shared core transcriptional program in TP53 wild-type MOLM-13 and TP53-mutant KASUMI-1 acute myeloid leukemia (AML) cells, downregulates key oncogenic pathways such as glycolysis and DNA repair, and upregulates p53 target genes and p53 pathway-associated transcriptional signatures[1].
Kevetrin (85-340 μM; 48 h) upregulates p21 in a dose-dependent manner in TP53 wild-type AML cells, increases the expression level of p53 and promotes its nuclear localization, and also induces the accumulation of p53 in apoptotic cells, with a stronger induction effect of p53 in TP53-mutant AML cell lines[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
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Concentration:85, 170, 340 μM
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Incubation Time:24 h; 48 h
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Result:Barely altered cell viability across all cell lines after 24 h treatment.
Significantly reduced viability in MOLM-13 cells at 340 μM, in OCI-AML3 cells at 170 and 340 μM, and in KASUMI-1 and NOMO-1 cells in a dose-dependent manner at all tested concentrations after 48 h treatment.
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Cell Line:TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
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Concentration:85, 170, 340 μM (24 h; 48 h)
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Incubation Time:24 h; 48 h
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Result:Induced significant apoptosis (Annexin V+ cells) in KASUMI-1 cells at 340 μM after 24 h treatment.
Increased Annexin V+ cells to 54.95 ± 5.63% in MOLM-13 cells at 340 μM, 10.03 ± 3.79% in OCI-AML3 cells at 340 μM, 79.70 ± 4.57% in KASUMI-1 cells at 340 μM, and 60.93 ± 2.63% in NOMO-1 cells at 340 μM after 48 h treatment.
Caused a dose-dependent increase in Annexin V+ cells in KASUMI-1 cells at 48 h.
Confirmed apoptosis in MOLM-13 and KASUMI-1 cells via mitochondrial depolarization, DNA fragmentation, and caspase-3 activation.
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Cell Line:TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
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Concentration:85, 170, 340 μM
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Incubation Time:24 h; 48 h
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Result:Caused no cell cycle alterations in MOLM-13 and KASUMI-1 cells at any tested concentration or time point.
Induced accumulation in the G0/G1 phase and a decrease in S phase cells after 24 and 48 h of treatment at all tested concentrations in NOMO-1 and OCI-AML3 cells.
Increased G2/M phase cells after treatment in OCI-AML3 cells.
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS. Nr. 500863-50-3
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Molecular Weight 143.21
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Formel C5H9N3S
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SMILES
N#CCCCSC(=N)N
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Synonyms
3-Cyanopropyl carbamimidothioate; 4-Isothioureidobutyronitrile
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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J Ethnopharmacol
Naoxintong capsule accelerates mitophagy in cerebral ischemia-reperfusion injury via TP53/PINK1/PRKN pathway based on network pharmacology analysis and experimental validation. [Abstract]2024 Aug 20:118721. PMID: 39173723 -
Int Immunopharmacol
Kaempferol inhibits atherosclerotic plaque development via dual-targeting of p53-p21-p16 senescence pathway and Nrf2/HO-1/NQO1 antioxidant mechanism: Insights from combined in vivo and in vitro research. [Abstract]2025 Sep 20:166:115587. PMID: 40976052 -
Invest Ophthalmol Vis Sci
2025 Jun 2;66(6):28. PMID: 40488714 -
J Bioenerg Biomembr
Total favonoids of Desmodium Styracifolium relieve renal ischemia-reperfusion injury by suppressing ferroptosis through P53/SLC7A11/GPX4 signaling pathway : (Running title) TFDS relieved renal ischemia-reperfusion injury. [Abstract]2025 Oct 9. PMID: 41065914
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