872866-28-9

Upstream product

• 406233-31-6 4-fluoro-3-nitrobenzenesulfonamide 
• 870812-94-5 (1R)-3-(4-morpholinyl)-3-oxo-1-((phenylsulfanyl)methyl)propylamine 
• 1027345-35-2 (R)-tert-butyl 3-amino-4-(phenylthio)butanoate 
• 882-33-7 diphenyldisulfane 
• 3888-84-4 4-fluoro-3-nitro-benzenesulfonic acid 
• 870812-93-4 benzyl (1R)-3-(4-morpholinyl)-3-oxo-1-((phenylsulfanyl)methyl)propylcarbamate 
• 870812-92-3 benzyl (1R)-1-(hydroxymethyl)-3-(4-morpholinyl)-3-oxopropylcarbamate 
• 1493-27-2 ortho-nitrofluorobenzene 
• 108-98-5 thiophenol 
• 6668-56-0 4-fluoro-3-nitrobenzene-1-sulfonyl chloride 
• 406233-30-5 (R)-3-(9H-fluoren-9-ylmethyloxycarbonylamino)-4-phenylsulfanylbutyric acid tert-butyl ester 
• 406233-32-7 (R)-3-(2-nitro-4-sulfamoylphenylamino)-4-phenylsulfanylbutyric acid tert-butyl ester 
• 872866-27-8 4-((R)-3-(morpholin-4-yl)-3-oxo-1-phenylsulfanylmethylpropylamino)-3-nitrobenzenesulfonamide 

Downstream Products

• 852808-14-1 (R)-4-(4-((4'-chlorobiphenyl)methyl)piperazin-1-yl)-N-(4-(4-morpholino-1-(phenylthio)butan-2-ylamino)-3-nitrophenylsulfonyl)benzamide 
• 1027344-93-9 N-{7-[4-((4'-chloro-(1,1'-biphenyl)-2-yl)methyl)piperazin-1-yl]quinazolin-4-yl}-4-(((R)-3-(morpholin-4-yl)-1-(phenylsulfanylmethyl)prop-1-yl)amino)-3-nitrobenzenesulfonamide 
• 1027345-01-2 N-(7-{4-[(2-(4-chlorophenyl)-5,5-dimethylcyclohex-1-en-1-yl)methyl]piperazin-1-yl}quinazolin-4-yl)-4-(((R)-3-(morpholin-4-yl)-1-(phenylsulfanylmethyl)prop-1-yl)amino)-3-nitrobenzenesulfonamide 

Relevant academic research and scientific papers

NANOPARTICLE FORMULATION OF BCL-2 INHIBITOR

Various albumin nanoparticle Bcl-2 inhibitor formulations are described, along with methods of using them to treat conditions characterized by excessive cellular proliferation, such as cancer and tumors. In various embodiments, such Bcl-2 inhibitor formulations contain albumin and a compound of the following Formula (I), or a pharmaceutically acceptable salt thereof, where the variables in Formula (I) are defined herein.

BENZAMIDE COMPOUNDS

Compounds of Formula (I) are provided herein. Such compounds, as well as pharmaceutically acceptable salts and compositions thereof, are useful for treating diseases or conditions, including conditions characterized by excessive cellular proliferation, such as cancer and tumors, as well as viral infections such as HIV.

APOPTOSIS-INDUCING AGENTS

Disclosed are compounds which inhibit the activity of anti-apoptotic Bcl-xL proteins, compositions containing the compounds and methods of treating diseases during which is expressed anti apoptotic Bcl-xL protein.

CHEMICAL COMPOUNDS

The present invention relates to compounds of Formula (I): and to their salts, pharmaceutical compositions, methods of use, and methods for their preparation. These compounds inhibit Bcl-2 and/or Bcl-XL activities and may be used for the treatment of cancer.

ARYLSULFONAMIDE COMPOUNDS

The invention relates generally to small molecules that mimic the biological activity of certain peptides and proteins, to compositions containing them and to their use. In particular, the invention relates to compounds of the general formula (I) that mim

Discovery and structure-activity relationship of antagonists of B-cell lymphoma 2 family proteins with chemopotentiation activity in vitro and in vivo

Development of a rationally designed potentiator of cancer chemotherapy, via inhibition of Bcl-XL function, is described. Lead compounds generated by NMR screening and directed parallel synthesis displayed sub-μM binding but were strongly deactivated in the presence of serum. The dominant component of serum deactivation was identified as domain III of human serum albumin (HSA); NMR solution structures of inhibitors bound to both Bcl-X L and HSA domain III indicated two potential optimization sites for separation of affinities. Modifications at both sites resulted in compounds with improved Bcl-XL binding and greatly increased activity in the presence of human serum, culminating in 73R, which bound to Bcl-XL with a Ki of 0.8 μM. In a cellular assay 73R reversed the protection afforded by Bcl-XL overexpression against cytokine deprivation in FL5.12 cells with an EC50 of 0.47 μM. 73R showed little effect on the viability of the human non small cell lung cancer cell line A549. However, consistent with the proposed mechanism, 73R potentiated the activity of paclitaxel and UV irradiation in vitro and potentiated the antitumor efficacy of paclitaxel in a mouse xenograft model.