Ixekizumab 80mg/1ml solution for injection pre-filled syringes
Requires a prescription from a doctor or prescriber
Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody (mAb) against interleukin-17A (IL-17A) and prevents it from interacting with the IL-17A receptor.
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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 Ixekizumab
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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 Ixekizumab
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1 branded products available
MHRA licensed products
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Taltz 80mg/1ml solution for injection pre-filled syringes
WHO defined daily dose (DDD)
2.9 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(15)
Ixekizumab for treating moderate to severe plaque psoriasis (TA442)
Ixekizumab for treating active ankylosing spondylitis and non-radiographic axial spondyloarthritis (TA718)
Ixekizumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA537)
Upadacitinib for treating active non-radiographic axial spondyloarthritis (TA861)
Guselkumab for treating moderate to severe plaque psoriasis (TA521)
Bimekizumab for treating active psoriatic arthritis (TA916)
Bimekizumab for treating active ankylosing spondylitis and non-radiographic axial spondyloarthritis (TA918)
Bimekizumab for treating moderate to severe plaque psoriasis (TA723)
Upadacitinib for treating active ankylosing spondylitis (TA829)
Tofacitinib for treating active ankylosing spondylitis (TA920)
Spondyloarthritis in over 16s: diagnosis and management (NG65)
Tildrakizumab for treating moderate to severe plaque psoriasis (TA575)
Certolizumab pegol for treating moderate to severe plaque psoriasis (TA574)
Brodalumab for treating moderate to severe plaque psoriasis (TA511)
Guselkumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA815)
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
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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: 18 · Randomised trials: 28 · 2015–2026
Showing the 50 most relevant studies, sorted by most relevant.
P. Mease, D. M. van der Heijde, C. Ritchlin, et al.
Annals of the Rheumatic Diseases, 2016
P. Nash, B. Kirkham, M. Okada, et al.
Lancet, 2017
P. Mease, J. Smolen, F. Behrens, et al.
Annals of the Rheumatic Diseases, 2019
A. Deodhar, D. Poddubnyy, C. Pacheco-Tena, et al.
Arthritis & Rheumatology (Hoboken, N.j.), 2019
A. Deodhar, D. van der Heijde, L. Gensler, et al.
Lancet, 2019
Yonghong Zhang, Zhiya Yang, J. Gong, et al.
Frontiers in Medicine, 2024
Gao S, Xie X, Fan L, et al.
2025
- Arthritis, Psoriatic
- Antirheumatic Agents
- Interleukin-12
BackgroundPsoriatic arthritis (PsA) is a chronic inflammatory disease that impacts both the skin and joints. Currently, interleukin (IL)-17, IL-12/23, and IL-23 inhibitors have become integral components of PsA treatment regimens. Nevertheless, the comparative effectiveness of these IL-targeted therapies remains a subject of ongoing debate. This study employs a network meta-analysis (NMA) approach to systematically evaluate the therapeutic efficacy and safety profiles of various IL-17, IL-12/23, and IL-23 inhibitors.MethodsWe searched PubMed, Web of Science, and Embase for randomized controlled trials (RCTs) to identify eligible research articles. This NMA was implemented by Stata 14.0 software, with odds ratios (ORs) and 95% confidence intervals (CIs) serving as effect and safety measures to evaluate clinical efficacy and safety profiles. Drugs were ranked based on their efficacy and safety profiles using the surface under the cumulative ranking curve values, enabling a comprehensive comparative assessment of interventional strategies. The CINeMA (Confidence in Network Meta-Analysis) online tool was utilized to evaluate the confidence level of the NMA results.ResultsThis NMA included 22 RCTs and 9,241 patients. All intervention groups demonstrated superior efficacy to the placebo group. Based on efficacy endpoints and subgroup analyses, bimekizumab, secukinumab, and ixekizumab exhibited superior short-term efficacy. Notably, subgroup analyses suggested that tildrakizumab may represent a promising therapeutic option for PsA. Regarding safety and the risk of adverse events, all treatments demonstrated no significant differences compared to placebo, except bimekizumab 160 mg every 4 weeks (Q4W) (OR = 1.37, 95% CI: 1.08-1.74). There were no significant differences in terms of serious adverse events and upper respiratory tract infection. Bimekizumab 160 mg Q4W showed heightened risk of nasopharyngitis (OR = 2.30, 95% CI: 1.26-4.22).ConclusionsThis NMA showed that IL-17, IL-12/23, and IL-23 inhibitors demonstrated remarkable efficacy in attaining ACR20, ACR50, ACR70, and MDA after 12, 16, or 24 weeks of treatment. Among these, IL-17 inhibitors-particularly bimekizumab, secukinumab, and ixekizumab-exhibited notably pronounced therapeutic effects. However, bimekizumab showed a less favorable clinical safety profile compared to other biological agents. In contrast, secukinumab and ixekizumab demonstrated a favorable balance of relatively high efficacy and low risk when considering safety profiles.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251023787, identifier CRD420251023787.
