79779-66-1

Usage

InChI:InChI=1/C8H4BrCl3O/c9-3-6(13)4-1-2-5(10)8(12)7(4)11/h1-2H,3H2

Upstream product

• 13608-87-2 2',3',4'-trichloroacetophenone 

Downstream Products

• 91064-45-8 2-(2-imino-thiazolidin-3-yl)-1-(2,3,4-trichloro-phenyl)-ethanone 
• 5028-86-4 2-(2-acetylimino-thiazolidin-3-yl)-1-(2,3,4-trichloro-phenyl)-ethanol 
• 6649-41-8 2-(2-acetylimino-thiazolidin-3-yl)-1-(2,3,4-trichloro-phenyl)-ethanone 
• 156897-39-1 [6,6-Dimethyl-1-phenyl-2-(2,3,4-trichloro-phenyl)-6,7-dihydro-5H-pyrrolizin-3-yl]-acetic acid ethyl ester 
• 178449-61-1 6-(2,3,4-Trichloro-phenyl)-imidazo[2,1-b]thiazole-5-carbaldehyde 
• 178449-62-2 6-(2,3,4-Trichloro-phenyl)-2,3-dihydro-imidazo[2,1-b]thiazole-5-carbaldehyde 
• 936105-14-5 5-[1,2,4]triazol-1-yl-4-(2,3,4-trichloro-phenyl)-thiazol-2-ylamine 
• 178449-58-6 6-(2,3,4-Trichloro-phenyl)-imidazo[2,1-b]thiazole 
• 178449-59-7 6-(2,3,4-Trichloro-phenyl)-2,3-dihydro-imidazo[2,1-b]thiazole 
• 156897-25-5 2,2-Dimethyl-7-phenyl-6-(2,3,4-trichloro-phenyl)-2,3-dihydro-1H-pyrrolizine 

Relevant academic research and scientific papers

Structural design, synthesis and structure-activity relationships of thiazolidinones with enhanced anti-Trypanosoma cruzi activity

Pharmacological treatment of Chagas disease is based on benznidazole, which displays poor efficacy when administered during the chronic phase of infection. Therefore, the development of new therapeutic options is needed. This study reports on the structural design and synthesis of a new class of anti-Trypanosoma cruzi thiazolidinones (4 a-p). (2-[2-Phenoxy-1-(4-bromophenyl) ethylidene)hydrazono]-5-ethylthiazolidin-4-one (4 h) and (2-[2-phenoxy-1-(4- phenylphenyl)ethylidene)hydrazono]-5-ethylthiazolidin-4-one (4 l) were the most potent compounds, resulting in reduced epimastigote proliferation and were toxic for trypomastigotes at concentrations below 10 μM, while they did not display host cell toxicity up to 200 μM. Thiazolidinone 4 h was able to reduce the in vitro parasite burden and the blood parasitemia in mice with similar potency to benznidazole. More importantly, T. cruzi infection reduction was achieved without exhibiting mouse toxicity. Regarding the molecular mechanism of action, these thiazolidinones did not inhibit cruzain activity, which is the major trypanosomal protease. However, investigating the cellular mechanism of action, thiazolidinones altered Golgi complex and endoplasmic reticulum (ER) morphology, produced atypical cytosolic vacuoles, as well as induced necrotic parasite death. This structural design employed for the new anti-T. cruzi thiazolidinones (4 a-p) led to the identification of compounds with enhanced potency and selectivity compared to first-generation thiazolidinones. These compounds did not inhibit cruzain activity, but exhibited strong antiparasitic activity by acting as parasiticidal agents and inducing a necrotic parasite cell death. Stop the cycle! The attachment of an aryl ring to the iminic carbon produced thiazolidinones that are conformationally more restricted than first-generation thiazolidinones. This enhanced the potency of antiparasitic thiazolidinones, as observed under treatment with compound 4 h where parasite development and invasion in host cells were substantially reduced. Copyright

Heme oxygenase inhibition by 1-Aryl-2-(1H-imidazol-1-yl/1H-1,2,4-triazol-1- yl)ethanones and their derivatives

Previous studies by our research group have been concerned with the design of selective inhibitors of heme oxygenases (HO-1 and HO-2). The majority of these were based on a four-carbon linkage of an azole, usually an imidazole, and an aromatic moiety. In the present study, we designed and synthesized a series of inhibition candidates containing a shorter linkage between these groups, specifically, a series of 1-aryl-2-(1H-imidazol-1-yl/1H-1,2,4-triazol-1-yl) ethanones and their derivatives. As regards HO-1 inhibition, the aromatic moieties yielding best results were found to be halogen-substituted residues such as 3-bromophenyl, 4-bromophenyl, and 3,4-dichlorophenyl, or hydrocarbon residues such as 2-naphthyl, 4-biphenyl, 4-benzylphenyl, and 4-(2-phenethyl)phenyl. Among the imidazole-ketones, five (36-39, and 44) were found to be very potent (IC5050 in favor of HO-1. In the case of the azole-dioxolanes, two of them (80 and 85), each possessing a 2-naphthyl moiety, were found to be particularly potent and selective HO-1 inhibitors. Three non-carbonyl analogues (87, 89, and 91) of 1-(4-chlorophenyl)-2-(1H-imidazol-1-yl)ethanone were found to be good inhibitors of HO-1. For the first time in our studies, two azole-based inhibitors (37 and 39) were found to exhibit a modest selectivity index in favor of HO-2. The present study has revealed additional candidates based on inhibition of heme oxygenases for potentially useful pharmacological and therapeutic applications.

Synthesis, structure, and biological activity of novel 1H-1,2,4-triazol-1- yl-thiazole derivatives

2-Amino-4-aryl-5-(1H-1,2,4-triazol-1-yl)thiazole derivatives were synthesized from the reaction of α-bromo substituted acetophenone and thiourea. The structures were confirmed by elemental analysis, 1H NMR and single crystal X-ray diffraction analysis. Biological evaluation showed that some of them possess antifungal and plant growth regulatory activities. Copyright Taylor & Francis Group, LLC.

Phenylpiperazines which are useful in the treatment of schistosomiasis

A compound of the formula STR1 in which A is STR2 n is 1, 2 or 3, and R is phenyl optionally substituted with halogen, alkyl, phenyl, cyano, hydroxy, alkoxy, mercapto, sulfinyl, sulfonyl, amino, nitro, trifluoromethyl and/or naphthyl radicals; or a furan, thiophene, pyridine, benzofuran, dibenzothiophene or thianthrene radical, or a pharmacologically acceptable salt thereof, for treating schistosomiasis.