93718-83-3

Usage

Uses

Used in Pharmaceutical Industry:
NSC 95397 is used as a Cdc25 inhibitor for its ability to inhibit the growth of several human tumor cell lines and block G2/M cell cycle transition. Its potency and selectivity make it a promising candidate for cancer research and drug development.
NSC 95397 is used as a caspase-3 activator for its role in inducing cell cycle arrest and apoptosis in cancer cells, which can be beneficial in the development of targeted cancer therapies.
NSC 95397 is used as an ERK activator for its ability to activate ERK-1 and -2, which can play a role in the regulation of cell growth and survival, making it a potential target for cancer treatment.
NSC 95397 is used as an MKP inhibitor for its role in inhibiting carboxyl-terminal binding protein, a transcriptional corepressor that suppresses multiple pro-apoptotic and epithelial genes, which can contribute to the development of novel cancer therapies.
Used in Research Applications:
NSC 95397 is used as a research tool for studying the role of Cdc25 phosphatase, ERK activation, and caspase-3 in various cellular processes, particularly in the context of cancer biology. Its ability to induce cell cycle arrest, apoptosis, and eryptosis in human erythrocytes makes it a valuable compound for investigating the mechanisms underlying these processes and their potential applications in therapeutic interventions.

Biological Activity

Potent and selective irreversible inhibitor of Cdc25 dual specificity phosphatases (K i values are 32, 96 and 40 nM for inhibition of Cdc25A, -B and -C respectively). Displays 125-180-fold selectivity over VH1-related dual-specificity phosphatase and protein tyrosine phosphatase 1b. Inhibits carcinoma cell growth and blocks G 2 /M phase transition in vitro .

Biochem/physiol Actions

Irreversible Cdc25 dual specificity phosphatase inhibitor.

References

1) Lazo et al. (2002), Identification of a potent and selective pharmacophore for Cdc25 dual specificity phosphatase inhibitors; Mol. Pharmacol., 61 720 2) Melchheier et al. (2005), Quinone-induced Cdc25A inhibition causes ERK-dependent connexin phosphorylation; Biochem. Biophys. Res. Commun., 327 1016 3) Blevins et al. (2015), Small Molecule, NSC95397, inhibits the CtBP1-Protein Partner Interaction and CtBP1-Mediated Transcriptional Repression; J. Biomol. Screen., 20 663 4) Jemaa et al. (2016), Stimulation of Suicidal Erythrocyte Death by the CDC25 Inhibitor NSC-95397; Cell. Physiol. Biochem., 40 597

InChI:InChI=1/C14H14O4S2/c15-5-7-19-13-11(17)9-3-1-2-4-10(9)12(18)14(13)20-8-6-16/h1-4,15-16H,5-8H2

Upstream product

• 117-80-6 2,3-Dichloro-1,4-naphthoquinone 
• 60-24-2 2-hydroxyethanethiol 

Relevant academic research and scientific papers

Synthesis, antitumor activity and docking of 2,3-(substituted)-1,4-naphthoquinone derivatives containing nitrogen, oxygen and sulfur

Eleven 2,3-(substituted)-1,4-naphthoquinone derivatives were synthesized in yields ranging from 52-89percent. These derivatives were evaluated for their cytotoxic effects on human lungs (H460), triple-negative breast (MDA-MB-231) and ovarian (A2780) cancer cell lines. Compounds 5f and 8 showed IC50 values of 3.048 × 10-5 mol L-1 and 4.24 × 10-6 mol L-1 for H460; 5c and 8 showed IC50 values of 2.16 × 10-5 mol L-1 and 1.60 × 10-5 mol L-1 for MDA-MB-231, and 5g and 8 showed IC50 values of 2.68 × 10-6 mol L-1 and 3.89 × 10-6 mol L-1 for A2780. Additionally, we conducted a docking study with the four most active compounds and the therapeutic targets PI3K and topoisomerase II showing the pharmacophoric conformation of these compounds.