Lamivudine is a nucleoside antiviral drug. It has a strong inhibitory effect on hepatitis B virus (HBV) in vitro and in experimentally infected animals. Lamivudine can be metabolized in HBV-infected cells and normal cells to produce lamivudine triphosphate, which is the active form of lamivudine and is both an inhibitor of HBV polymerase and a substrate of this polymerase. Lamivudine triphosphate penetrates into the viral DNA chain and blocks the synthesis of viral DNA. Lamivudine triphosphate does not interfere with the metabolism of deoxynucleosides in normal cells. It has a weak inhibitory effect on mammalian DNA polymerase a and b and has almost no effect on the DNA content of mammalian cells. Lamivudine has no obvious toxicity to the structure, DNA content and function of mitochondria. The results of serum HBVDNA detection in most hepatitis B patients showed that lamivudine can rapidly inhibit HBV replication, and its inhibitory effect lasts throughout the treatment process, while reducing serum aminotransferase to normal.

Lamivudine and zidovudine are effective selective inhibitors of HIV-1 and HIV-2. The two have strong synergistic effects and can inhibit HIV replication in cell culture. Lamivudine-TP and zidovudine-TP are substrate competitive inhibitors of HIV reverse transcriptase. Their main antiviral activity is incorporation into the viral DNA chain in the form of monophosphate, resulting in the termination of the viral DNA chain. The triphosphate hydrochloride of lamivudine and zidovudine has a much lower affinity for host cell DNA polymerase than for viral DNA. Clinical trials have shown that the combined use of lamivudine and zidovudine can reduce HIV viral load and increase CD4 cell counts. Zidovudine-resistant virus strains can transform into zidovudine-sensitive strains while acquiring lamivudine resistance. In vitro experiments have confirmed that the combination of the two drugs can delay the emergence of zidovudine-resistant strains.

Zidovudine and lamivudine are effective selective inhibitors of HIV-1 and HIV-2. The two have strong synergistic effects and can inhibit HIV replication in cell culture. Zidovudine-TP and lamivudine-TP are substrate competitive inhibitors of HIV reverse transcriptase. Their main antiviral activity is incorporation into the viral DNA chain in the form of monophosphate, resulting in the termination of the viral DNA chain. In vivo experiments have shown that zidovudine has no genetic toxicity when the blood concentration reaches 40-50 times the clinical blood concentration. Zidovudine-resistant virus isolates can become zidovudine-sensitive strains when they also acquire lamivudine resistance. Clinical phenomena have shown that in vivo experiments have delayed the development of zidovudine resistance in patients who have never been treated with antiretroviral drugs by combining lamivudine and zidovudine.

In human HepG2 cells transfected with wild-type hepatitis B virus, the concentration required to inhibit 50% viral DNA synthesis (EC50) was 0.004 μM. The median EC50 for lamivudine-resistant virus strains (rtL180M, rtM204V) was 0.026 μM (range 0.01 to 0.059 μM). Co-administration with HIV nucleoside reverse transcriptase inhibitors (NRTIs) is unlikely to reduce the anti-HBV efficacy of entecavir or the anti-HIV efficacy of any of the latter drugs. Abacavir, didanosine, lamivudine, stavudine, tenofovir or zidovudine did not antagonize the anti-HBV activity of entecavir over a wide range of concentrations. When entecavir concentrations were greater than 4 times the peak in vivo concentration, there was no antagonism of the anti-HIV activity of the six NRTIs in cell culture.

Lamivudine is the 2-deoxy-3-thiocytosine left-handed enantiomer and a dideoxynucleoside analog. It is phosphorylated to form lamivudine triphosphate under the action of intracellular enzymes, which competitively inhibits HIV-1 reverse transcriptase (RT) and leads to the termination of the DNA chain. It has anti-HIV-1, HIV-2 and hepatitis B virus activity.

Tenofovir disoproxil fumarate is converted into tenofovir in the body, which is a monophosphate nucleoside (nucleotide) analog. Tenofovir is phosphorylated by intracellular enzymes to form tenofovir diphosphate, which competitively inhibits HIV-1 reverse transcriptase (RT) and leads to the termination of the DNA chain. It has anti-HIV-1, HIV-2 and hepatitis B virus activity.

Lamivudine is a nucleoside antiviral drug. It has a strong inhibitory effect on hepatitis B virus (HBV) in vitro and in experimentally infected animals. Lamivudine can be metabolized in HBV-infected cells and normal cells to produce lamivudine triphosphate, which is the active form of lamivudine and is both an inhibitor of HBV polymerase and a substrate of this polymerase. Lamivudine triphosphate penetrates into the viral DNA chain and blocks the synthesis of viral DNA. Lamivudine triphosphate does not interfere with the metabolism of deoxynucleosides in normal cells. It has a weak inhibitory effect on mammalian DNA polymerase a and b and has almost no effect on the DNA content of mammalian cells. Lamivudine has no obvious toxicity to the structure, DNA content and function of mitochondria. The results of serum HBVDNA detection in most hepatitis B patients showed that lamivudine can rapidly inhibit HBV replication, and its inhibitory effect lasts throughout the treatment process, while reducing serum aminotransferase to normal.