184002-61-7

Upstream product

• 84758-55-4 N-(tert-butoxycarbonyl)-α-methylalanine methyl ester 
• 30992-29-1 Boc-Aib-OH 

Downstream Products

• 880166-85-8 tert-Butyl {1-methyl-1-[4-methyl-5-(2-methylphenyl)-1,2,4-triazol-3-yl]ethyl}carbamate 
• 959841-70-4 7-[(Benzyloxy)carbonyl]-3-{1-[(tert-butoxycarbonyl)amino]-1-methylethyl}-5,6,7,8-tetrahydro[1,2,4]triazolo[4,3-a]pyrazin-1-ium Trifluoroacetate 
• 959841-68-0 Benzyl 5-(2-{2-[(tert-butoxycarbonyl)amino]-2-methylpropanoyl}hydrazino)-3,6-dihydropyrazine-1(2H)-carboxylate 

Relevant academic research and scientific papers

Pyridinone and Pyridazinone Derivatives as Inhibitors of Poly (Adp-Ribose) Polymerase (Parp)

The present invention relates to compounds of formula I: and pharmaceutically acceptable salts or tautomers thereof which are inhibitors of poly(ADP-ribose)polymerase (PARP) and thus useful for the treatment of cancer, inflammatory diseases, reperfusion injuries, ischaemic conditions, stroke, renal failure, cardiovascular diseases, vascular diseases other than cardiovascular diseases, diabetes mellitus, neurodegenerative diseases, retroviral infections, retinal damage, skin senescence and UV-induced skin damage, and as chemo- or radiosensitizers for cancer treatment.

Synthesis of chemoreversible prodrugs of ara-C with variable time-release profiles. Biological evaluation of their apoptotic activity

N4-Dipeptidyl slow-release forms of the anticancer drug ara-C were prepared by acylation of the lithiated nucleotide with 4,4-dialkyloxazolinones. An azapeptide prodrug of ara-C was obtained by condensation of an amino acid hydrazide with an activated nucleotide urea. The use of unnatural amino acid residues at N4 prevented nonspecific proteolytic cleavage in biological medium. Ara-C prodrugs 10, 15, 17, and 19 released active drug with half-lives from a few minutes to several days, respectively. Activation via intramolecular N4-deacylation did not require enzymatic intervention but was strictly dependent on the structure of the peptide chain. The prodrugs 10, 15, and 17 produced similar growth inhibition as ara-C in cultured murine leukemia cells while the azapeptide prodrug 19 was less potent reflecting the slow release of active drug with this compound. All four prodrugs retained the ability to induce apoptosis in human HL-60 leukemia cells with kinetics dictated by the rate of intramolecular N4-deacylation. This is the first demonstration for the control of apoptotic cell death by the modulation of drug release from prodrugs.