32826-88-3

Upstream product

• 598-21-0 2-Bromoacetyl bromide 
• 104-94-9 4-methoxy-aniline 
• 2365-48-2 Methyl thioglycolate 
• 530-62-1 1,1'-carbonyldiimidazole 
• 1219-96-1 N-(p-methoxyphenyl)-N'-phenylthiourea 
• 1219-96-1 N¹-phenyl-N²-(p-methoxyphenyl)thiourea 
• 2284-20-0 4-Methoxyphenyl isothiocyanate 
• 32826-80-5 3-(4-methoxy-phenyl)-2-phenylimino-thiazolidin-4-one 
• 79-11-8 chloroacetic acid 
• 1227-45-8 1,3-bis-(p-methoxyphenyl)thiourea 

Downstream Products

• 1273422-85-7 C₁₇H₁₂BrNO₄S 
• 104268-08-8 N,N'-bis-[3-(4-methoxy-phenyl)-2,4-dioxo-thiazolidin-5-yl]-2,2'-piperazine-1,4-diyl-bis-acetamide 
• 92696-07-6 5-(2-chloro-acetylamino)-3-(4-methoxy-phenyl)-thiazolidine-2,4-dione 
• 85350-19-2 5-amino-3-(4-methoxylphenyl)-thiazolidine-2,4-dione 
• 93150-61-9 N,N-diethyl-glycine 3-(4-methoxy-phenyl)-2,4-dioxo-thiazolidin-5-ylamide 
• 35077-57-7 (4-methoxy-phenyl)-thiazolidinetrione 5-phenylhydrazone 

Relevant academic research and scientific papers

Novel N-phenyl-substituted thiazolidinediones protect neural cells against glutamate- and tBid-induced toxicity

Mitochondrial demise is a key feature of progressive neuronal death contributing to acute and chronic neurological disorders. Recent studies identified a pivotal role for the BH3-only protein B-cell lymphoma-2 interacting domain death antagonist (Bid) for such mitochondrial damage and delayed neuronal death after oxygen-glucose deprivation, glutamate-induced excitotoxicity, or oxidative stress in vitro and after cerebral ischemia in vivo. Therefore, we developed new N-phenyl-substituted thiazolidine-2,4-dione derivatives as potent inhibitors of Bid-dependent neurotoxicity. The new compounds 6, 7, and 16 were identified as highly protective by extensive screening in a model of glutamate toxicity in immortalized mouse hippocampal neurons (HT-22 cells). These compounds significantly prevent truncated Bid-induced toxicity in the neuronal cell line, providing strong evidence that inhibition of Bid was the underlying mechanism of the observed protective effects. Furthermore, Bid-dependent hallmarks of mitochondrial dysfunction, such as loss of mitochondrial membrane potential, ATP depletion, as well as impairments in mitochondrial respiration, are significantly prevented by compounds 6, 7, and 16. Therefore, the present study identifies a class of N-phenyl thiazolidinediones as novel Bid-inhibiting neuroprotective agents that provide promising therapeutic perspectives for neurodegenerative diseases, in which Bid-mediated mitochondrial damage and associated intrinsic death pathways contribute to the underlying progressive loss of neurons. Copyright

Reaction of O-alkyl-N-substituted iminothiocarbonates with bromoacetyl bromide. A general method for the synthesis of 3-substituted 1,3-thiazolidine-2,4-diones

Reaction of sodium salts of O-methyl-N-substituted iminothiocaibonates with bromoacetyl bromide represents a new general method for preparation of 3-substituted 1,3-thiazolidine-2,4-diones in good yields and high purity. The structure of the synthesized products has been confirmed by 1H NMR, 13C NMR, IR and mass spectroscopy as well as by independent synthesis.

Influence of Substituents on the Synthesis of Thiazolidinones

The influence of substituents (subunits) in the synthesis of thiazolidinones by the reaction of unsymmetrical thioureas with monochloroacetic acid in ethanol has been rationalised by the characterisation of the hydrolysis products of the resulting thiazolidinones.The formation of thiol from thiourea, which is the key intermediate in thiazolidinone synthesis, invariably involves the -NH- group adjacent to more electron withdrawing subunits.