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.
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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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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 Brodalumab
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1 branded products available
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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 the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
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.
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
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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. 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.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 24 · Randomised trials: 15 · 2014–2026
Showing the 50 most relevant studies, sorted by most relevant.
Tan B, Chen M, Hu X, et al.
2025
BackgroundPyoderma gangrenosum (PG) is a rare disease causing painful skin ulcers, typically starting with tender pustules that quickly develop into painful ulcers. Traditional treatments like glucocorticoids and immunosuppressants often have adverse effects and limited efficacy, making them unsuitable for all patients. Recent evidence shows that biological agents are more effective and safer, leading to increased acceptance. However, selecting the most suitable biological agent from the many available options remains a significant challenge for both physicians and patients.ObjectiveTo systematically review the treatment outcomes of two biologics: TNF (tumour necrosis factors)-α inhibitors and IL (interleukin) inhibitors in pyoderma gangrenosum.MethodsA search of Pubmed was conducted on September 7, 2024. A total of 107 studies were included using Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines.ResultsA total of 139 patients were included. Ninety-two were treated with TNF-α inhibitors and 47 with IL inhibitors. The number of included cases and the efficacy are Infliximab (n=52, 88.4%), Adalimumab (n=23, 91.3%), Etanercept (n=13, 84.6%), Certolizumab (n=3, 66.6%), Golimumab (n=1, 100.0%), Anakinra (n=11, 100.0%), Canakinumab (n=7, 100.0%), Secukinumab (n=5, 40.0%), Brodalumab (n=3, 100.0%), Ixekizumab (n=1, 100.0%), Ustekinumab (n=12, 100.0%), Spesolimab (n=3, 100.0%), Guselkumab (n=2, 100.0%), Tildrakizumab (n=2, 100.0%), Risankizuma (n=1, 100.0%). Among them, 46.0% (n=64) achieved complete remission, including 47 (33.8%) who used TNF-α inhibitors and 17 (12.2%) with IL inhibitors. And the total effective rate of IL- inhibitors (93.6%) was higher than that of TNF-α inhibitors (88.0%), but had no statistical significance (p>0.05). However, it takes less time for IL inhibitors to reach partial remission or complete remission. Additionally, in infliximab group, the number of adverse events that occurred was large and varied.ConclusionDifference in effective rate shows no statistical significance between two kinds of agents. However, IL inhibitors demonstrate an advantage with shorter treatment cycles. Additionally, Infliximab has a wider range of side effects and should be used with caution.PROSPERO number: CRD42024608039.
Abstract licence: CC BY-NC
Shahsavaripoor B, Karami S, Sahebi A, et al.
2026
- Psoriasis
- Biological Products
- Depression
BackgroundPsoriasis is a long-lasting inflammatory condition of the skin associated with various comorbidities, including depression and suicidal ideation. Management strategies for psoriasis include symptom alleviation, quality-of-life enhancement, and prevention of disease progression. Psoriasis treatments include topical therapies, phototherapy, oral systemic medications, and biologics.ObjectivesIn this review, we evaluate the impact of psoriasis treatments on depression and suicidal ideation in affected patients.MethodsWe systematically searched multiple databases, including PubMed, Scopus, and Web of Science, until September 30, 2024, to identify relevant articles. Studies that examined the effects of psoriasis therapies on depression and suicidal thoughts were included. Data on treatment modalities, psychological health outcomes, and psoriasis severity was obtained. Quality evaluation instruments, such as JBI, consolidated standards of reporting trials (CONSORTs), Center for Evidence-Based Management (CEMBa), and appraisal tool for cross-sectional studies (AXIS), were used to appraise study quality.ResultsTen studies met inclusion criteria, predominantly focusing on biologic therapies. Biologics like guselkumab, brodalumab, and bimekizumab have shown notable reductions in depression symptoms, probably through the alleviation of psoriasis severity and the enhancement of quality-of-life. Suicidal ideation occurred in some cases, especially with brodalumab; however, a definitive causal relationship was not established.ConclusionsTreatments for psoriasis, especially biologics, have shown some advantages in reducing depression symptoms as well as relieving skin symptoms. However, cautious monitoring is required due to the possible hazards of suicidal thoughts with certain therapeutic options such as biologics. Addressing the complex issues of psoriasis requires comprehensive therapy that includes dermatologists and mental health specialists.
Abstract licence: CC BY
Dahyeon Kim, Nickoulet Babaei, Minka Gill, et al.
Archives of Dermatological Research, 2026
Gupta AK, Bamimore MA, Wang T, et al.
2026
- Scalp Dermatoses
- Psoriasis
- Immunomodulating Agents
BackgroundRecently, the literature has expanded with peer-reviewed studies on immunomodulatory agents' efficacy on scalp psoriasis-which, in turn, widened knowledge gaps regarding these agents' relative effectiveness. We determined the relative efficacy of immunomodulatory monotherapies for scalp psoriasis.MethodsWe ran Bayesian network meta-analyses (NMAs) using outcomes related to Psoriasis Scalp Severity Index (PSSI) and scalp-specific Physician's Global Assessment of clear (0) or almost clear (1) (Sc-PGA 0/1).ResultsWe estimated the relative efficacy of 22 interventions (including placebo), and analyzed 9 outcomes, namely: proportion of participants who attained Sc-PGA 0/1, proportion of participants who achieved 100% improvement in PSSI (PSSI-100), and proportion of participants who achieved 90% improvement in PSSI (PSSI-90) at 8, 12, and 16 weeks.ConclusionsWe are the first to provide comparative evidence on the efficacy of newly investigated agents such as deucravacitinib, tildrakizumab, roflumilast and icotrokinra. In general, the IL-17 inhibitors (bimekizumab, ixekizumab, secukinumab, brodalumab) and IL-23 inhibitors (icotrokinra, guselkumab, tildrakizumab) were effective depending upon the outcome and time-point being considered. At 16 weeks, for PSSI-100, ixekizumab 150 mg at weeks 0, 2, 4, 8, and 12 ranked highest; at 16 weeks, for Sc-PGA 0/1 bimekizumab 320 mg every 4 weeks ranked highest; at 8 weeks, for PSSI-100 ixekizumab 80 mg every 2 weeks ranked highest; at 8 weeks, for Sc-PGA 0/1 secukinumab 300 mg at weeks 1, 2, 3 and then every 4 weeks ranked highest. Small-molecule therapies (apremilast, deucravacitinib, roflumilast) improved scalp psoriasis modestly. Our work would guide the design of future studies and clinical decision-making.
Abstract licence: CC BY
Fan Bai, Gang Li, Qingmin Liu, et al.
Journal of Immunology Research, 2019
L. Puig, M. Lebwohl, H. Bachelez, et al.
Journal of the American Academy of Dermatology, 2020
Matteo Megna, Gabriella Fabbrocini, Maria Ferrillo, et al.
Dermatologic Therapy, 2020
Drew J. B. Kurtzman (5024465), Jaren Trost (5024474), Jawad Bilal (5024462), et al.
2018
Yukari Okubo, Satomi Kobayashi, Masamoto Murakami, et al.
American Journal of Clinical Dermatology, 2024
- Psoriasis
- Receptors, Interleukin-17
- Antibodies, Monoclonal, Humanized
Rothery, Claire, South, Emily, Grosso, Alessandro, et al.
2019
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study 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 medicines. 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
Show
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:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72