EGYFERON 5 M.I.U. VIAL

INDICATION FOR THE TREATMENT OF HAIRY CELL LEUKEMIA MALIGNANT MELANOMA AND AIDS-RELATED KAPOSI S SARCOMA. PHARMACODYNAMICS 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)