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BVM: A Promising Agent for Future HIV-1 Treatment

Alex Joseph, Suthar Sharad Kumar, Sandeep Lohan, Abhishek Mathur, Srinivasan K.K, Angel Treasa Thomas


More than 20 individual and fixed-dose combinations of anti-HIV drugs are available for the treatment of human immunodeficiency virus (HIV) infection. However, owing to the development of viral-drug resistance and adverse effects associated with currently available drug therapy regimen there is a continuous need to explore new drug candidates. BVM is the first in class of maturation inhibitors, which inhibits HIV-1 maturation by blocking a late step in the Gag processing pathway specifically the cleavage of SP1 from the C terminus of capsid (CA). BVM has a side chain at position 3 of betulinic acid. It is well absorbed after oral administration and a long half-life indicating once daily dosing. Metabolism of BVM takes place predominantly by glucuronidation via uridine diphosphate glucuronosyltransferases (UGTs). Elimination of bevirimat is primarily by hepatic glucuronidation and hepatobiliary excretion. Single amino acid substitution at or near the CA-SP1 cleavage site confers resistance to BVM, which is not a known target for resistance to existing antiretroviral drugs. Encouraging results obtained in preclinical and limited clinical trials indicates that BVM is promising agent for the future HIV-1 treatment, henceforth needs further investigations in humans.


BVM, HIV-1, Maturation inhibitors, Glucuronidation, CA-SP1 cleavage

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