6703-51-1

Usage

Uses

Used in Pharmaceutical Industry:
5,6-Dihydro-imidazo[2,1-b]thiazol-3-one is used as a drug candidate for the treatment of various diseases, such as cancer and neurodegenerative disorders, due to its potential therapeutic effects.
Used in Medicinal Chemistry:
5,6-Dihydro-imidazo[2,1-b]thiazol-3-one is used as a building block in organic synthesis and pharmaceutical development, leveraging its versatile reactivity to create novel chemical structures with valuable biological activities.
Used in Anti-inflammatory and Analgesic Applications:
5,6-Dihydro-imidazo[2,1-b]thiazol-3-one is used as an anti-inflammatory and analgesic agent, given its potential to alleviate inflammation and pain, making it a candidate for further research and development in these therapeutic areas.

InChI:InChI=1/C5H6N2OS/c8-4-3-9-5-6-1-2-7(4)5/h1-3H2

Upstream product

• 96-45-7 N,N'-ethylenethiourea 
• 105-39-5 chloroacetic acid ethyl ester 
• 19951-23-6 2-((4,5-dihydro-1H-imidazol-2-yl)thio)acetic acid 
• 91774-37-7 ethyl [(4,5-dihydro-2-imidazolyl)thio]acetate hydrochloride 
• 92114-17-5 (4,5-dihydro-1H-imidazol-2-ylsulfanyl)-thioacetic acid S-(4,5-dihydro-1H-imidazol-2-yl) ester 
• 105-36-2 ethyl bromoacetate 

Downstream Products

• 17886-71-4 (Z)-2-benzylidene-5,6-dihydroimidazo[2,1-b]thiazol-3(2H)-one 
• 17886-71-4 2-benzylidene-5,6-dihydro-imidazo[2,1-b]thiazol-3-one 
• 59816-55-6 3-(4-Chloro-3-dimethylsulfamoylphenyl)-3-hydroxy-2,3,5,6-tetra-hydro-imidazo[2,1-b]thiazol-hydrobromide 
• 1255207-84-1 (2Z)-2-(2-chlorobenzylidene)-5,6-dihydroimidazo[2,1-b]thiazol-3(2H)-one 
• 1443655-30-8 (2Z)-2-(4-morpholinobenzylidene)-5,6-dihydroimidazo[2,1-b]thiazol-3(2H)-one 

Relevant academic research and scientific papers

Identification of (Z)-2-benzylidene-dihydroimidazothiazolone derivatives as tyrosinase inhibitors: Anti-melanogenic effects and in silico studies

As part of our continuous search for novel tyrosinase inhibitors, we designed 5,6-dihydroimindazo[2,1-b]thiazol-3(2H)-one (DHIT) derivatives based on the structure of MHY773; a potent tyrosinase inhibitor with a 2-iminothiazolidin-4-one template. Of the 11 DHIT derivatives synthesized using a Knoevenagel condensation, three DHIT derivatives 1a (IC50 = 36.14 ± 3.90 μM), 1b (IC50 = 0.88 ± 0.91 μM), and 1f (IC50 = 17.10 ± 1.01 μM) inhibited mushroom tyrosinase more than kojic acid (IC50 = 84.41 ± 2.87 μM). Notably, compound 1b inhibited mushroom tyrosinase around 100- and 3.3-fold more potently than kojic acid and MHY773, respectively. Lineweaver-Burk plots demonstrated that compounds 1b and 1f competitively inhibited mushroom tyrosinase, and in silico docking results supported our kinetic results and indicated that these two compounds bind more strongly to the active site of tyrosinase than kojic acid. Docking simulation results using a human tyrosinase homology model confirmed the abilities of 1b and 1f to strongly inhibit human tyrosinase. B16F10 murine melanoma cells were used to investigate whether these two compounds display tyrosinase inhibitory activities and anti-melanogenesis effects in cells. Both compounds were found to significantly and dose-dependently inhibit cellular tyrosinase activity and intracellular and extracellular melanin production more potently than kojic acid. The similarities observed between the cellular tyrosinase and melanogenesis inhibitory effects of 1b and 1f suggest their observed anti-melanogenic effects were due to tyrosinase inhibition. These results indicate that compounds 1b and 1f, which possess the DHIT template, are promising candidates as anti-browning agents and therapeutic agents for hyperpigmentation disorders.

cGAS ANTAGONIST COMPOUNDS

Disclosed are novel compounds of Formula (I) that are cGAS antagonists, methods of preparation of the compounds, pharmaceutical compositions comprising the compounds, and their use in medical therapy.

Synthesis and biological evaluation of novel thiazolidinone derivatives as potential anti-inflammatory agents

The modulation of pro-inflammatory cytokines provides a target for controlling inflammatory diseases and attracts much attention in current anti-inflammatory drug development. Here, four series of thiazolidinone derivatives were synthesized and screened for anti-inflammatory activities. A majority of these compounds showed excellent inhibition on the expression of TNF-α and IL-6 in LPS-stimulated macrophages. Discussions are given regarding the structure-activity relationships. Compounds 12d and 12h inhibited LPS-induced TNF-α and IL-6 release in a dose-dependent manner. Furthermore, 12d exhibited a significant protection against LPS-induced septic death in mouse model. Together, these data present a series of new thiazolidinones with potential therapeutic effects in acute inflammatory diseases and they could be important leads in the continuing anti-inflammatory drug research.

Discovery, synthesis and SAR analysis of novel selective small molecule S1P4-R agonists based on a (2Z,5Z)-5-((pyrrol-3-yl)methylene)-3- alkyl-2-(alkylimino)thiazolidin-4-one chemotype

High affinity and selective S1P4 receptor (S1P4-R) small molecule agonists may be important proof-of-principle tools used to clarify the receptor biological function and effects to assess the therapeutic potential of the S1P4-R in diverse disease areas including treatment of viral infections and thrombocytopenia. A high-throughput screening campaign of the Molecular Libraries-Small Molecule Repository was carried out by our laboratories and identified (2Z,5Z)-5-((1-(2-fluorophenyl)-2,5-dimethyl-1H- pyrrol-3-yl)methylene)-3-methyl-2-(methylimino) thiazolidin-4-one as a promising S1P4-R agonist hit distinct from literature S1P4-R modulators. Rational chemical modifications of the hit allowed the identification of a promising lead molecule with low nanomolar S1P4-R agonist activity and exquisite selectivity over the other S1P 1-3,5-Rs family members. The lead molecule herein disclosed constitutes a valuable pharmacological tool to explore the effects of the S1P4-R signaling cascade and elucidate the molecular basis of the receptor function.