Brodalumab 210mg/1.5ml solution for injection pre-filled syringes
Requires a prescription from a doctor or prescriber
Brodalumab has been used in trials studying the treatment of Asthma, Psoriasis, Crohn's Disease, Psoriatic Arthritis, and Rheumatoid Arthritis.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Brodalumab
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Submit a Yellow Card report to the MHRA
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.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Brodalumab
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Brodalumab on the MHRA register
Kyntheum 210mg/1.5ml solution for injection pre-filled syringes
WHO defined daily dose (DDD)
15 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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
Brodalumab
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(6)
Brodalumab for treating moderate to severe plaque psoriasis (TA511)
Bimekizumab for treating moderate to severe plaque psoriasis (TA723)
Certolizumab pegol for treating moderate to severe plaque psoriasis (TA574)
Tildrakizumab for treating moderate to severe plaque psoriasis (TA575)
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.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
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
Not available
Mechanism
Brodalumab binds with high affinity to interleukin (IL)-17 receptor A, thereby i…
Food interactions
None known
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Volume of distribution
4.62 L
Clearance
0.223 L
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 681 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:17911633 PMID:9367539
Receptor for IL17F .
PMID:17911633 PMID:19838198
Binds to IL17A with higher affinity than to IL17F .
PMID:17911633
Binds IL17A and IL17F homodimers as part of a heterodimeric complex with IL17RC .
PMID:16785495
Also binds heterodimers formed by IL17A and IL17F as part of a heterodimeric complex with IL17RC .
PMID:18684971
Cytokine binding triggers homotypic interaction of IL17RA and IL17RC chains with TRAF3IP2 adapter, leading to 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:16785495 PMID:17911633 PMID:18684971 PMID:21350122 PMID:24120361
Involved in antimicrobial host defense primarily promoting neutrophil activation and recruitment at infection sites to destroy extracellular bacteria and fungi (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).
Plays a role in the maintenance of the integrity of epithelial barriers during homeostasis and pathogen infection. 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). Involved in antiviral host defense through various mechanisms.
Enhances immunity against West Nile virus by promoting T cell cytotoxicity. Contributes to Influenza virus 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). Receptor for IL17C as part of a heterodimeric complex with IL17RE PMID:21993848
PMID:16785495
Receptor for the heterodimer formed by IL17A and IL17B as part of a heterodimeric complex with IL17RA .
PMID:18684971
Has also been shown to be the cognate receptor for IL17F and to bind IL17A with high affinity without the need for IL17RA .
PMID:17911633
Upon binding of IL17F homodimer triggers downstream activation of TRAF6 and NF-kappa-B signaling pathway .
PMID:16785495 PMID:32187518
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 (By similarity).
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). Binding of IL17A-IL17F to IL17RA-IL17RC heterodimeric receptor complex triggers 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:17911633 PMID:18684971
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)
PMID:12807873 PMID:12958313
Regulates the nuclear ERK signaling pathway by spatially blocking nuclear translocation of activated ERK without inhibiting cytoplasmic phosphorylation of ERK .
PMID:15239952
Mediates JNK activation and may be involved in apoptosis (By similarity). May inhibit FGF-induced FGFR1 tyrosine phosphorylation (By similarity). Might have a role in the early stages of fate specification of GnRH-secreting neurons (By similarity).
Inhibits TGFB-induced epithelial-to-mesenchymal transition in lens epithelial cells (By similarity)
May be a crucial regulator in innate immunity to bacterial pathogens. Isoform 2 and isoform 4 may be either cytoplasmic inactive or dominant active forms. Isoform 3 and isoform 5 may act as soluble decoy receptors
ATC L04AC12
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)
Brodalumab
Additional database identifiers
Drugs Product Database (DPD)
22941
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5985
GeneCards
IL17RA
Guide to Pharmacology
1738
UniProt Accession
I17RA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18015
GeneCards
IL17RB
UniProt Accession
I17RB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18358
GeneCards
IL17RC
UniProt Accession
I17RC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17616
GeneCards
IL17RD
UniProt Accession
I17RD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18439
GeneCards
IL17RE
UniProt Accession
I17RE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5981
GeneCards
IL17A
UniProt Accession
IL17_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: