Chemical: Drug
interferon beta-1a

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PharmGKB contains no Clinical Variants that meet the highest level of criteria.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

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The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page.

Links in the "Gene" column lead to PharmGKB Gene Pages.

List of all variant annotations for interferon beta-1a

Gene ? Variant?
Alternate Names ? Chemicals ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
No VIP available CA VA HLA-B *15:01:01:01 N/A N/A N/A
No VIP available CA VA HLA-DRB1 *04:01:01 N/A N/A N/A
No VIP available CA VA
rs10494227 NC_000001.10:g.120137445A>G, NC_000001.11:g.119594822A>G, rs17186150, rs60091301
A > G
No VIP available CA VA
rs10760397 NC_000009.11:g.128133207T>C, NC_000009.12:g.125370928T>C, rs58258954
T > C
No VIP available CA VA
rs10819043 NC_000009.11:g.128037245C>T, NC_000009.12:g.125274966C>T, NM_001282679.1:c.-150+5982C>T, NM_001282680.1:c.-150+5982C>T, NM_015635.3:c.-33+13007C>T, XM_005251899.1:c.-150+5982C>T, XM_005251900.1:c.-150+5982C>T, XM_005251901.1:c.-33+5982C>T, XM_005251901.2:c.-33+5982C>T, XM_005251902.1:c.-150+5982C>T, XM_005251903.1:c.-33+5982C>T, XM_005251904.1:c.-33+5982C>T, XM_005251904.2:c.-33+5982C>T, XM_006717044.2:c.-33+5982C>T, XM_011518499.1:c.-33+5982C>T, XM_011518500.1:c.-150+5982C>T, XM_011518501.1:c.-33+5982C>T, XM_011518502.1:c.-33+5982C>T, XM_011518503.1:c.-125+14073C>T, XM_011518504.1:c.-33+17837C>T, XM_011518505.1:c.-34+11265C>T, XM_011518506.1:c.-33+5982C>T, XM_011518507.1:c.-33+5982C>T, XM_011518508.1:c.-34+13006C>T, rs59535510
C > T
No VIP available CA VA
rs12044852 NC_000001.10:g.117087779C>A, NC_000001.11:g.116545157C>A, NM_001144822.1:c.71-553G>T, NM_001779.2:c.71-553G>T, NR_026665.1:n.192-553G>T, XR_947739.1:n.210+333C>A, XR_947740.1:n.210+333C>A, rs386522642, rs60002408, rs60224328
C > A
No VIP available CA VA
rs1448673 NC_000007.13:g.17605070A>G, NC_000007.14:g.17565446A>G, rs10368730, rs386532310, rs61485269
A > G
No VIP available No Clinical Annotations available VA
rs1799752 NC_000017.10:g.61565890_61565891insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NC_000017.10:g.61565890_61565891insG, NC_000017.11:g.63488529_63488530insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NC_000017.11:g.63488529_63488530insG, NG_011648.1:g.16457_16458insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NG_011648.1:g.16457_16458insG, NM_000789.3:c.2306-119_2306-118insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NM_000789.3:c.2306-119_2306-118insG, NM_001178057.1:c.584-119_584-118insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NM_001178057.1:c.584-119_584-118insG, NM_152830.2:c.584-119_584-118insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, NM_152830.2:c.584-119_584-118insG, XM_005257110.1:c.1757-119_1757-118insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, XM_005257110.1:c.1757-119_1757-118insG, XM_006721737.2:c.644-119_644-118insATACAGTCACTTTTTTTTTTTTTTTGAGACGGAGTCTCGCTCTGTCGCCC, XM_006721737.2:c.644-119_644-118insG, rs13447447 (retired), rs4340, rs4340 (retired), rs4646994
- > G
No VIP available CA VA
rs2291858 NC_000009.11:g.128128782A>G, NC_000009.12:g.125366503A>G, rs386563938, rs59761820
A > G
No VIP available CA VA
rs3133084 NC_000011.10:g.126157578A>G, NC_000011.9:g.126027473A>G, rs59153754
A > G
No VIP available CA VA
rs4278350 NC_000001.10:g.88555928C>T, NC_000001.11:g.88090245C>T, rs61141471
C > T
No VIP available No Clinical Annotations available VA
rs4961252 NC_000008.10:g.142104944A>G, NC_000008.11:g.141094845A>G, rs17546440, rs58686754
A > G
No VIP available CA VA
rs760316 NC_000003.11:g.60098968C>T, NC_000003.12:g.60113241C>T, NG_007551.1:g.1143166G>A, NM_001166243.1:c.104-99090G>A, NM_002012.2:c.104-99090G>A, XM_005264951.1:c.125-99090G>A, XM_005264952.1:c.104-99090G>A, XM_005264953.1:c.104-99090G>A, XM_005264954.1:c.104-99090G>A, XM_005264955.1:c.104-99090G>A, XM_011533481.1:c.104-99089G>A, XM_011533482.1:c.104-99089G>A, XM_011533483.1:c.104-99089G>A, XM_011533484.1:c.104-99089G>A, XM_011533485.1:c.104-99089G>A, XM_011533486.1:c.104-99089G>A, rs59412671
C > T
No VIP available CA VA
rs9272105 NC_000006.11:g.32599999G=, NC_000006.11:g.32599999G>A, NC_000006.12:g.32632222G=, NC_000006.12:g.32632222G>A, NT_113891.2:g.4050375A=, NT_113891.2:g.4050375A>G, NT_113891.3:g.4050269A=, NT_113891.3:g.4050269A>G, NT_167245.1:g.3881721G=, NT_167245.1:g.3881721G>A, NT_167245.2:g.3876136G=, NT_167245.2:g.3876136G>A, NT_167246.1:g.4056154G=, NT_167246.1:g.4056154G>A, NT_167246.2:g.4050534G=, NT_167246.2:g.4050534G>A, NT_167247.1:g.3938863G=, NT_167247.1:g.3938863G>A, NT_167247.2:g.3933278G=, NT_167247.2:g.3933278G>A, NT_167248.1:g.3836834A=, NT_167248.1:g.3836834A>G, NT_167248.2:g.3831238A=, NT_167248.2:g.3831238A>G, NT_167249.1:g.4033445G=, NT_167249.1:g.4033445G>A, NT_167249.2:g.4034147G=, NT_167249.2:g.4034147G>A, rs112115374, rs12198540, rs35395657, rs78375203
G > A
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147


