220349-91-7

Upstream product

• 623-73-4 diazoacetic acid ethyl ester 
• 622-97-9 1-ethenyl-4-methylbenzene 
• 20754-20-5 3-p-tolyl-acrylic acid methyl ester 
• 1866-39-3 trans-p-methylcinnamic acid 
• 72228-97-8 methyl trans-2-(p-methyphenyl)cyclopropanecarboxylate 
• 16633-44-6 (±)-trans-2-p-tolylcyclopropanecarboxylic acid 

Relevant academic research and scientific papers

C-H activation enables a rapid structure-activity relationship study of arylcyclopropyl amines for potent and selective LSD1 inhibitors

We describe the structure-activity relationship of various arylcyclopropylamines (ACPAs), which are potent LSD1 inhibitors. More than 45 ACPAs were synthesized rapidly by an unconventional method that we have recently developed, consisting of a C-H borylation and cross-coupling sequence starting from cyclopropylamine. We also generated NCD38 derivatives, which are known as LSD1 selective inhibitors, and discovered a more effective inhibitor compared to the original NCD38.

Exploring distal regions of the A3 adenosine receptor binding site: Sterically constrained N6-(2-phenylethyl)adenosine derivatives as potent ligands

We synthesized phenyl ring-substituted analogues of N6-(1S,2R)- (2-phenyl-1-cyclopropyl)adenosine, which is highly potent in binding to the human A3AR with a Ki value of 0.63nM. The effects of these structural changes on affinity at human and rat adenosine receptors and on intrinsic efficacy at the hA3AR were measured. A 3-nitrophenyl analogue was resolved chromatographically into pure diastereomers, which displayed 10-fold stereoselectivity in A3AR binding in favor of the 1S,2R isomer. A molecular model defined a hydrophobic region (Phe168) in the putative A3AR binding site around the phenyl moiety. A heteroaromatic group (3-thienyl) could substitute for the phenyl moiety with retention of high affinity of A3AR binding. Other related N6-substituted adenosine derivatives were included for comparison. Although the N 6-(2-phenyl-1-cyclopropyl) derivatives were full A3AR agonists, several other derivatives had greatly reduced efficacy. N 6-Cyclopropyladenosine was an A3AR antagonist, and adding either one or two phenyl rings at the 2-position of the cyclopropyl moiety restored efficacy. N6-(2,2-Diphenylethyl)adenosine was an A 3AR antagonist, and either adding a bond between the two phenyl rings (N6-9-fluorenylmethyl) or shortening the ethyl moiety (N 6-diphenylmethyl) restored efficacy. A QSAR study of the N 6 region provided a model that was complementary to the putative A3AR binding site in a rhodopsin-based homology model. Thus, a new series of high-affinity A3AR agonists and related nucleoside antagonists was explored through both empirical and theoretical approaches.

Triazolo(4,5-d)pyrimidine compounds

Triazolo[4,5-d]pyrimidine compounds are provided of the formula (I) wherein R1, R2, R3, R4, R5and R6are as defined in the specification. Compositions containing the compounds are also provided, together with processes for their preparation and methods of use in the treatment of diseases, including myocardial infarction and unstable angina.