Interferon-beta: mechanism of action and dosing issues.
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Markowitz CE
Interferon-beta: mechanism of action and dosing issues.
Neurology. 2007 Jun 12;68(24 Suppl 4):S8-11. doi: 10.1212/01.wnl.0000277703.74115.d2.
- PubMed ID
- 17562848 [ View in PubMed]
- Abstract
In patients with multiple sclerosis (MS), activation of immune cells and breakdown of the blood-brain barrier (BBB) lead to demyelination and axon injury. Although repairing damage to neurons is not possible, immunomodulating therapies can reduce the inflammatory processes that lead to demyelination. Interferon-beta (IFN-beta) is a polypeptide, normally produced by fibroblasts, that has antiviral and antiproliferative effects. Binding of IFN-beta to its receptor induces a complex transcriptional response. In immune cells (the most likely target of IFN-beta's therapeutic effect in MS), IFN-beta reduces antigen presentation and T-cell proliferation, alters cytokine and matrix metalloproteinase (MMP) expression, and restores suppressor function. Therapeutic forms of IFN-beta can be produced in bacterial expression systems (IFN-beta1b) or in mammalian cells (IFN-beta1a). These forms have some differences in their amino acid sequence and posttranslational modifications, but the transcriptional response to IFN- beta1b and IFN-beta1a appears to be similar, if not indistinguishable. However, the biological response and the clinical effect do vary with changes in the dosing frequency of IFN-beta. In clinical trials, IFN-beta1a IM administered weekly elicits a transient biological response compared to IFN-beta1b administered SC every other day or IFN-beta1a (administered SC three times per week). Comparative clinical trials suggest that the differences in the biological response are clinically meaningful: more frequent IFN-beta administration produces superior clinical responses.
DrugBank Data that Cites this Article
- Drugs
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Human interferon beta Interferon alpha/beta receptor 1 Protein Humans YesBinderDetails