Interferon beta 1b

K K Jain MD†

Neuropharmacology & Neurotherapeutics

Updated 09.12.2021
Released 12.19.2002
Expires For CME 09.12.2024

Interferon beta 1b

Author: K K Jain MD†

See Contributor Disclosures

Interferon beta 1b

In This Article

Quick Link

Introduction

Historical note and terminology

Interferons are glycoproteins secreted in the body in response to viral infections and are presumed to provide protection to other cells against viral infection. The name derives from the term "viral interference" used in the first description of these proteins by their discoverers (18). In addition to the antiviral properties, immunomodulatory and antineoplastic properties of interferons were discovered later (05). Use of interferons in multiple sclerosis was based on the belief that the disease may be due to a latent virus infection of the brain in persons with impairment of the immune system (07). Trials with interferon have been conducted in various diseases of the nervous system including multiple sclerosis (11). Two types of interferons have been identified: type 1 (interferon alpha and interferon beta) and type 2 (interferon gamma). Type 2 is synthesized mainly by lymphocytes and type 1 beta by fibroblasts, but both have a similar amino acid composition and genetic coding. Gamma interferon differs from type 1 interferons by its amino acid composition and cell surface receptor. Interferon alpha has been developed mostly for applications in virology and oncology. Interferon beta has a beneficial effect on the course of multiple sclerosis, and interferon alpha has an equivocal effect, whereas interferon gamma exacerbated the disease. Reasons for these varying effects are not well understood.

Interferons are now manufactured commercially in large quantities by recombinant DNA technology. Interferon beta 1b was approved for the treatment of multiple sclerosis by the United States Food and Drug Administration in 1993. Interferon beta 1a is described elsewhere in MedLink Neurology.

Pharmacology

Interferons are cytokines that mediate antiviral, antiproliferative, and immunomodulatory activities in response to viral infections and other biological inducers.

Pharmacodynamics. Interferon beta exerts its effect by binding to specific receptors on human cells. This leads to a complex chain of events that, in turn, lead to expression of various interferon-induced gene products that are believed to be the mediators of the biological actions of interferon beta 1b. The exact mechanism of action is not fully understood, but it may decrease the synthesis of inflammatory cytokines interferon gamma and tumor necrosis factor alpha.

Interferon beta 1b stabilizes the blood-brain barrier, which is damaged in multiple sclerosis. This might help improve the management of multiple sclerosis. Interferon beta 1b achieves this by blocking apoptosis of the endothelial cells of the blood-brain-barrier that is induced by serum from multiple sclerosis patients (15). Measurement of immunological biomarkers such as cytokines and neurotrophic factors in patients treated with interferon beta 1b for 1 year indicate their usefulness as indicators of clinical response (08).

Pharmacokinetics. Because serum concentrations of interferon beta 1b are low or undetectable following subcutaneous administration of 0.25 mg or less, pharmacokinetic information in patients with multiple sclerosis receiving the recommended dose of the drug is not available. In healthy volunteers, serum interferon beta 1b concentrations are generally below 100 IU/mL following single and multiple daily subcutaneous administrations of 0.5 mg of the drug. Peak serum interferon beta 1b concentrations occur between 1 and 8 hours. The pharmacokinetic profile is similar after intravenous administration. In patients receiving single intravenous doses up to 2.0 mg, increases in serum concentrations are dose proportional. Mean terminal elimination half-life values ranged from 8.0 minutes to 4.3 hours. Prolonged treatment does not result in accumulation of interferon beta 1b in the serum of patients.

Formulations. A refrigeration-free formulation of interferon beta 1b, based on mannitol, is stable at room temperature for up to 2 years. The safety and efficacy of the refrigeration-free formulation of interferon beta 1b is comparable with that of the original glucose.

Pharmacogenetics/pharmacogenomics. Nonresponder and responders to interferon beta differ in their ex vivo gene expression profile as determined by cDNA microarrays, longitudinal gadolinium-enhanced MRI scans, and clinical disease activity. These findings will help to better understand the mechanism of action of interferon beta in relation to different disease patterns and enable optimized therapy. Several differentially regulated genes have been identified in healthy volunteers in response to interferon beta 1b, and this biomarker panel may become a valuable tool for assessment of clinical drug effects.

