One-pot synthesis of thiazolo[3,2-a]pyrimidine derivatives, their cytotoxic evaluation and molecular docking studies.

An economical, simple and efficient one-pot method has been developed for the synthesis of thiazolo[3,2-a]pyrimidine hydrobromide derivatives. 2,4-diaryl-6,7,8,9-tetrahydro-4H-benzo[4,5]thiazolo[3,2-a]pyrimidine hydrobromides were synthesized by the α-bromination of cyclohexanone with N-Bromosuccinamide (NBS) and followed by cyclization with 3,4-dihydropyrimidine-2(1H)-thiones, respectively, in the presence of p-toluenesulfonic acid (PTSA) in acetonitrile. However when cyclohexanone was replaced by acetyl acetone and alpha-tetralone gave the corresponding 1-(3-methyl-5,7-diaryl-5H-thiazolo[3,2-a]pyrimidin-2-yl)ethan-1-one hydrobromide and 9,11-diaryl-6,11-dihydro-5H-naphtho[1',2':4,5]thiazolo[3,2-a]pyrimidine hydrobromide derivatives, respectively.

Synthesis and bioassay of a new class of heterocycles pyrrolyl oxadiazoles/thiadiazoles/triazoles.

A new class of heterocycles pyrrolyl thiadiazoles, pyrrolyl oxadiazoles and pyrrolyl triazoles were prepared from arylsulfonylethenesulfonylacetic acid methyl ester and tested for their antimicrobial and cytotoxic activities.

Synthesis and antimicrobial activity of novel sulfone-linked bis heterocycles.

Novel sulfone-linked bis heterocycles pyrazolines in combination with thiadiazoles, oxadiazoles and triazoles were prepared from E-styrylsulfonylacetic acid methyl ester and tested for their antimicrobial activity. The compound 8 showed pronounced activity than the compounds 6 and 7.

Biological evaluation of sulfone derivatives as anti-inflammatory and tumor cells growth inhibitory agents.

A variety of sulfone derivatives including three dimethyl arylsulfonyl malonates (1-3), two bis-(arylethenesulfonyl)-vinyl benzenes (4 and 5) and a sulfone triazole (6) were evaluated for their anti-inflammatory as well as tumor cells growth inhibitory activities in vitro. The sulfone derivatives 1, 2, 3 and 6 significantly and dose-dependently inhibited the production of inflammatory mediators such as nitric oxide (NO), and cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-12), in lipopolysaccharide (LPS) and interferon (IFN)-gamma activated murine peritoneal macrophages, without displaying cytotoxicity. The inhibitory mechanism is found through reducing iNOS protein expression.