country

Change Language

EN - English
FR - Français
DE - Deutsch
ES - Español
JA - 日本語
KO - 한국어

Country or Region:

United States

Product Name	Size / Unit Price	Qty

Total: USD 0.00 Checkout

Cat. No.: HY-16270

Copy Link Print Information

Kevetrin

(Synonyms: 3-Cyanopropyl carbamimidothioate; 4-Isothioureidobutyronitrile)

4 Cited Publications

고객리뷰

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.

연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.

CAS No.: 500863-50-3
화학식: C₅H₉N₃S
분자량:143.21

보관:

Please store the product under the recommended conditions in the Certificate of Analysis.

Kevetrin Chemical Structure

CAS No.: 500863-50-3

사이즈

가격

재고

수량

Amount: USD 0.00

* 장바구니에 담기 전 물품의 수량을 선택해 주십시오.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

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

Biological Activity
- 제품 설명
- Cellular Effect
- In Vitro
- Clinical Trial
Chemical Information
Publications (4)
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

Cellular Effect

Cell Line	Type	Value	Description	References
Caco-2	Inhibition	-5.91 % Compound: KEVETRIN (HYDROCHLORIDE)	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	10.21203/rs.3.rs-23951/v1

In Vitro

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.

Cell Viability Assay^[1]

Cell Line:

TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
Concentration:

85, 170, 340 μM
Incubation Time:

24 h; 48 h
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.

Apoptosis Analysis^[1]

Cell Line:

TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
Concentration:

85, 170, 340 μM (24 h; 48 h)
Incubation Time:

24 h; 48 h
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.

Cell Cycle Analysis^[1]

Cell Line:

TP53-wild-type OCI-AML3, MOLM-13, and TP53-mutant KASUMI-1, NOMO-1 acute myeloid leukemia (AML) cell lines
Concentration:

85, 170, 340 μM
Incubation Time:

24 h; 48 h
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.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 500863-50-3
분자량 143.21
화학식 C₅H₉N₃S
SMILES

N#CCCCSC(=N)N
Synonyms

3-Cyanopropyl carbamimidothioate; 4-Isothioureidobutyronitrile
선적

Room temperature in continental US; may vary elsewhere.
보관

Please store the product under the recommended conditions in the Certificate of Analysis.

Publications (4)

All

Sort by:

Journal Impact Factor

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

Corneal Sensory Denervation Causes Epithelial Ferroptosis and Delayed Healing in Mice. [Abstract]

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Napolitano R, et al. Kevetrin induces apoptosis in TP53 wild‑type and mutant acute myeloid leukemia cells. Oncol Rep. 2020;44(4):1561-1573. [Content Brief]

Calculators

몰농도 계산기

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

농도 희석 계산기

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

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.

Keywords

MOQ

Minimum order quantity

100 mg

견적 받기 해외재고보유

Other size

견적 받기

Amount: USD 0.00

Biological Activity
- 제품 설명
- In Vitro
- Clinical Trial
Chemical Information
Publications (4)
순도&문서
References

상품명:
Cat. No.:
수량:
MCE Japan Authorized Agent:

상품명:
CAS No.:
Species:
Purity:
수량:

Kevetrin

Publications Citing Use of MedChemExpress (MCE) Kevetrin