73763-86-7

Upstream product

• 67-56-1 methanol 
• 4744-50-7 2,3-pyrazinedicarboxylic anhydride 
• 89-01-0 2,3-dicarboxypyrazine 

Downstream Products

• 6164-79-0 methyl pyrazine-2-carboxylate 
• 1401246-73-8 8-[(4-chlorophenyl)methyl]-6-[(2R)-2-pyrrolidinylmethyl]pyrazino[2,3-d]pyridazin-5(6H)-one 
• 1401246-74-9 C₁₉H₂₀ClN₅O 
• 1401246-71-6 8-[(4-chlorophenyl)methyl]pyrazino[2,3-d]pyridazin-5(6H)-one 
• 1401246-72-7 C₂₃H₂₆ClN₅O₃ 
• 1401246-68-1 methyl 3-[2-(4-chlorophenyl)-3-(methyloxy)-3-oxopropanoyl]-2-pyrazinecarboxylate 
• 1401246-69-2 3-[2-(4-chlorophenyl)-3-(methyloxy)-3-oxopropanoyl]-2-pyrazinecarboxylic acid 
• 6164-77-8 pyrazine-2,3-dicarboxylic acid dimethyl ester 
• 98-96-4 pyrazinamide 
• 1355613-00-1 methyl 3-(3-(tert-butoxy)-3-oxopropanoyl)pyrazine-2-carboxylate 
• 1355612-71-3 zopolrestat 
• 16298-03-6 Methyl 3-amino-2-pyrazinecarboxylate 

Relevant academic research and scientific papers

Synthesis and pharmacological investigation of azaphthalazinone human histamine H1 receptor antagonists

5-Aza, 6-aza, 7-aza and 8-aza-phthalazinone, and 5,8-diazaphthalazinone templates were synthesised by stereoselective routes starting from the appropriate pyridine/pyrazine dicarboxylic acids by activation with CDI, reaction with 4-chlorophenyl acetate ester enolate to give a β-ketoester, which was hydrolysed, and decarboxylated. The resulting ketone was condensed with hydrazine to form the azaphthalazinone core. The azaphthalazinone cores were alkylated with N-Boc-D-prolinol at N-2 by Mitsunobu reaction, de-protected, and then alkylated at the pyrrolidine nitrogen to provide the target H 1 receptor antagonists. All four mono-azaphthalazinone series had higher affinity (pKi) for the human H1 receptor than azelastine, but were not as potent as the parent non-aza phthalazinone. The 5,8-diazaphthalazinone was equipotent with azelastine. The least potent series were the 7-azaphthalazinones, whereas the 5-azaphthalazinones were the most lipophilic. The more hydrophilic series were the 8-aza series. Replacement of the N-methyl substituent on the pyrrolidine with the n-butyl group caused an increase in potency (pA2) and a corresponding increase in lipophilicity. Introduction of a β-ether oxygen in the n-butyl analogues (2-methoxyethyl group) decreased the H1 pA2 slightly, and increased the selectivity against hERG. The duration of action in vitro was longer in the 6-azaphthalazinone series. The more potent and selective 6-azaphthalazinone core was used to append an H3 receptor antagonist fragment, and to convert the series into the long acting single-ligand, dual H1 H3 receptor antagonist 44. The pharmacological profile of 44 was very similar to our intranasal clinical candidate 1.

ALDOSE REDUCTASE INHIBITORS AND USES THEREOF

The present invention relates to novel compounds and pharmaceutical compositions thereof, and methods for promoting healthy aging of skin, the treatment of skin disorders, the treatment of cardiovascular disorders, the treatment of renal disorders, the treatment of angiogenesis disorders, such as cancer, treatment of tissue damage, such as non-cardiac tissue damage, the treatment of evolving myocardial infarction, and the treatment of various other disorders, such as complications arising from diabetes with the compounds and compositions of the invention. Other disorders can include, but are not limited to, atherosclerosis, coronary artery disease, diabetic nephropathy, diabetic neuropathy, diabetic retinopathy, infections of the skin, peripheral vascular disease, stroke, and the like.

Application of the Curtius rearrangement in a convenient preparation of 3-amino-pyrazinecarboxylic acid, methyl ester

An efficient and convenient synthesis of 3-aminopyrazinecarboxylic acid, methyl ester (7) has been achieved through the use of a Curtius rearrangement.