Clinical trials

Several clinical trials have been conducted with interferon beta 1b. Some of these are shown in Table 1.

Table 1. Clinical Trials for Interferon beta 1b

Method and reference	Results
Multicenter, randomized, placebo-controlled trial in patients in secondary progressive phase of multiple sclerosis receiving 8 million IU interferon beta 1b every other day subcutaneously for up to 3 years (02).	Treatment with interferon beta 1b delayed sustained neurologic deterioration.
Randomized, placebo-controlled trial of interferon beta 1b in patients with secondary progressive multiple sclerosis in the European Study Group with MRI studies (27).	Interferon beta 1b reduced the accumulation of new inflammatory disease foci, which might be the mechanism of positive clinical benefits of treatment.
A prospective European multicenter, double-blind, randomized, placebo-controlled trial with patients treated for up to 36 months (21).	Interferon beta 1b treatment delays neurologic deterioration in patients with secondary progressive multiple sclerosis.
An open pilot study of the safety of combining mitoxantrone with interferon in patients with worsening relapsing-remitting or secondary progressive multiple sclerosis (19).	The combination was safe and enhanced the effect of interferon on disease progression.
A randomized, multicenter study in Japanese patients with relapsing-remitting multiple sclerosis (37).	Interferon beta 1b significantly reduced relapse rates and change in MRI lesion area in classical as well as optic-spinal multiple sclerosis.
Examination of detailed MRI findings from the first 2 years of Betaseron/Betaferon in the Newly Emerging Multiple Sclerosis for Initial Treatment (BENEFIT) study, which is a double-blind, placebo-controlled, randomized, parallel-group, multicenter, phase 3 study.	Interferon beta 1b treatment had a robust effect on MRI measures, supporting its value as an early intervention in this patient group (04).
Interferon beta 1b treatment effect was analyzed by Cox proportional hazards regression in a subgroup of the BENEFIT study.	Interferon beta 1b treatment effect was robust across the study population, including patients without MRI disease activity and patients not receiving steroids for the clinically isolated syndrome (33).
The 5-year active treatment extension of the BENEFIT study compared effects of early and delayed treatment with interferon beta 1b on time to clinically definite multiple sclerosis and other disease outcomes (20).	Favorable long-term safety support with early initiation of treatment with interferon beta 1b, although delay in treatment by up to 2 years did not affect long-term disability outcomes.
Betaferon Efficacy Yielding Outcomes of a New Dose (BEYOND) trial, compared efficacy, safety, and tolerability of 250 microg or 500 microg interferon beta-1b with glatiramer acetate for treating relapsing-remitting multiple sclerosis (OConnor et al 2009).	500 microg interferon beta-1b was not more effective than the standard 250 microg dose, and both doses had similar clinical effects to glatiramer acetate.

Modest but beneficial effects of interferon beta 1b on clinical variables and brain atrophy development were observed 5 years after termination of a 2-year clinical trial of interferon beta 1b for the treatment of primary progressive multiple sclerosis (41).

In the BENEFIT study, the impact of interferon beta-1b on cognitive performance at the clinically isolated stage of multiple sclerosis was evaluated by Paced Auditory Serial Addition Test-3 scores (31). IFNβ-1b treatment had a sustained positive effect on the test scores over the 5-year duration of the study. A 16-year longitudinal study has shown beneficial effects of interferon beta-1b on cognition outcomes in multiple sclerosis (23). In a randomized placebo-controlled trial of clinically isolated syndrome with follow-up of 5 years, interferon beta-1b was shown to reduce the number of black holes (ie, persisting T1 hypointensities on MRI) (28).

