Lamivudine

Lamivudine’s anti- HBV activity, like its anti-HIV activity, has been shown to depend on the ability of LMV-TP to serve as both substrate and inhibitor of the DNA- and RNA-dependent polymerase activities of the HBV P gene product. Lamivudine owes its activity to the remarkably broad substrate specificity of deoxycytidine kinase and the unusual substrate preference of the HBV polymerases for dNTPs with the unnatural L-conformation, whereas the anti-HBV activity of PCV appears to depend on several factors including optimal phosphorylation (sufficient for antiviral activity but not cytotoxicity) by key cellular enzymes, the long intracellular half-life of PCV-TP and the ability of PCV-TP to inhibit the HBV RT priming reaction as well as RT and DNA polymerase activity. ^[1]

Lamivudine and Penciclovir inhibits duck hepatitis B virus (DHBV) replication to a comparable extent when used alone, and in combination, the two nucleoside analogs acts synergistically over a wide range of clinically relevant concentrations. Lamivudine combined with Penciclovir is more effective in reducing the normally recalcitrant viral covalently closed circular (CCC) DNA form of DHBV than either drug alone. ^[2]

Lamivudine inhibits p24 antigen production by HIV-I in PBMC, with ED50s ranging from 0.07 μM to 0.2 μM. ^[3]

• Cell lines

  Neonatal rat ventricular cardiomyocytes

• Concentrations

  5 μM

• Incubation Time

  24 h

• Method

  Cells were treated with indicated concentrations of drug for 24 h.