Generic Names
  • Fibroblast interferon
  • IFN-beta
  • Interferon beta precursor
Trade Names
  • Avonex
  • Avonex (Biogen Inc)
  • Belerofon
Brand Mixture Names

PharmGKB Accession Id





Human interferon beta (166 residues), glycosylated, MW=22.5kD. It is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta.

Source: Drug Bank



Commercially available interferons (INF) include IFN-beta-1b and IFN-beta-1a [Article:11971121]. The difference between the two IFNs is that IFN-beta-1a is glycosylated, whereas IFN-beta-1b is not [Article:11971121]. IFN-beta-1a is used for relapsing-remitting multiple sclerosis (MS) [Article:19783688]. IFN-beta-1a is thought to exert its therapeutic effects by down-modulating the immune response by multiple potential pathways [Article:19559654]. A microarray analysis of peripheral blood mononuclear cells from MS patients detected a profile of immune cell activation, autoantigen upregulation, and enhanced E2F pathway transcription [Article:15081262]. Jurkat T cells were exposed to IFN-beta-1a with the result that the cell surface expression of the IFN receptor subunit (IFNAR1) decreased significantly, and the cells were unresponsive to further IFN treatment [Article:12034032]. The treatment with IFN-beta-1a down regulated the expression of interleukin 1 beta (IL1B) and interleukin 23 alpha subunit p19 (IL23A) in dendritic cells and it induced the gene expression of interleukin 12A (IL12A) and interleukin 27 (IL27) [Article:19783688]. A study, which examined the molecular mechanisms potentially capable of modulating bone homeostasis in response to INF-beta-1a, found that the treatment modulated receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) [Article:17086898]. An investigation of the heterogeneity of clinical response to INF-beta treatment found decreased integrin (ITGB1and ITGB2) gene expression in patients with MS responding to INF-beta treatment [Article:15081256]. Drug-responders could be distinguished from non-responders by early and sustained induction of TNF-related apoptosis inducing ligand (TNFSF10) [Article:12814715].