Regression analysis of patients with relapsing-remitting multiple sclerosis from BEYOND clinical trial has examined the predictive value of patient characteristics at baseline and after 1 year of treatment with interferon beta-1b 250 μg every other day (16). Higher number of relapses in year 1 predicted the future occurrence of relapses, whereas age, MRI activity, and the presence of neutralizing antibodies in the first year were mainly predictive of future MRI activity.

A 2-year prospective cohort study assessed serum 25-hydroxyvitamin D levels to determine association of interferon beta-1 treatment with the course of multiple sclerosis in participants of BEYOND clinical trial because low 25-hydroxyvitamin D levels indicate increased disease activity and rate of progression (10). Results showed that in patients treated with interferon beta-1b, higher 25-hydroxyvitamin D levels were associated with lower rates of disease activity observed on MRI.

A 2-year longitudinal study was conducted to estimate the prevalence of growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis in clinically isolated syndrome (CIS) patients and their correlation with conversion to multiple sclerosis in interferon beta 1b treated patients (24). GH/IGF-1 axis function was found to be frequently altered in CIS patients, but this was not related to conversion to multiple sclerosis despite improvement of growth hormone deficiency during interferon therapy.

Goals and duration of treatment

The aim is to slow the accumulation of physical disability and decrease the frequency of clinical exacerbations. It is not a curative treatment. The therapy can be continued for an indefinite period. A 21-year follow-up of multiple sclerosis patients treated with interferon beta-1b has reported better life (22).

An MRI study has shown that lack of size decrease of contrast enhancing lesions, which represent inflammatory events during interferon beta 1a therapy, suggests a limited therapeutic effect of the drug due to increased severity of brain tissue damage associated with blood-brain barrier breakdown (12).

In an observational extension study of the BENEFIT clinical trial, 8-year results provide further evidence supporting early initiation of treatment with interferon beta 1b in patients with a first event suggestive of multiple sclerosis (09). Patients originally randomized to interferon beta 1b had a reduced risk of developing clinically definite multiple sclerosis by 32.2% over the 8-year observation period.

A study on patients with relapsing-remitting multiple sclerosis showed that serum neutralizing antibodies (Nabs) were more frequent in patients receiving interferon beta 1b treatment than in those treated with subcutaneous or intramuscular interferon beta 1a, supporting Nabs as a biomarker to identify multiple sclerosis patients with a high probability of showing an optimal response to interferon beta 1b (01).

Predictive validity for negative disability outcomes at 16 years and survival at 21 years postrandomization were assessed in a follow-up of a randomized trial of interferon beta 1b for no evidence of disease activity (13). Clinical assessment of no disease activity predicted long-term disability outcome, whereas MRI variables did not increase the predictive validity.

The goal of a digital observational study, which was a mixed prospective and retrospective study, conducted among users of autoinjector BETACONNECT^® (80% of the patients) was to establish a method that enables the collection of medication usage data on a medical app (myBETAapp) and to assess medication usage among patients with multiple sclerosis treated with interferon beta 1b (ClinicalTrials.gov NCT03134573). This study provides important information on interferon beta 1b usage among patients with multiple sclerosis as well as on the consenting behavior of patients in digital studies, and in future clinical studies, this approach may enable patients' feedback to be rapidly implemented in existing digital solutions (26).

Following the introduction of BETACONNECT^® (an electronic autoinjector), an exploratory study suggested that persons with multiple sclerosis taking interferon beta 1b were more adherent compared with those taking interferon beta 1a, with higher persistence (06). More than 90% reached a medication possession ratio of 80%, a threshold commonly used to define good adherence.

Special considerations

All patients should have blood chemistry and hematology tests prior to initiating interferon beta 1b therapy and at periodic intervals thereafter: hemoglobin, complete and differential white blood cell counts, platelet counts, and blood chemistries including liver function tests. In the controlled clinical trials, patients were monitored every 3 months. The study protocol stipulated that interferon beta 1b therapy should be discontinued in the event the absolute neutrophil count fell below 750/mm3. When the absolute neutrophil count had returned to a value greater than 750/mm3, therapy could be restarted at a 50% reduced dose. Similarly, if hepatic transaminase levels exceeded 10 times the upper limit of normal or if the serum bilirubin exceeded 5 times the upper limit of normal, therapy was discontinued. In each instance during the controlled trials, hepatic enzyme abnormalities returned to normal following discontinuation of therapy.

