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indicationFor the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age.
pharmacologyUpregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R.
mechanism of actionInterferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.
absorptionFollowing a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life (t½ ka) was 4.6 hours.
half lifeThe mean elimination half-life is approximately 40 hours (range 22 to 60 hours) in patients with HCV infection.
route of eliminationRenal elimination accounts for 30% of the clearance.
drug interactionsAminophylline: Interferon increases the effect and toxicity of theophylline
Dyphylline: Interferon increases the effect and toxicity of theophylline
Oxtriphylline: Interferon increases the effect and toxicity of theophylline
Theophylline: Interferon increases the effect and toxicity of theophylline