1394157-98-2

Basic information

• Product Name: C₄₉H₇₅NO₅
• Synonyms: C₄₉H₇₅NO₅
• CAS NO: 1394157-98-2
• Molecular Weight: 758.138
• Mol File: 1394157-98-2.mol

Chemical Properties

• CAS DataBase Reference: C₄₉H₇₅NO₅(CAS DataBase Reference)
• NIST Chemistry Reference: C₄₉H₇₅NO₅(1394157-98-2)
• EPA Substance Registry System: C₄₉H₇₅NO₅(1394157-98-2)

Safety Data

• Hazardous Substances Data: 1394157-98-2(Hazardous Substances Data)

Upstream product

• 10376-50-8 3-O-acetylbetulinic acid 
• 1394158-05-4 benzyl 9-amino nonanoate 
• 59868-82-5 3-O-acetylbetulinic acid chloride 

Relevant articles and documents

Synthesis of betulinic acid derivatives as entry inhibitors against HIV-1 and bevirimat-resistant HIV-1 variants

Betulinic acid derivatives modified at the C28 position are HIV-1entry inhibitors such as compound A43D; however, modified at the C3 position instead of C28 give HIV-1 maturation inhibitor such as bevirimat. Bevirimat exhibited promising pharmacokinetic profiles in clinical trials, but its effectiveness was compromised by the high baseline drug resistance of HIV-1 variants with polymorphism in the putative drug binding site. In an effort to determine whether the viruses with bevirimat resistant polymorphism also altered their sensitivities to the betulinic acid derivatives that inhibit HIV-1 entry, a series of new betulinic acid entry inhibitors were synthesized and tested for their activities against HIV-1 NL4-3 and NL4-3 variants resistant to bevirimat. The results show that the bevirimat resistant viruses were approximately 5- to10-fold more sensitive to three new glutamine ester derivatives (13, 15 and 38) and A43D in an HIV-1 multi-cycle replication assay. In contrast, the wild type NL4-3 and the bevirimat resistant variants were equally sensitive to the HIV-1 RT inhibitor AZT. In addition, these three new compounds markedly improved microsomal stability compared to A43D.

New betulinic acid derivatives for bevirimat-resistant human immunodeficiency virus type-1

Bevirimat (1, BVM) is an anti-HIV agent that blocks HIV-1 replication by interfering with HIV-1 Gag-SP1 processing at a late stage of viral maturation. However, clinical trials of 1 have revealed a high baseline drug resistance that is attributed to naturally occurring polymorphisms in HIV-1 Gag. To overcome the drug resistance, 28 new derivatives of 1 were synthesized and tested against compound 1-resistant (BVM-R) HIV-1 variants. Among them, compound 6 exhibited much improved activity against several HIV-1 strains carrying BVM-R polymorphisms. Compound 6 was at least 20-fold more potent than 1 against the replication of NL4-3/V370A, which carries the most prevalent clinical BVM-R polymorphism in HIV-1 Gag-SP1. Thus, compound 6 merits further development as a potential anti-AIDS clinical trial candidate.