Caution should be exercised in giving interferon beta 1b to patients with depression and patients with seizure disorders. Patients with cardiac disease should be closely monitored.

Anesthesia. No relevant information is available.

Pregnancy. Interferon beta 1b is contraindicated for pregnant women. It is not known if interferon beta is excreted in human milk. Nursing mothers should either discontinue nursing or interferon beta treatment. The rates of spontaneous abortions and birth defects in a study with the largest number of interferon beta 1bexposed pregnancies do not differ from available population estimates, and no pattern of specific birth defects was observed (36). However, the number of cases is not large enough to make a final assessment of the safety of interferon beta 1b during pregnancy.

Pediatric. Safety and efficacy in patients below the age of 18 years has not been established. A retrospective study, however, supports the safety and tolerability of interferon beta 1b in children with multiple sclerosis and related diseases, but regular monitoring of liver function is recommended (03).

Geriatric. No relevant information is available.

Adverse effects

Adverse events reported during clinical trials and postmarketing experience are listed in the Physicians Desk Reference. Some of the adverse reactions are:

	• Flu-like symptoms, which include fever, chills, myalgias, and arthralgias. These symptoms can be reduced by slower titration of the drug.
	• Injection-site inflammation. This can be reduced by use of an autoinjector.
	• Interferon beta 1b subcutaneous has been reported to result in ulceration due to multiple superficial thrombosed vessels.
	• Neutralizing antibodies to interferon beta occur in some multiple sclerosis patients, particularly during the first year of treatment, and may be associated with an attenuation of the therapeutic effect. However, another study shows that most patients with poor clinical response are negative for neutralizing bodies, suggesting that this explains only partially the suboptimal response to interferon beta (38). The IDEA (Interferon Dose Escalation Assessment) extension study demonstrated that when neutralizing antibodies develop in patients receiving higher doses of interferon beta 1b they tend to persist for a prolonged period, although neutralizing antibody titers tend to decrease over time and some patients may revert to neutralizing antibody-negative status (14). In 1 study, patients who produced neutralizing antibodies differed from those who did not by higher incidence of cognitive deficit and higher lesion load, and this might be a biomarker of a more aggressive form of multiple sclerosis (25). Methylprednisolone combined with interferon beta 1b reduces the incidence of neutralizing bodies during the first year of treatment. Neutralizing antibodies to interferon beta are linked to aggregation of the peptide during manufacturing and storage. Dodecylmaltoside, a nontoxic alkylsaccharide surfactant, reduces aggregation of interferon beta in vitro and reduces its immunogenicity in vivo in rodent models (35).
	• Interferon syndrome.
	• Exacerbation of multiple sclerosis may occur in some cases. It is difficult to ascertain if this is the natural progression of the disease with a lack of efficacy of treatment or an adverse reaction to the drug.
	• Drug-induced systemic lupus erythematosus has been reported in a patient suffering from multiple sclerosis after 8-year use of interferon beta 1b, and the symptoms gradually resolved after discontinuation of the drug (40).
	• Postmenopausal bleeding has been reported in a patient with the use of interferon beta 1b therapy, which could be due to elevated serum estradiol levels (32).
	• Thrombotic microangiopathy manifested by headache, thrombocytopenia, renal dysfunction, severe hypertension, posterior reversible encephalopathy syndrome, and gastrointestinal involvement has been reported in a patient after 8 years of therapy with interferon beta 1b (30). Rapid improvement followed discontinuation of the medication and initiation of antihypertensive treatment.
	• Severe active pulmonary tuberculosis has been reported in patients with multiple sclerosis undergoing interferon beta-1b therapy due to impact on cellular immunity. Screening is recommended for latent infection with Mycobacterium tuberculosis prior to interferon beta-1b therapy (39).

