70059-80-2

Basic information

• Product Name: 4-PHENYL-5-(2-PHENYLQUINOLIN-4-YL)-4H-1,2,4-TRIAZOLE-3-THIOL
• Synonyms: 4-phenyl-3-(2-phenylquinolin-4-yl)-1H-1,2,4-triazole-5-thione
• CAS NO: 70059-80-2
• Molecular Formula: C₂₃H₁₆N₄S
• Molecular Weight: 380.4649
• Mol File: 70059-80-2.mol
• Article Data: 3

Chemical Properties

• Boiling Point: 565.3°Cat760mmHg
• Flash Point: 295.7°C
• Appearance: /
• Density: 1.29g/cm³
• Vapor Pressure: 8.43E-13mmHg at 25°C
• Refractive Index: 1.721
• CAS DataBase Reference: 4-PHENYL-5-(2-PHENYLQUINOLIN-4-YL)-4H-1,2,4-TRIAZOLE-3-THIOL(CAS DataBase Reference)
• NIST Chemistry Reference: 4-PHENYL-5-(2-PHENYLQUINOLIN-4-YL)-4H-1,2,4-TRIAZOLE-3-THIOL(70059-80-2)
• EPA Substance Registry System: 4-PHENYL-5-(2-PHENYLQUINOLIN-4-YL)-4H-1,2,4-TRIAZOLE-3-THIOL(70059-80-2)

Safety Data

• Hazardous Substances Data: 70059-80-2(Hazardous Substances Data)

Usage

InChI:InChI=1/C23H16N4S/c28-23-26-25-22(27(23)17-11-5-2-6-12-17)19-15-21(16-9-3-1-4-10-16)24-20-14-8-7-13-18(19)20/h1-15H,(H,26,28)

Upstream product

• 4779-54-8 2-phenylquinoline-4-carboxylic acid hydrazide 
• 103-72-0 phenyl isothiocyanate 
• 132-60-5 cinchophen 
• 91-56-5 indole-2,3-dione 

Relevant articles and documents

Design and synthesis of novel quinoline/chalcone/1,2,4-triazole hybrids as potent antiproliferative agent targeting EGFR and BRAFV600E kinases

New quinoline / chalcone hybrids containing 1,2,4-triazole moiety have been designed, synthesized and their structures elucidated and confirmed by various spectroscopic techniques. The designed compounds showed moderate to good activity on different NCI 60 cell lines in a single-dose assay with a growth inhibition rate ranging from 50% to 94%. Compounds 7b, 7d, 9b, and 9d were the most active compounds in most cancer cell lines with a growth inhibition percent between 77% and 94%. Newly synthesized hybrids were evaluated for their anti-proliferative activity against a panel of four human cancer cell lines. Compounds 7a, 7b, 9a, 9b, and 9d showed promising antiproliferative activities. These compounds were further tested for their inhibitory potency against EGFR and BRAFV600E kinases with erlotinib as a reference drug. The molecular docking study of compounds 7a, 7b, 9a, 9b, and 9d revealed nice fitting into the active site of EGFR and BRAFV600E kinases. Compounds 7b, 9b, and 9d displayed the highest binding affinities and similar binding pattern to those of erlotinib.

NO-releasing STAT3 inhibitors suppress BRAF-mutant melanoma growth

Constitutive activation of STAT3 can play a vital role in the development of melanoma. STAT3-targeted therapeutics are reported to show efficacy in melanomas harboring the BRAFV600E mutant and also in vemurafenib-resistant melanomas. We designed and synthesized a series of substituted nitric oxide (NO)-releasing quinolone-1,2,4-triazole/oxime hybrids, hypothesizing that the introduction of a STAT3 binding scaffold would augment their cytotoxicity. All the hybrids tested showed a comparable level of in vitro NO production. 7b and 7c exhibited direct binding to the STAT3-SH domain with IC50 of ～ 0.5 μM. Also, they abrogated STAT3 tyrosine phosphorylation in several cancer cell lines, including the A375 melanoma cell line that carries the BRAFV600E mutation. At the same time, they did not affect the phosphorylation of upstream kinases or other STAT isoforms. 7c inhibited STAT3 nuclear translocation in mouse embryonic fibroblast while 7b and 7c inhibited STAT3 DNA-binding activity in the A375 cell line. Their anti-proliferating activity is attributed to their ability to trigger the production of reactive oxygen species and induce G1 cell cycle arrest in the A375 cell line. Interestingly, 7b and 7c showed robust cell growth suppression and apoptosis induction in two pairs of BRAF inhibitor-na?ve (-S) and resistant (-R) melanoma cell lines containing a BRAF V600E mutation. Surprisingly, MEL1617-R cells that are known to be more resistance to MEK inhibition by GSK1120212 than MEL1617-S cells exhibit a similar response to 7b and 7c.