An association was found between glypican 5 (GPC5) polymorphisms and the response to INF-beta therapy in patients with MS [Article:19556317]. A genome-wide pharmacogenomic analysis identified genes linked to interindividual differences in the efficacy of INF-beta therapy [Article:18195134]. Responders and non-responders had significantly different genotype frequencies for polymorphisms located in many genes, including glypican 5 (GPC5), collagen type 25 alpha1 (COL25A1), hyaluronan proteoglycan link protein (HAPLN1), calpastatin (CAST), and neuronal PAS domain protein 3 (NPAS3) [Article:18195134]. A candidate genes study identified polymorphisms in JAK2-IL10RB-GBP1-PIAS1 genes as most significant allelic combinations that differed in frequency between responders and non-responders [Article:19604093].

Source: PharmGKB


For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Interferon beta 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) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha.

Source: Drug Bank


Interferon beta 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. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity


10 hrs

Source: Drug Bank


* 33-55 L/hour [Healthy SC injection of 60 mcg]

Source: Drug Bank

Chemical Properties

Chemical Formula


Source: Drug Bank

Canonical SMILES

Not Available

Source: Drug Bank

Average Molecular Weight


Source: Drug Bank

Genes that are associated with this drug in PharmGKB's database based on (1) variant annotations, (2) literature review, (3) pathways or (4) information automatically retrieved from DrugBank, depending on the "evidence" and "source" listed below.

Curated Information ?

Drug Targets

Gene Description
IFNAR1 (source: Drug Bank )
IFNAR2 (source: Drug Bank )
No related drugs are available.

Curated Information ?

Relationships from National Drug File - Reference Terminology (NDF-RT)

May Treat
Contraindicated With

Publications related to interferon beta-1a: 9

No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
HLA genes as modifiers of response to IFN-beta-1a therapy in relapsing-remitting multiple sclerosis. Pharmacogenomics. 2016. Mazdeh Mehrdokht, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Response to interferon-beta treatment in multiple sclerosis patients: a genome-wide association study. The pharmacogenomics journal. 2016. Mahurkar S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacogenetics of multiple sclerosis: personalized therapy with immunomodulatory drugs. Pharmacogenetics and genomics. 2015. Tsareva Ekaterina, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Association of CD58 Polymorphism with Multiple Sclerosis and Response to Interferon ß Therapy in A Subset of Iranian Population. Cell journal. 2015. Torbati Sara, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacogenomic update on multiple sclerosis: a focus on actual and new therapeutic strategies. The pharmacogenomics journal. 2012. Foti Cuzzola V, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Single-nucleotide polymorphisms in HLA- and non-HLA genes associated with the development of antibodies to interferon-beta therapy in multiple sclerosis patients. The pharmacogenomics journal. 2011. Weber F, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Network analysis of transcriptional regulation in response to intramuscular interferon-beta-1a multiple sclerosis treatment. The pharmacogenomics journal. 2010. Hecker M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Genetic polymorphisms, their allele combinations and IFN-beta treatment response in Irish multiple sclerosis patients. Pharmacogenomics. 2009. O'Doherty Catherine, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Genome-wide pharmacogenomic analysis of the response to interferon beta therapy in multiple sclerosis. Archives of neurology. 2008. Byun Esther, et al. PubMed


Web Resource:
National Drug Code Directory:
Drugs Product Database (DPD):
Therapeutic Targets Database:
FDA Drug Label at DailyMed:

Clinical Trials

These are trials that mention interferon beta-1a and are related to either pharmacogenetics or pharmacogenomics.

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NURSA Datasets

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No NURSA datasets available.

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Sources for PharmGKB drug information: DrugBank, PubChem.