Chemical structure of lamivudine.
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Lamivudine

Lamivudine (2',3'-dideoxy-3'-thiacytidine, 3TC) has the trade name EpivirĀ®. It is a potent reverse transcriptase inhibitor of the class nucleoside analog reverse transcriptase inhibitor (NARTI). more...

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Lamivudine has been used for treatment of chronic hepatitis B at a lower dose than for treatment of HIV. It improves the seroconversion of e-antigen positive hepatitis B and also improves histology staging of the liver. Long term use of lamivudine unfortunately leads to emergence of a resistant hepatitis B virus (YMDD) mutant. Despite this, lamivudine is still used widely as it is well tolerated.

History

Lamivudine was invented by Bernard Belleau and Nghe Nguyen-Ba at the Montreal-based IAF BioChem International, Inc. laboratories in 1989. The drug was later licensed to the British pharmaceutical company Glaxo for a 14 percent royalty.

Lamivudine was approved by the Food and Drug Administration (FDA) on Nov 17, 1995 for use with Zidovudine (AZT) and again in 2002 as a once-a-day dosed medication. The fifth antiretroviral drug on the market, it was the last NRTI for three years while the approval process switched to protease inhibitors. Its patent will expire in the United States on 2016-05-18.

Mechanism of action

Lamivudine is an analogue of cytidine. It can inhibit both types (1 and 2) of HIV reverse transcriptase and also the reverse transcriptase of hepatitis B. It needs to be phosphorylated to its triphosphate form before it is active. 3TC-triphosphate also inhibits cellular DNA polymerase.

Lamivudine is administered orally, and it is rapidly absorbed with a bio-availability of over 80%. Some research suggests that lamivudine can cross the blood-brain barrier. Lamivudine is often given in combination with zidovudine, with which it is highly synergistic. Lamivudine treatment has been shown to restore zidovudine sensitivity of previously resistant HIV. Several mutagenicity tests show that lamivudine should not show mutagenic activity in therapeutical doses.


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Treatment of chronic hepatitis B infection
From American Family Physician, 10/15/05 by Anne D. Walling

Chronic hepatitis B infection can lead to cirrhosis, hepatic failure, and hepatocellular carcinoma. Current therapies are successful in a minority of patients. Approximately 19 percent of patients respond to interferon alfa, and 10 to 15 percent respond to lamivudine (Epivir). The long-term efficacy of current agents may be worse. For lamivudine, viral resistance is reported in more than one half of patients within three years. Janssen and colleagues reasoned that the combination of interferon alfa and lamivudine in a long-term treatment regimen could improve sustained response rates in chronic hepatitis B infection.

The authors conducted a randomized, double-blind controlled trial at 42 centers in 15 countries to compare the safety and effectiveness of interferon alfa monotherapy with combination therapy using interferon alfa plus lamivudine. Participants were at least 16 years of age and had been positive for hepatitis B surface antigen for at least six months. In the eight weeks before randomization, participants were required to be positive for hepatitis B e antigen (HBeAg) on at least two occasions and to have two documented measurements of alanine transaminase levels that were at least twice the upper limit of the normal range. Patients were excluded from the study if they had antibodies against hepatitis C or D viruses or if they were positive for human immunodeficiency virus. Patients with a history of antiviral or immunosuppressive therapy within the previous six months; pregnancy or inadequate contraception in women; substance abuse; liver, thyroid, psychiatric, or serious medical conditions; and inadequate leucocyte, granulocyte, or platelet counts also were excluded. After screening, patients were randomly assigned to therapy with 100 mcg pegylated interferon alfa-2b once per week plus 100 mg lamivudine (combination therapy), or to monotherapy using 100 mcg pegylated alfa-2b weekly plus a daily placebo. After 32 weeks, the interferon dose in both groups was lowered to 50 mcg per week. Patients were monitored at outpatient clinics every four weeks during the 52 weeks of the study and for 26 weeks after treatment. In addition to monitoring of laboratory markers and reported adverse effects, participants underwent liver biopsy at the beginning of the study and were offered repeat biopsy after treatment.

Of the 307 patients randomized, 266 (87 percent) were included in the analysis. Reasons for exclusion included nonadherence with medication or follow-up visits, clearance of HBeAg before starting therapy, and problems in data verification from one study center. The patients in the two treatment groups were comparable at recruitment and at conclusion of the study. By the end of the 52 weeks, significantly more patients using combination therapy responded with loss of HBeAg (44 percent compared with 29 percent). However, by the end of the follow-up period (at 78 weeks), 35 percent of the combination therapy group and 36 percent of the monotherapy group had sustained response. This pattern was shown in two other markers of hepatitis B infection. Fibrosis scores improved in 33 percent of the 52 combination therapy patients who agreed to two biopsies, compared with 22 percent of the 58 patients assigned to monotherapy. Biopsies revealed deteriorating fibrosis scores in 38 percent of available patients in both treatment groups. Regardless of treatment group, the sustained response rate was significantly influenced by the hepatitis B virus genotype. For genotypes A and B, the sustained response rates were 47 and 44 percent, respectively. For genotypes C and D, the comparable rates were 28 and 25 percent. Side effects were common, especially influenza-like syndrome, which affected 62 to 74 percent of patients. Thirty-two serious adverse effects were reported, of which one half were attributed to therapy. Despite adverse effects, 91 percent of patients remained on therapy after the study.

The authors conclude that combination therapy was superior to monotherapy over 52 weeks, but this advantage was not sustained during follow-up. They emphasize that long-term use of lamivudine is contraindicated because of drug resistance, and that the virus genotype is a key predictor of response to antiviral therapy.

ANNE D. WALLING, M.D. Janssen HLA, et al. Pegylated interferon alfa-2b alone or in combination with lamivudine for HBeAg-positive chronic hepatitis B: a randomised trial. Lancet January 8, 2005;365:123-9.

COPYRIGHT 2005 American Academy of Family Physicians
COPYRIGHT 2005 Gale Group

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