Interferon alfa

Interferon alfa
Interferon alfa
Clinical data
AHFS/Drugs.com International Drug Names
Pregnancy cat. C(US)
Legal status  ?
Routes Subcutaneous, intramuscular
Identifiers
ATC code L03AB01
Chemical data
Formula  ?
 N(what is this?)  alfa (verify)

Interferon alfa (INN, or HuIFN-alpha-Le, trade name Multiferon) is a natural interferon alpha (IFN-α) which is obtained from the leukocyte fraction of human blood following induction with Sendai virus. Interferon alfa contains several naturally occurring IFN-α subtypes and is purified by affinity chromatography.

Contents

Composition

Interferon alfa contains a mixture of several proteins all with structural, serological and functional properties typical for natural interferon alpha (IFN α). The major subtypes identified are: IFN-α1 -α2, -α8, -α10, -α14 and -α21; IFN-α2 and IFN-α14 are glycosylated. The IFN-α content is expressed in international units per ml and the drug product is formulated in isotonic phosphate buffer solution (pH 7.2) supplemented with human albumin, 1.5 mg/ml. The albumin used is a medicinal product, which is approved in several countries, indicated for subcutane injection therapy.

Pharmacology

Summary of differences between IFN subtypes

IFN-α8 enhances the proliferation of human B cells as well as being able to activate natural killer NK cells.

The subtypes α10 and α2 along with α8 are the best NK cell activators.

Subtypes α21 and α2 enhance the expression of IFN-gamma-inducible protein-10 (IP-10) in dendritic cells. Activated dendritic cells initiate immune responses and the expression of IP-10, a chemokine which promotes a Th1 inflammatory response.

IFN-α1 causes increased HLA-II expression and can directly inhibit tumour cell growth in vitro, but is a poor activator of NK cells, has poor anti-viral activity, does not induce B cell proliferation and does not enhance HLA-I or tumour antigen expression. Despite its apparent inactivity, it is used clinically in the treatment of metastatic renal carcinoma, with a reported lower toxicity than the recombinant IFN-α2.

Overall, IFN-α has a general inflammatory action which skews the immune response towards a Th1 profile.

Subtype α2 increased the expression of HLA-I molecules which correlate with IFN-α mediated activation of memory CD8 cells and increased cytolytic action against virally infected cells and tumour cells via cytotoxic CD8 cells.

References