References

01: Alenda R, Costa-Frossard L, Alvarez-Lafuente R, et al. Blood lymphocyte subsets identify optimal responders to IFN-beta in MS. J Neurol 2018;265(1):24-31.** PMID 29027004
02: Anonymous. Placebo-controlled multicentre randomised trial of interferon beta-1b in treatment of secondary progressive multiple sclerosis. European Study Group on interferon beta-1b in secondary progressive MS. Lancet 1998;352(9139):1491-7. PMID 9820296
03: Banwell B, Reder AT, Krupp L, et al. Safety and tolerability of interferon beta-1b in pediatric multiple sclerosis. Neurology 2006;66:472-6. PMID 16505297
04: Barkhof F, Polman CH, Radue EW, et al. Magnetic resonance imaging effects of interferon beta-1b in the BENEFIT study: integrated 2-year results. Arch Neurol 2007;64(9):1292-8. PMID 17846268
05: Borden EC, Ball LA. Interferons: biochemical, cell growth inhibitory and immunological effects. In: Brown EB, editor. Progress in hematology. New York: Grune & Stratton, 1981:299-339.
06: Butler O, Heeg S, Holl K, et al. Real-world assessment of interferon-β-1b and interferon-β-1a adherence before and after the introduction of the BETACONNECT® autoinjector: a retrospective cohort study. Drugs Real World Outcomes 2021;8(3):359-67.** PMID 33928518
07: Cook SD, Dowling PC. Multiple sclerosis and viruses: an overview. Neurology 1980;30:80-91. PMID 6248821
08: Dhib-Jalbut S, Sumandeep S, Valenzuela R, Ito K, Patel P, Rametta M. Immune response during interferon beta-1b treatment in patients with multiple sclerosis who experienced relapses and those who were relapse-free in the START study. J Neuroimmunol 2013;254(1-2):131-40. PMID 22999187
09: Edan G, Kappos L, Montalbán X, et al. Long-term impact of interferon beta-1b in patients with CIS: 8-year follow-up of BENEFIT. J Neurol Neurosurg Psychiatry 2014;85(11):1183-9.** PMID 24218527
10: Fitzgerald KC, Munger KL, Köchert K, et al. Association of vitamin D levels with multiple sclerosis activity and progression in patients receiving interferon beta-1b. JAMA Neurol 2015;72(12):1458-65.** PMID 26458124
11: Fleishman WR, Ramamurthy V, Stanton JG, et al. Interferon: mode of action and clinical applications. In: Smith RA, editor. Interferon treatment in neurological disorders. New York: Marcel Dekker Inc, 1988:1-42.
12: Gaindh D, Jeffries N, Ohayon J, et al. The effect of interferon beta-1b on size of short-lived enhancing lesions in patients with multiple sclerosis. Expert Opin Biol Ther 2008;8(12):1823-9. PMID 18990070
13: Goodin DS, Reder AT, Traboulsee AL, et al. Predictive validity of NEDA in the 16- and 21-year follow-up from the pivotal trial of interferon beta-1b. Mult Scler 2019;25(6):837-47.** PMID 29761737
14: Gottesman MH, Friedman-Urevich S, Boylan E, Cheng D. Neutralizing antibodies to 500 microg interferon beta-1b: 28-month results of the IDEAS extension trial. Mult Scler 2010;16(1):78-80. PMID 19995836
15: Haghjooy Javanmard S, Saadatnia MM, Homayouni VV, et al. Interferon-beta-1b protects against multiple sclerosis-induced endothelial cells apoptosis. Front Biosci (Elite Ed) 2012;4:1368-74. PMID 22201961
16: Hartung HP, Kappos L, Goodin DS, et al. Predictors of disease activity in 857 patients with MS treated with interferon beta-1b. J Neurol 2015;262(11):2466-71. PMID 26239222
17: Hung IF, Lung KC, Tso EY, et al. Triple combination of interferon beta-1b, lopinavir-ritonavir, and ribavirin in the treatment of patients admitted to hospital with COVID-19: an open-label, randomised, phase 2 trial. Lancet 2020;395(10238):1695-704. PMID 32401715
18: Isaacs A, Lindemann J. Virus interference. I. The interferon. Proc R Soc Lond B Biol Sci 1957;147:258-67. PMID 13465720
19: Jeffery DR, Chepuri N, Durden D, Burdette J. A pilot trial of combination therapy with mitoxantrone and interferon beta-1b using monthly gadolinium-enhanced magnetic resonance imaging. Mult Scler 2005;11(3):296-301. PMID 15957510
20: Kappos L, Freedman MS, Polman CH, et al. Long-term effect of early treatment with interferon beta-1b after a first clinical event suggestive of multiple sclerosis: 5-year active treatment extension of the phase 3 BENEFIT trial. Lancet Neurol 2009;8(11):987-97. PMID 19748319
21: Kappos L, Polman C, Pozzilli C, et al. Final analysis of the European multicenter trial on IFNbeta-1b in secondary-progressive MS. Neurology 2001;57(11):1969-75. PMID 11739811
