Bimekizumab 320mg/2ml solution for injection pre-filled disposable devices
Requires a prescription from a doctor or prescriber
Drugs affecting the immune response
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Yellow Card reports
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Suspected adverse reactions reported for Bimekizumab
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Bimekizumab
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1 branded products available
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Bimzelx 320mg/2ml solution for injection pre-filled pens
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Bimekizumab
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(7)
Bimekizumab for treating active psoriatic arthritis (TA916)
Bimekizumab for treating moderate to severe plaque psoriasis (TA723)
Bimekizumab for treating active ankylosing spondylitis and non-radiographic axial spondyloarthritis (TA918)
Bimekizumab for treating moderate to severe hidradenitis suppurativa (terminated appraisal) (TA1028)
Spondyloarthritis in over 16s: diagnosis and management (NG65)
Deucravacitinib for treating moderate to severe plaque psoriasis (TA907)
Psoriasis: assessment and management (CG153)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
23 days
Mechanism
The pathophysiology of psoriasis involves a dysregulation of the immune system a…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
70.1%
[L39665]
Half-life
23 days
[L39665]
Volume of distribution
11.2 L
[L39665]
Metabolism
[L39665]
Clearance
0.337 L
[L39665]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L48546][L51053]
It is also approved in the US for adults with moderate to severe hidradenitis suppurativa (HS).
[L51409]
In Canada, it is also approved for the treatment of active psoriatic arthritis in adults alone or in combination with a conventional non-biologic disease-modifying antirheumatic drug (cDMARD).
[L51053]
It is also used to treat adults with active ankylosing spondylitis who have responded inadequately or are intolerant to conventional therapy.
[L51053]
Bimekizumab is also used for the treatment of adult patients with active non-radiographic axial spondyloarthritis with objective signs of inflammation as indicated by elevated C-reactive protein (CRP) and/or magnetic resonance imaging (MRI) who have responded inadequately or are intolerant to nonsteroidal anti-inflammatory drugs (NSAIDs).
[L51053]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1351 interactions
[L39665]
If overdosage of bimekizumab is suspected, monitor the patient for adverse reactions and institute symptomatic treatment as clinically indicated.
Bimekizumab is a monoclonal antibody targeted against IL-17A, IL-17F, and a heterodimer of the two called IL-17AF.[L39665] It blocks the interaction of these interleukins with their respective receptors, thus reducing psoriatic inflammation.
Bimekizumab may increased the risk of infection, including upper respiratory tract infections and oral candidiasis.[L39665] Any clinically important active infections should be resolved prior to therapy. In addition, the use of live vaccines during bimekizumab therapy is not recommended - ensure patients beginning therapy have completed all age appropriate immunizations prior to initiation.[L39665]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L39665]
[L39665]
[L39665]
[L39665]
[L39665]
Proteins and enzymes this drug interacts with in the body
PMID:24120361
Signals via IL17RA-IL17RC heterodimeric receptor complex, triggering homotypic interaction of IL17RA and IL17RC chains with TRAF3IP2 adapter. This leads to downstream TRAF6-mediated activation of NF-kappa-B and MAPkinase pathways ultimately resulting in transcriptional activation of cytokines, chemokines, antimicrobial peptides and matrix metalloproteinases, with potential strong immune inflammation .
PMID:17911633 PMID:18684971 PMID:19825828 PMID:21350122 PMID:24120361 PMID:8676080
Plays an important role in connecting T cell-mediated adaptive immunity and acute inflammatory response to destroy extracellular bacteria and fungi. As a signature effector cytokine of T-helper 17 cells (Th17), primarily induces neutrophil activation and recruitment at infection and inflammatory sites (By similarity).
In airway epithelium, mediates neutrophil chemotaxis via induction of CXCL1 and CXCL5 chemokines (By similarity). In secondary lymphoid organs, contributes to germinal center formation by regulating the chemotactic response of B cells to CXCL12 and CXCL13, enhancing retention of B cells within the germinal centers, B cell somatic hypermutation rate and selection toward plasma cells (By similarity). Effector cytokine of a subset of gamma-delta T cells that functions as part of an inflammatory circuit downstream IL1B, TLR2 and IL23A-IL12B to promote neutrophil recruitment for efficient bacterial clearance (By similarity).
Effector cytokine of innate immune cells including invariant natural killer cell (iNKT) and group 3 innate lymphoid cells that mediate initial neutrophilic inflammation (By similarity). Involved in the maintenance of the integrity of epithelial barriers during homeostasis and pathogen infection .
PMID:21350122
Upon acute injury, has a direct role in epithelial barrier formation by regulating OCLN localization and tight junction biogenesis (By similarity). As part of the mucosal immune response induced by commensal bacteria, enhances host's ability to resist pathogenic bacterial and fungal infections by promoting neutrophil recruitment and antimicrobial peptides release (By similarity).
In synergy with IL17F, mediates the production of antimicrobial beta-defensins DEFB1, DEFB103A, and DEFB104A by mucosal epithelial cells, limiting the entry of microbes through the epithelial barriers (By similarity). Involved in antiviral host defense through various mechanisms (By similarity). Enhances immunity against West Nile virus by promoting T cell cytotoxicity (By similarity).
May play a beneficial role in influenza A virus (H5N1) infection by enhancing B cell recruitment and immune response in the lung (By similarity). Contributes to influenza A virus (H1N1) clearance by driving the differentiation of B-1a B cells, providing for production of virus-specific IgM antibodies at first line of host defense (By similarity)
PMID:21350122
IL17A-IL17F signals via IL17RA-IL17RC heterodimeric receptor complex, triggering homotypic interaction of IL17RA and IL17RC chains with TRAF3IP2 adapter through SEFIR domains. This leads to downstream TRAF6-mediated activation of NF-kappa-B and MAPkinase pathways ultimately resulting in transcriptional activation of cytokines, chemokines, antimicrobial peptides and matrix metalloproteinases, with potential strong immune inflammation .
PMID:11574464 PMID:11591732 PMID:11591768 PMID:17911633 PMID:18684971 PMID:21350122 PMID:28827714
IL17A-IL17F is primarily involved in host defense against extracellular bacteria and fungi by inducing neutrophilic inflammation (By similarity). As signature effector cytokine of T-helper 17 cells (Th17), primarily induces neutrophil activation and recruitment at infection and inflammatory sites (By similarity).
Stimulates the production of antimicrobial beta-defensins DEFB1, DEFB103A, and DEFB104A by mucosal epithelial cells, limiting the entry of microbes through the epithelial barriers (By similarity). IL17F homodimer can signal via IL17RC homodimeric receptor complex, triggering downstream activation of TRAF6 and NF-kappa-B signaling pathway .
PMID:32187518
Via IL17RC induces transcriptional activation of IL33, a potent cytokine that stimulates group 2 innate lymphoid cells and adaptive T-helper 2 cells involved in pulmonary allergic response to fungi. Likely via IL17RC, promotes sympathetic innervation of peripheral organs by coordinating the communication between gamma-delta T cells and parenchymal cells.
Stimulates sympathetic innervation of thermogenic adipose tissue by driving TGFB1 expression (By similarity). Regulates the composition of intestinal microbiota and immune tolerance by inducing antimicrobial proteins that specifically control the growth of commensal Firmicutes and Bacteroidetes (By similarity)
ATC L04AC21
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Bimekizumab
Additional database identifiers
Drugs Product Database (DPD)
23699
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5981
GeneCards
IL17A
UniProt Accession
IL17_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16404
GeneCards
IL17F
UniProt Accession
IL17F_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: