24386-91-2

Upstream product

• 291535-38-1 4-chloro-5-iodo-7-[5-O-[(1,1-dimethylethyl)dimethysilyl]-2,3-O-(1-methylethylidene)-β-D-ribofuranosyl]-7H-pyrrolo[2,3-d]pyrimidine 

Downstream Products

• 24386-93-4 5-iodotubercidin 
• 1039752-81-2 4-benzylthio-5-iodo-7-(β-D-ribofuranosyl)pyrrolo[2,3-d]pyrimidine 

Relevant academic research and scientific papers

TRICYCLIC-NUCLEOSIDE COMPOUNDS FOR TREATING VIRAL INFECTIONS

Disclosed are tricyclic nucleoside compounds of formula (I), and methods thereof for treating viral infections mediated at least in part by a Flaviviridae family virus.

Structure-activity relationships of 7-deaza-6-benzylthioinosine analogues as ligands of Toxoplasma gondii adenosine kinase

Several 7-deaza-6-benzylthioinosine analogues with varied substituents on aromatic ring were synthesized and evaluated against Toxoplasma gondii adenosine kinase (EC.2.7.1.20). Structure-activity relationships indicated that the nitrogen atom at the 7-position does not appear to be a critical structural requirement. Molecular modeling reveals that the 7-deazapurine motif provided flexibility to the 6-benzylthio group as a result of the absence of H-bonding between N7 and Thr140. This flexibility allowed better fitting of the 6-benzylthio group into the hydrophobic pocket of the enzyme at the 6-position. In general, single substitutions at the para or meta position enhanced binding. On the other hand, single substitutions at the ortho position led to the loss of binding affinity. The most potent compounds, 7-deaza-p-cyano-6- benzylthioinosine (IC50 = 5.3 μM) and 7-deaza-p-methoxy-6- benzylthioinosine (IC50 = 4.6 μM), were evaluated in cell culture to delineate their selective toxicity.

Nucleoside compounds for treating viral infections

Disclosed are compounds, compositions and methods for treating viral infections caused by a Flaviviridae family virus, such as hepatitis C virus.

Study on the synthesis and PKA-I binding activities of 5-alkynyl tubercidin analogues

5-Alkynyl tubercidin analogues were synthesized and their biologica activities were evaluated. It was found that protein kinase A could be activated by 5-alkynyl tubercidin (9a) and cAMP- binding ability to PKA-I was selectively inhibited by it. Molecular

Adenosine kinase inhibitors. 1. Synthesis, enzyme inhibition, and antiseizure activity of 5-iodotubercidin analogues

Adenosine receptor agonists produce a wide variety of therapeutically useful pharmacologies. However, to date they have failed to undergo successful clinical development due to dose-limiting side effects. Adenosine kinase inhibitors (AKIs) represent an alternative strategy, since AKIs may raise local adenosine levels in a more site- and event-specific manner and thereby elicit the desired pharmacology with a greater therapeutic window. Starting with 5-iodotubercidin (IC50 = 0.026 μM) and 5'-amino-5'- deoxyadenosine (IC50 = 0.17 μM) as lead inhibitors of the isolated human AK, a variety of pyrrolo[2,3-d]pyrimidine nucleoside analogues were designed and prepared by coupling 5-substituted-4-chloropyrrolo[2,3-d]pyrimidine bases with ribose analogues using the sodium salt-mediated glycosylation procedure. 5'-Amino-5'-deoxy analogues of 5-bromo- and 5-iodotubercidins were found to be the most potent AKIs reported to date (IC50s 0.001 μM). Several potent AKIs were shown to exhibit anticonvulsant activity in the rat maximal electric shock (MES) induced seizure assay.