166954-96-7

Upstream product

• 2969-81-5 Ethyl 4-bromobutyrate 
• 123-31-9 hydroquinone 
• 20449-79-0 melittin from honey bee venom 
• 137215-27-1 7-mercapto-4-methyl-2H-chromen-2-one 
• 143216-03-9 4-(4-ethoxy-4-oxobutoxy)benzoic acid 
• 92991-64-5 ethyl 4-(4-formylphenoxy)butyrate 
• 123-08-0 4-hydroxy-benzaldehyde 
• 287392-85-2 4-(4-benzyloxy-phenoxy)-butyric acid ethyl ester 

Downstream Products

• 166953-72-6 ethyl 4-[4-[(4-dimethylaminopyrid-3-yl)methoxy]phenoxy]butanoate 
• 1133001-19-0 ethyl 4-(4-(5-((5-tert-butyloxazol-2-yl)methylthio)thiazol-2-ylcarbamoyloxy)phenoxy)butanoate 
• 34918-52-0 1-isopropylamino-3-(p-3-carbamoylpropoxyphenoxy)propan-2-ol 
• 84822-51-5 4-(4-hydroxyphenoxy)butanoic acid 

Relevant academic research and scientific papers

Identification of 5-Substituted 2-Acylaminothiazoles That Activate Tat-Mediated Transcription in HIV-1 Latency Models

The persistent reservoir of cells latently infected with human immunodeficiency virus (HIV)-integrated proviral DNA necessitates lifelong suppressive antiretroviral therapy (ART). Epigenetic targeted compounds have shown promise as potential latency-reversing agents; however, these drugs have undesirable toxicity and lack specificity for HIV. We utilized a novel HEK293-derived FlpIn dual-reporter cell line, which quantifies specific HIV provirus reactivation (LTR promoter) relative to nonspecific host cell gene expression (CMV promoter), to identify the 5-substituted 2-acylaminothiazole hit class. Here, we describe the optimization of the hit class, defining the functionality necessary for HIV gene activation and for improving in vitro metabolism and solubility. The optimized compounds displayed enhanced HIV gene expression in HEK293 and Jurkat 10.6 latency cellular models and increased unspliced HIV RNA in resting CD4+ T cells isolated from HIV-infected individuals on ART, demonstrating the potential of the 2-acylaminothiazole class as latency-reversing agents.

Chemoselective and site-selective peptide and native protein modification enabled by aldehyde auto-oxidation

We report a chemoselective and site-selective formylation of ?-amine in native proteins. The aldehyde auto-oxidation re-routing, regulated generation of formate, and reversible N-terminus protection drive the transformation. It labels a single ?-amine in a pool of its copies, other nucleophilic residues, and α-amine. The extension of the methodology leads to site-selective acylation.

General method for the synthesis of salicylic acids from phenols through palladium-catalyzed silanol-directed C-H carboxylation

A silanol-directed, palladium-catalyzed C-H carboxylation reaction of phenols to give salicylic acids has been developed. This method features high efficiency and selectivity, and excellent functional-group tolerance. The generality of this method was demonstrated by the carboxylation of estrone and by the synthesis of an unsymmetrically o,o′-disubstituted phenolic compound through two sequential C-H functionalization processes.

CDK INHIBITORS

The present invention relates to CDK inhibitors and their use in the treatment of cell proliferative diseases such as cancer.

CDK INHIBITORS CONTAINING A ZINC BINDING MOIETY

The present invention relates to CDK inhibitors and their use in the treatment of cell proliferative diseases such as cancer. The compounds of the invention may further act as HDAC inhibitors.

Alkynyl containing hydroxamic acid compounds as matrix metalloproteinase and tace inhibitors

Compounds of the formula are useful in treating disease conditions mediated by TNF-α, such as rheumatoid arthritis, osteoarthritis, sepsis, AIDS, ulcerative colitis, multiple sclerosis, Crohn's disease and degenerative cartilage loss.