25960-41-2

Upstream product

• 2657-25-2 4'-hydroxychalcone 
• 869-24-9 2-chloro-N,N-diethylethylamine hydrochloride 
• 1195876-29-9 (E)-1-(4-(2-bromoethyloxy)phenyl)-3-phenylprop-2-en-1-one 
• 109-89-7 diethylamine 
• 2657-25-2 (E)-1-(4-hydroxyphenyl)-3-phenylprop-2-en-1-one 
• 100-52-7 benzaldehyde 
• 99-93-4 4-Hydroxyacetophenone 

Downstream Products

• 5679-53-8 1-[4-(2-diethylamino-ethoxy)-phenyl]-3-phenyl-propan-1-ol 
• 113181-57-0 1-[4-(2-diethylamino-ethoxy)-phenyl]-3-phenyl-butan-1-one 
• 74631-85-9 1-[4-(2-diethylamino-ethoxy)-phenyl]-3-phenyl-pentan-1-one 

Relevant academic research and scientific papers

Design and synthesis of new bioisosteres of spirooxindoles (MI-63/219) as anti-breast cancer agents

We report herein the design and synthesis of bioisosteres of spirooxindole (MI-63/219), a small-molecule inhibitors of the MDM2-p53 interaction as anti-breast cancer agents. Compound 5b has been exhibiting significant anti-proliferative activity in nude mice bearing MCF-7 xenograft tumor. The compound 5b was found to act via modulation of MDM2 and p53 expression in breast cancer cells expressing wild type p53. Compound 5b stimulated p53 activation, caused modulation of downstream effectors p21, pRb, and cyclin D1 which regulate cell cycle. Thus, compound triggered G1-S phase cell cycle arrest, which was evident by flow cytometric analysis of treated breast cancer cells. Thus, compound 5b restores the p53 function, which triggers molecular events consistent with cell cycle arrest at G1/S phase.

Design, synthesis and pharmacological evaluation of chalcone derivatives as acetylcholinesterase inhibitors

A novel series of chalcone derivatives (4a-8d) were designed, synthesized, and evaluated for the inhibition activity against acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The log P values of the compounds were shown to range from 1.49 to 2.19, which suggested that they were possible to pass blood brain barriers in vivo. The most promising compound 4a (IC50: 4.68 μmol/L) was 2-fold more potent than Rivastigmine against AChE (IC50: 10.54 μmol/L) and showed a high selectivity for AChE over BuChE (ratio: 4.35). Enzyme kinetic study suggested that the inhibition mechanism of compound 4a was a mixed-type inhibition. Meanwhile, the result of molecular docking showed its potent inhibition of AChE and high selectivity for AChE over BuChE.