942045-32-1

Upstream product

• 371-40-4 4-fluoroaniline 

Downstream Products

• 1279692-10-2 (E)-N-(4-fluorophenyl)-4-morpholino-6-[2-(naphthalen-2-ylmethylene)hydrazinyl]-1,3,5-triazin-2-amine 
• 1454695-05-6 C₂₆H₂₈ClFN₈O 
• 1454694-94-0 C₂₅H₂₆ClFN₈O 
• 1454694-90-6 C₂₄H₂₄ClFN₈O 
• 1279692-09-9 (E)-N-(4-fluorophenyl)-4-morpholino-6-[2-(naphthalen-1-ylmethylene)hydrazinyl]-1,3,5-triazin-2-amine 
• 330569-41-0 (4-fluorophenyl)-(4-hydrazino-6-morpholin-4-yl-[1,3,5]triazin-2-yl)amine 

Relevant academic research and scientific papers

Toward the Discovery of Novel Anti-HIV Drugs. Second-Generation Inhibitors of the Cellular ATPase DDX3 with Improved Anti-HIV Activity: Synthesis, Structure-Activity Relationship Analysis, Cytotoxicity Studies, and Target Validation

A hit optimization protocol applied to the first nonnucleoside inhibitor of the ATPase activity of human DEAD-box RNA helicase DDX3 led to the design and synthesis of second-generation rhodanine derivatives with better inhibitory activity toward cellular DDX3 and HIV-1 replication. Additional DDX3 inhibitors were identified among triazine compounds. Biological data were rationalized in terms of structure-activity relationships and docking simulations. Antiviral activity and cytotoxicity of selected DDX3 inhibitors are reported and discussed. A thorough analysis confirmed human DDX3 as a valid anti-HIV target. The compounds described herein represent a significant advance in the pursuit of novel drugs that target HIV-1 host cofactors.

Design and development of novel thiazolidin-4-one-1,3,5-triazine derivatives as neuro-protective agent against cerebral ischemia–reperfusion injury in mice via attenuation of NF-?B

The present study enumerates the discovery and development of novel thiazolidin-4-one-1,3,5-triazine as neuro-protective agent against cerebral ischemia–reperfusion injury in mice. These compounds showed significant inhibition of NF-?B transcriptional activity in LPS-stimulated RAW264.7 cells, displaying compound 8k as most potent inhibitor among the tested derivative. The compound 8k was further studied in in vivo middle cerebral artery occlusion (MCAO) mice model for neuro-protective action. Results suggest that compound 8k causes attenuation of inflammation (TNF-α, IL-β, and IL-6), oxidative stress (SOD, GSH, and MDA), and apoptosis (Bcl-2, Bax, and cleaved caspase-3) in MCAO mice in concentration-dependent manner. Collectively, our results documented that compound 8k pre-treatment protects cerebral I/R. This novel lead scaffold may be helpful for investigation of new neuro-protective agent by inactivation of NF-?B.