indication

For treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma.

pharmacology

Upregulates 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 action

Interferon 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.

half life

Terminal half life is 80 hours (range 50 to 140 hours).

drug interactions

Aminophylline: 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

Telbivudine: Co-administration of Peginterferon alpha-2a and Telbivudine may increase the risk of serious peripheral neuropathy.

Theophylline: Interferon increases the effect and toxicity of theophylline