204125-01-9

Upstream product

• 204124-97-0 7-trichloroacetylbaccatin III 

Downstream Products

• 261728-77-2 7-trichloroacetyl-3'-debenzoylpaclitaxel 
• 502626-35-9 C₅₁H₆₂Cl₃NO₁₅ 
• 502626-31-5 C₅₀H₅₈Cl₃NO₁₅ 
• 502626-32-6 C₅₀H₆₀Cl₃NO₁₅ 
• 502626-33-7 C₅₀H₅₈Cl₃NO₁₅ 
• 502626-34-8 C₅₁H₅₀Cl₃NO₁₅ 
• 502626-29-1 C₄₉H₅₈Cl₃NO₁₅ 
• 502626-30-4 C₅₀H₅₆Cl₃NO₁₅ 
• 502626-26-8 C₄₈H₅₄Cl₃NO₁₅ 
• 502626-23-5 C₄₇H₅₂Cl₃NO₁₅ 
• 502626-21-3 C₄₇H₅₂Cl₃NO₁₅ 
• 502626-17-7 C₄₆H₅₀Cl₃NO₁₅ 
• 502626-19-9 C₄₆H₅₀Cl₃NO₁₅ 
• 502626-20-2 C₄₆H₄₈Cl₃NO₁₅ 

Relevant academic research and scientific papers

Synthesis and biology of 3'-N-acyl-N-debenzoylpaclitaxel analogues

The 3'-N-acyl-N-debenzoylpaclitaxel analogues 1a-d were synthesized and evaluated on biological systems. Some of the analogues 1a-d exhibited higher cytotoxicities (up to 20-fold) and stronger abilities to induce apoptosis than paclitaxel. In an in vivo experiment against ip implanted B16 melanoma, the most cytotoxic compound 1b in vitro caused tumor growth inhibition more than paclitaxel.

Structure-activity relationship study at the 3'-N-position of paclitaxel: synthesis and biological evaluation of 3'-N-acyl-paclitaxel analogues.

A series of 3'-N-acyl-paclitaxel analogues 1a-v were synthesized and their cytotoxicities in vitro against several human tumor cell lines examined. It has been shown that distinct correlation between activity and N-acyl-substituent. The appropriate size of N-acyl group was indispensable for cytotoxicity, and moreover, the presence of beta-substituted conjugated double and triple bond to N-carbonyl generally resulted in increase of cytotoxicities.