| Indication |
For the treatment of HIV infection and chronic hepatitis B (HBV). |
| Pharmacodynamics |
Lamivudine is a nucleoside reverse transcriptase inhibitor
(NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1)
and hepatitis B (HBV). Lamivudine is phosphorylated to active
metabolites that compete for incorporation into viral DNA. They inhibit
the HIV reverse transcriptase enzyme competitively and act as a chain
terminator of DNA synthesis. The lack of a 3'-OH group in the
incorporated nucleoside analogue prevents the formation of the 5' to 3'
phosphodiester linkage essential for DNA chain elongation, and
therefore, the viral DNA growth is terminated. |
| Mechanism of action |
Lamivudine is a synthetic nucleoside analogue and is
phosphorylated intracellularly to its active 5'-triphosphate metabolite,
lamivudine triphosphate (L-TP). This nucleoside analogue is
incorporated into viral DNA by HIV reverse transcriptase and HBV
polymerase, resulting in DNA chain termination. |
| Absorption |
Lamivudine was rapidly absorbed after oral administration in
HIV-infected patients. Absolute bioavailability in adults is 86% ± 16%
for the tablet and 87% ± 13% for the oral solution. |
| Volume of distribution |
Not Available |
| Protein binding |
36% |
| Metabolism |
The only detected metabolite of lamivudine is trans-sulfoxide. |
| Route of elimination |
The primary routes of elimination of abacavir are metabolism by
alcohol dehydrogenase to form the 5′-carboxylic acid and glucuronyl
transferase to form the 5′-glucuronide. Lamivudine is excreted in human
breast milk and into the milk of lactating rats. |
| Half life |
5 to 7 hours |
| Clearance |
- Renal cl=280.4 +/- 75.2 mL/min [HIV-infected patients given a single IV doses ranging from 0.25 to 8 mg/kg]
|
| Toxicity |
Not Available |