22: Komoly S. [Better life expectations of SM patients: 21 years follow up of patients treated with interferon beta-1b]. Ideggyogy Sz 2013;66(3-4):143-4. PMID 23750430
23: Lacy M, Hauser M, Pliskin N, Assuras S, Valentine MO, Reder A. The effects of long-term interferon-beta-1b treatment on cognitive functioning in multiple sclerosis: a 16-year longitudinal study. Mult Scler 2013;19(13):1765-72. PMID 23652214
24: Lanzillo R, Di Somma C, Quarantelli M, et al. Growth hormone/IGF-1 axis longitudinal evaluation in clinically isolated syndrome patients on interferon β-1b therapy: stimulation tests and correlations with clinical and radiological conversion to multiple sclerosis. Eur J Neurol 2017;24(2):446-9. PMID 27982500
25: Lanzillo R, Orefice G, Prinster A, et al. Predictive factors of neutralizing antibodies development in relapsing-remitting multiple sclerosis patients on interferon Beta-1b therapy. Neurol Sci 2011;32(2):287-92. PMID 21308385
26: Limmroth V, Hechenbichler K, Müller C, Schürks M. Assessment of medication adherence using a medical app among patients with multiple sclerosis treated with interferon beta-1b: pilot digital observational study (PROmyBETAapp). J Med Internet Res 2019;21(7):e14373.** PMID 31359863
27: Miller DH, Molyneux PD, Barker GJ, MacManus DG, Moseley IF, Wagner K. Effect of interferon-beta1b on magnetic resonance imaging outcomes in secondary progressive multiple sclerosis: results of a European multicenter, randomized, double-blind, placebo-controlled trial. European Study Group on Interferon-beta1b in secondary progressive multiple sclerosis. Ann Neurol 1999;46(6):850-9. PMID 10589537
28: Nagtegaal GJ, Pohl C, Wattjes MP, et al. Interferon beta-1b reduces black holes in a randomised trial of clinically isolated syndrome. Mult Scler 2014;20(2):234-42. PMID 23842212
29: O'Connor P, Filippi M, Arnason B, et al. 250 microg or 500 microg interferon beta-1b versus 20 mg glatiramer acetate in relapsing-remitting multiple sclerosis: a prospective, randomised, multicentre study. Lancet Neurol 2009;8(10):889-97. PMID 19729344
30: Omoto S, Utsumi T, Matsuno H, Terasawa Y, Iguchi Y. Thrombotic microangiopathy presenting with intestinal involvement following long-term interferon-β1b treatment for multiple sclerosis. Intern Med 2018;57(5):741-4. PMID 29151517
31: Penner IK, Stemper B, Calabrese P, et al. Effects of interferon beta-1b on cognitive performance in patients with a first event suggestive of multiple sclerosis. Mult Scler 2012;18(10):1466-71. PMID 22492127
32: Perlman B, Heller D, Cracchiolo B. Interferon beta-1b-induced postmenopausal bleeding in a patient with multiple sclerosis. Climacteric 2016;19(6):599-600. PMID 27749097
33: Polman C, Kappos L, Freedman MS, et al. Subgroups of the BENEFIT study: risk of developing MS and treatment effect of interferon beta-1b. J Neurol 2008;255(4):480-7. PMID 18004635
34: Rahmani H, Davoudi-Monfared E, Nourian A, et al. Interferon β-1b in treatment of severe COVID-19: a randomized clinical trial. Int Immunopharmacol 2020;88:106903. PMID 32862111
35: Rifkin RA, Maggio ET, Dike S, Kerr DA, Levy M. n-Dodecyl-β-D-maltoside inhibits aggregation of human interferon-β-1b and reduces its immunogenicity. J Neuroimmune Pharmacol 2011;6(1):158-62. PMID 20532646
36: Romero RS, Lünzmann C, Bugge JP. Pregnancy outcomes in patients exposed to interferon beta-1b. J Neurol Neurosurg Psychiatry 2015;86(5):587-9. PMID 25185209
37: Saida T, Tashiro K, Itoyama Y, et al. Interferon beta-1b is effective in Japanese RRMS patients: a randomized, multicenter study. Neurology 2005;64(4):621-30. PMID 15728282
38: Sbardella E, Tomassini V, Gasperini C, et al. Neutralizing antibodies explain the poor clinical response to interferon beta in a small proportion of patients with multiple sclerosis: a retrospective study. BMC Neurol 2009;9:54. PMID 19825153
39: Sirbu CA, Dantes E, Plesa CF, Docu Axelerad A, Ghinescu MC. Active pulmonary tuberculosis triggered by interferon beta-1b therapy of multiple sclerosis: four case reports and a literature review. Medicina (Kaunas) 2020;56(4):202. PMID 32344653
40: Sladkova V, Mares J, Lubenova B, Hlustik P, Kanovsky P. Drug-induced systemic lupus erythematosus in interferon beta-1b therapy. Neuro Endocrinol Lett 2011;32(1):4-6. PMID 21407162
41: Tur C, Montalban X, Tintoré M, et al. Interferon β-1b for the treatment of primary progressive multiple sclerosis: five-year clinical trial follow-up. Arch Neurol 2011;68(11):1421-7. PMID 22084124

