169104-33-0

Upstream product

• 168960-17-6 (1R,4S)-2-(p-Methoxybenzyl)-2-azabicyclo<2.2.1>-5-hepten-3-one 
• 130931-83-8 (1S,4R)-2-azabicyclo[2,2,1]hept-5-en-3-one 
• 824-94-2 p-methoxybenzyl chloride 
• 640897-02-5 (1S,4S)-6-difluoromethylenyl-2-(4‘-methoxybenzyl)-2-azabicyclo[2.2.1]heptan-3-one 
• 79200-56-9 (-)-2-azabicyclo[2.2.1]hept-5-en-3-one 
• 918452-16-1 (1S,4R,6S)-6-hydroxy-2-(4-methoxybenzyl)-2-azabicyclo[2.2.1]-heptan-3-one 
• 918452-15-0 C₁₆H₁₉NO₄ 
• 918452-17-2 (1S,4R)-6-iodo-2-(4-methoxybenzyl)-2-azabicyclo[2.2.1]hept-5-en-3-one 

Downstream Products

• 918452-16-1 (1S,4R,6S)-6-hydroxy-2-(4-methoxybenzyl)-2-azabicyclo[2.2.1]-heptan-3-one 
• 130931-83-8 (1S,4R)-2-azabicyclo[2,2,1]hept-5-en-3-one 

Relevant academic research and scientific papers

Unexpected Retroaldol-Aldol Reaction during O-Alkylation of Hydroxylated Vince Lactam Derivatives

The unexpected retroaldol-aldol reaction during O-alkylation of a β-hydroxy lactam was found to be highly dependent on the temperature and shows a remarkable solvent effect. In DMF, O-alkylation is faster than retroaldol-aldol rearrangement giving exclusively products with retention of configuration. In THF, O-alkylation is slower than rearrangement, giving selectively products with inversion of stereochemistry. In DMSO, a retroaldol reaction followed by fast intramolecular proton transfer occurs to give the ring-opened aldehyde.

HORMONE RECEPTOR MODULATORS FOR TREATING METABOLIC MUTAGENIC AND FIBROTIC CONDITIONS AND DISORDERS

The invention relates to activators of FXR useful in the treatment of autoimmune disorders, liver disease, intestinal disease, kidney disease, cancer, and other diseases in which FXR plays a role, having the Formula (I): wherein L1, A, X1

Fluorinated conformationally restricted γ-aminobutyric acid aminotransferase inhibitors

On the basis of the structures of several potent inhibitor molecules for γ-aminobutryric acid aminotransferase (GABA-AT) that were previously reported, six modified fluorine-containing conformationally restricted analogues were designed, synthesized, and tested as GABA-AT inhibitors. The syntheses of all six molecules followed from a readily synthesized ketone intermediate. Three of the molecules were found to be irreversible inhibitors of GABA-AT with comparable or larger kinact/K1 values than that of vigabatrin, a clinically used antiepilepsy drug, and the other three were reversible inhibitors. A possible mechanism for inactivation by one of the inactivators is proposed.

Conversion of one enantiomer of the carbocyclic nucleoside synthon 2-azabicyclohept-5-en-3-one into the other

The lactam synthon 2-azabicyclohept-5-en-3-one was converted into its enantiomer by a 5-step sequence incorporating a skeletal rearrangement mediated by anchimeric assistance of the nitrogen atom; the route proceeded via a tosylate intermediate prone to racemization.