32558-16-0

Upstream product

• 30748-47-1 5-acetyl-4-methylthiazole-2-amine 
• 1694-29-7 3-chloropentane-2,4-dione 
• 32519-69-0 N-(5-acetyl-4-methylthiazol-2-yl)benzamide 

Downstream Products

• 39884-32-7 1-(2-benzoylamino-4-methyl-thiazol-5-yl)-2-bromo-ethanol 
• 113753-36-9 N-[2-(4-Carboethoxyphenyl)ethyl]-2-hydroxy-2-(2-benzoylamino-4-methyl-thiazol-5-yl)ethanamine 
• 958941-46-3 C₂₁H₁₈N₄OS₂ 
• 1030631-27-6 C₂₀H₁₄Cl₂N₄OS₂ 
• 958941-29-2 C₂₀H₁₅FN₄OS₂ 
• 958941-35-0 C₂₀H₁₅FN₄OS₂ 
• 315704-32-6 C₂₁H₁₈N₄O₂S₂ 
• 958972-79-7 C₂₁H₁₈N₄O₂S₂ 
• 958941-25-8 C₂₀H₁₅ClN₄OS₂ 
• 1144518-59-1 C₃₀H₃₃ClN₄O₆S₂ 
• 1391715-61-9 N-(5-(2-azidoacetyl)-4-methylthiazol-2-yl)benzamide 
• 1395082-15-1 N-(5-(2-(4-(methoxymethyl)-1H-1,2,3-triazol-1-yl)acetyl)-4-methylthiazol-2-yl)benzamide 

Relevant academic research and scientific papers

Click-based synthesis of triazolobithiazole Δf508-CFTR correctors for cystic fibrosis

Copper catalyzed azide-alkyne cycloaddition (CuAAC) chemistry is reported for the construction of previously unknown 5-(1H-1,2,3-triazol-1-yl)-4,5′- bithiazoles from 2-bromo-1-(thiazol-5-yl)ethanones. These novel triazolobithiazoles are shown to have cyst

Design and synthesis of a hybrid potentiator-corrector agonist of the cystic fibrosis mutant protein ΔF508-CFTR

A developing therapy of cystic fibrosis caused by the ΔF508 mutation in CFTR employs correction of defective CFTR chloride channel gating by a 'potentiator' and of defective CFTR protein folding by a 'corrector'. Based on SAR data for phenylglycine-type potentiators and bithiazole correctors, we designed a hybrid molecule incorporating an enzymatic hydrolysable linker to deliver the potentiator (PG01) fragment 2 and the corrector (Corr-4a) fragment 13. The hybrid molecule 14 contained PG01-OH and Corr-4a-linker-CO2H moieties, linked with an ethylene glycol spacer through an ester bond. The potentiator 2 and corrector 13 fragments (after cleavage) had low micromolar potency for restoration of ΔF508-CFTR channel gating and cellular processing, respectively. Cleavage of hybrid molecule 14 by intestinal enzymes under physiological conditions produced the active potentiator 2 and corrector fragments 13, providing proof-of-concept for small-molecule potentiator-corrector hybrids as a single drug therapy for CF caused by the ΔF508 mutation.

4′-Methyl-4,5′-bithiazole-based correctors of defective ΔF508-CFTR cellular processing

The synthesis and ΔF508-CFTR corrector activity of a 148-member methylbithiazole-based library are reported. Synthetic routes were devised and optimized to generate methylbithiazole analogs in four steps. Corrector potency and efficacy were assayed using epithelial cells expressing human ΔF508-CFTR. These structure-activity data establish that the bithiazole substructure plays a critical function; eight novel methylbithiazole correctors were identified with low micromolar potencies.