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Kevetrin hydrochloride (4-Isothioureidobutyronitrile hydrochloride) Sale

(Synonyms: 4-Isothioureidobutyronitrile hydrochloride; thioureidobutyronitrile hydrochloride; thioureido butyronitrile hydrochloride) 目录号 : GC32919

An activator of p53

Kevetrin hydrochloride (4-Isothioureidobutyronitrile hydrochloride) Chemical Structure

Cas No.:66592-89-0

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥693.00
现货
10mg
¥630.00
现货
50mg
¥1,980.00
现货
100mg
¥3,330.00
现货
500mg
¥9,990.00
现货

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产品描述

Kevetrin is an activator of p53.1,2 It increases levels of activated p53 and expression of p21 in A549 cells and decreases expression of the transcription factor E2F1 in a variety of cell lines.1,2 Kevetrin decreases cell viability in a panel of cancer cell lines with a mean IC50 value of 0.49 μM.3 It reduces tumor growth in MDA-MB-231, HT-29, PC3, HCT15, A549, NCI-H1975, CRL-1619, LNCaP, MIA PaCa, and SCC-5 mouse xenograft models when administered at a dose of 200 mg/kg.

1.Kumar, A., Hiran, T., Holden, S.A., et al.Abstract 4470: KevetrinTM, a novel small molecule, activates p53, enhances expression of p21, induces cell cycle arrest and apoptosis in a human cancer cell lineCancer Res.71(8 Supp)4470(2011) 2.Kumar, A., Holden, S.A., Chafai-Fadela, K., et al.Abstract 2874: Kevetrin targets both MDM2-p53 and Rb-E2F pathways in tumor suppressionCancer Res.72(8 Supp)2874(2012) 3.Menon, K.Nitrile derivatives and their pharmaceutical use and compositions(2012)

Chemical Properties

Cas No. 66592-89-0 SDF
别名 4-Isothioureidobutyronitrile hydrochloride; thioureidobutyronitrile hydrochloride; thioureido butyronitrile hydrochloride
Canonical SMILES NC(SCCCC#N)=N.[H]Cl
分子式 C5H10ClN3S 分子量 179.67
溶解度 DMSO : ≥ 40 mg/mL (222.63 mM) 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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1 mg 5 mg 10 mg
1 mM 5.5658 mL 27.8288 mL 55.6576 mL
5 mM 1.1132 mL 5.5658 mL 11.1315 mL
10 mM 0.5566 mL 2.7829 mL 5.5658 mL
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Research Update

Inhibition of mycobacteria proliferation in macrophages by low cisplatin concentration through phosphorylated p53-related apoptosis pathway

PLoS One 2023 Jan 31;18(1):e0281170.PMID:36719870DOI:PMC9888694

Background: Drug resistance is a prominent problem in the treatment of tuberculosis, so it is urgent to develop new anti- tuberculosis drugs. Here, we investigated the effects and mechanisms of cisplatin (DDP) on intracellular Mycobacterium smegmatis to tap the therapeutic potential of DDP in mycobacterial infection. Results: Macrophages infected with Mycobacterium smegmatis were treated with DDP alone or combined with isoniazid or rifampicin. The results showed that the bacterial count in macrophages decreased significantly after DDP (≤ 6 μg/mL) treatment. When isoniazid or rifampicin was combined with DDP, the number of intracellular mycobacteria was also significantly lower than that of isoniazid or rifampicin alone. Apoptosis of infected cells increased after 24 h of DDP treatment, as shown by flow cytometry and transmission electron microscopy detection. Transcriptome sequencing showed that there were 1161 upregulated and 645 downregulated differentially expressed genes (DEGs) between the control group and DDP treatment group. A Trp53-centered protein interaction network was found based on the top 100 significant DEGs through STRING and Cytoscape software. The expression of phosphorylated p53, Bax, JAK, p38 MAPK and PI3K increased after DDP treatment, as shown by Western blot analysis. Inhibitors of JAK, PI3K or p38 MAPK inhibited the increase in cell apoptosis and the reduction in the intracellular bacterial count induced by DDP. The p53 promoter Kevetrin hydrochloride scavenges intracellular mycobacteria. If combined with DDP, Kevetrin hydrochloride could increase the effect of DDP on the elimination of intracellular mycobacteria. In conclusion, DDP at low concentrations could activate the JAK, p38 MAPK and PI3K pathways in infected macrophages, promote the phosphorylation of p53 protein, and increase the ratio of Bax to Bcl-2, leading to cell apoptosis, thus eliminating intracellular bacteria and reducing the spread of mycobacteria. Conclusion: DDP may be a new host-directed therapy for tuberculosis treatment, as well as the p53 promoter Kevetrin hydrochloride.