Interferon beta-1b

Summary

Interferon beta-1b is a recombinant, non-glycosylated form of human interferon-β produced in E. coli, differing from the native protein by substitution of serine for cysteine at position 17. It is approved for the treatment of relapsing forms of multiple sclerosis (MS) to reduce the frequency of clinical exacerbations and delay physical disability. It was the first disease-modifying therapy approved for MS in the United States (1993).

Mechanism of Action

Binds to the type I interferon receptor (IFNAR1/IFNAR2) on cell surfaces, activating the JAK-STAT signaling pathway (JAK1/TYK2 → STAT1/STAT2), leading to expression of interferon-stimulated genes. In multiple sclerosis, reduces T-cell activation, inhibits lymphocyte migration across the blood-brain barrier by downregulating matrix metalloproteinases and adhesion molecules, shifts cytokine balance toward anti-inflammatory profiles, and reduces MRI lesion activity.

Routes of Administration

Goals & Uses

• Clinically isolated syndrome (CIS) — delay to definite MSNeurological / PreventiveHigh
• Reduction of MRI lesion burden in MSNeurological / Imaging BiomarkerHigh
• Delay of disability progression in MSNeurological / AutoimmuneHigh
• Treatment of secondary progressive MSNeurological / Disease ModificationModerate
• Reduction of relapse rate in relapsing-remitting MSNeurological / ImmunomodulationHigh

Contraindications

• Current severe depression or suicidal ideationPsychiatricHigh
• PregnancyPopulationHighPotential fetal risk or insufficient safety data
• Severe hepatic impairment or decompensated liver diseaseHepaticHigh
• Hypersensitivity to natural or recombinant interferon-β or human albuminAllergy / ImmunologicHigh

Adverse Effects

• Hepatotoxicity / elevated liver enzymesHepaticCommon
• Injection site reactions (pain, erythema, necrosis)Local / DermatologicCommon
• Flu-like symptoms (fever, chills, myalgia, malaise)Systemic / ImmunologicCommon
• LymphopeniaHematologicCommon
• Depression and suicidal ideationPsychiatricUncommon
• Neutralizing antibodies (NAbs)ImmunologicalCommon

Drug Interactions

• Antidepressants (e.g., SSRIs)Low
• CYP450 substrates (e.g., warfarin, phenytoin)Moderate
• Hepatotoxic drugs (e.g., isoniazid, valproate, statins)Moderate
• Myelosuppressive agents (e.g., azathioprine, methotrexate)Moderate

Population Constraints

• Pediatric patients (<18 years)AgeRelative
• Patients with epilepsyNeurologicalRelative
• Patients with thyroid disordersEndocrineRelative
• Patients with pre-existing depression or psychiatric disordersPsychiatricRelative
• Pregnant womenReproductiveRelative

Regulatory Status

• European UnionApprovedApproved: Relapsing-remitting multiple sclerosis, Secondary progressive multiple sclerosis with active disease, Clinically isolated syndrome (CIS)Betaferon (Bayer) approved by EMA; also available as Extavia. Broader label includes SPMS with relapses.
• United StatesApprovedApproved: Relapsing forms of multiple sclerosis (RRMS, active SPMS, CIS)FDA-approved 1993 (Betaseron); Extavia approved 2009. First disease-modifying therapy for MS in the US.
• United KingdomApprovedApproved: Relapsing-remitting multiple sclerosis, Secondary progressive multiple sclerosis with active disease, Clinically isolated syndromeApproved by MHRA post-Brexit under Betaferon and Extavia brand names. Consistent with EMA indications.

First MS disease-modifying therapy approved by the FDA (August 1993). Approved in the EU and other major jurisdictions. Betaseron and Extavia are FDA-approved brand names; Betaferon is the EU/UK brand name (Bayer). Extavia (Novartis) was approved as an additional brand in the US in 2009.

Evidence & Sources

No sources recorded yet.