Clevudine for hepatitis B
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Anderson, D.L. [1]
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[1] Medical Information Department, Prous Science, Provença 388, 08025 Barcelona, Spain
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- Localización: Medicamentos de actualidad = Drugs of today, ISSN 1699-3993, Vol. 45, Nº. 5, 2009, págs. 331-350
- Idioma: inglés
- Texto completo no disponible (Saber más ...)
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Resumen
Clevudine is distinguished from other oral agents by its sustained suppression of HBV DNA for several months after cessation of therapy, according to a comprehensive review of hepatitis B in the 2 October 2008 issue of the New England Journal of Medicine (1). Clevudine is differentiated by i) an unusual activation pathway to the biochemically active triphosphate; ii) a mechanism of action of clevudine triphosphate that inhibits multiple steps of the hepatitis B virus (HBV) intracellular life cycle; iii) a long half-life and iv) significant reduction of covalently closed circular DNA (cccDNA) in animal models. Clevudine was approved and is marketed in South Korea based on two 24-week phase III trials vs. placebo. In these studies with treatment-naïve patients, 59% of 248 HBeAg-positive patients had undetectable HBV DNA after 24 weeks of treatment compared with 92% of 89 HBeAg-negative patients, while the percentage of patients with normal liver enzymes was 68% in the HBeAg-positive patients and 75% in the HBeAg-negative patients (all statistically significant versus placebo). Follow-up studies include trials vs. lamivudine as well as a phase IV study of long-term clevudine. Larger and longer phase III trials in the United States, European Union, Asia and South America of clevudine vs. adefovir are ongoing. An ANRS-sponsored trial of clevudine vs. tenofovir vs. the combination of the two agents is poised to begin (2-4). Literature published through November 2008 and presentations from the 59th annual meeting of the American Association for the Study of Liver Diseases held 31 October to 4 November 2008 are included (5-7).