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Interferon beta 1b

Other Pertinent Drugs

ACTH
interferon alpha
interferon beta-1a
interferon gamma
glatiramer acetate
- methylprednisolone
- mitoxantrone
- natalizumab
- prednisone

Also Relevant

Autoantibodies: disease markers
Clinical trials in multiple sclerosis
Interferon beta 1a
Multiple sclerosis
Multiple sclerosis: neurobehavioral aspects
- Neuropharmacology
- Transverse myelitis
- Multiple sclerosis: treatment of its symptoms

Clinical Categories

Web References

Guidelines

AAN: Neutralizing antibodies to Interferon-beta: clinical and radiographic Impact

Package inserts

Interferon Beta-1b

Interferon beta 1b

Interferon beta 1b

Introduction

Historical note and terminology

Pharmacology

Clinical trials

Table 1. Clinical Trials for Interferon beta 1b

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Author

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Paraneoplastic syndromes

Anti-IgLON5 disease

Anti-LGI1 encephalitis

Progressive encephalomyelitis with rigidity and myoclonus and glycine receptor antibodies

Drug-induced myasthenic syndromes

Giant cell arteritis

Acupuncture

Chronic inflammatory demyelinating polyradiculoneuropathy

Interferon beta 1b

Introduction

Historical note and terminology

Pharmacology

Clinical trials

Table 1. Clinical Trials for Interferon beta 1b

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Author

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Paraneoplastic syndromes

Anti-IgLON5 disease

Anti-LGI1 encephalitis

Progressive encephalomyelitis with rigidity and myoclonus and glycine receptor antibodies

Drug-induced myasthenic syndromes

Giant cell arteritis

Acupuncture

Chronic inflammatory demyelinating polyradiculoneuropathy

This is an article preview.
Start a Free Account
to access the full version.