Abstract licence: CC BY
Zhang JX, Li WW, Huang LZ, et al.
2025
- Inflammatory Bowel Diseases
- Psoriasis
- Interleukins
BackgroundInterleukin inhibitors represent a standard therapeutic approach for psoriasis. However, there is still debate about the risk of new-onset inflammatory bowel disease (IBD) in psoriasis patients following interleukin inhibitor treatment. This systematic review and meta-analysis aims to evaluate the risk of new-onset IBD in psoriasis patients treated with five interleukin inhibitors (Bimekizumab, Ixekizumab, Secukinumab, Brodalumab, and Ustekinumab), providing insights to inform clinical decision-making.MethodThis study was registered in the PROSPERO with registration number of CRD42024608423. The databases PubMed, Embase, Cochrane Library, and Web of Science were comprehensively searched for observational studies published as full-length papers in English. The Mantel-Haenszel method with a fixed-effects model and risk difference was used to compare the risk of new-onset IBD between experimental groups (using interleukin inhibitors) and the control groups (using placebo or non-interleukin inhibitors). Sensitivity analysis was performed using the leave-one-out method for the meta-analysis. Additionally, considering the potential for underdiagnosis of IBD, a meta-analysis of the risk of diarrhea was conducted.ResultThis study included 17 articles covering 21 Randomized Controlled Trials(RCTs). A total of 22 new-onset IBD cases were reported in the experimental groups, with 3, 14, 4, 1, and 0 cases in the Bimekizumab, Ixekizumab, Secukinumab, Brodalumab, and Ustekinumab group, respectively. The control group only reported 1 case of new-onset IBD. No significant difference in the risk of new-onset IBD was found between these experimental groups and control groups. Based on the fixed-effects model, the pooled risk difference for Ixekizumab group was MH RD 0.0027 (95% CI 0.0001-0.0054, I² = 0%, P = 0.04). Sensitivity analysis indicated that the data was stable. Regarding diarrhea, a total of 95 cases were reported in the experimental groups, compared to 50 cases in the control groups. The experimental groups of Bimekizumab, Secukinumab, and Brodalumab reported 49, 45, and 1 case of diarrhea, respectively, while their control groups reported 11, 39, and 0 cases, respectively. Based on the fixed-effects model, compared to the control groups, there were no significant differences in the risk of diarrhea among psoriasis patients treated with these three interleukin inhibitors, and sensitivity analysis demonstrated good data robustness. Additionally, no cases of diarrhea were reported in the Ixekizumab group and Ustekinumab group.ConclusionsThere is insufficient evidence to confirm that Ustekinumab, Bimekizumab, Secukinumab, and Brodalumab significantly increase the risk of new-onset IBD. However, compared to the control group, Ixekizumab was significantly associated with an increased risk of new-onset IBD in psoriasis patients. Psoriasis patients receiving Ixekizumab treatment should remain vigilant for gastrointestinal symptoms, particularly in high-risk patients, to identify and manage potential IBD early. Additionally, compared to the control group, no significant difference was observed in the risk of diarrhea as an adverse event among patients treated with Bimekizumab, Secukinumab, and Brodalumab.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD42024608423, identifier CRD42024608423.
Abstract licence: CC BY
J. Maneiro, J. Carmona, Antonio Mera, et al.
JCR: Journal of Clinical Rheumatology, 2024
de Sena RR, de C Mesquita K, Barroso LF, et al.
2026
IntroductionRecent trials with withdrawal arms in patients with psoriasis have highlighted the need for updated clinical guidance. The aim of this investigation was to compare the effects and safety of planned limited-time withdrawal versus continuous maintenance of interleukin (IL) inhibitors in patients with psoriasis.MethodsOn August 5, 2025, the following platforms were systematically searched: PubMed, Embase, Clarivate (Web of Science), Scopus, and Ovid. Titles and abstracts, followed by full-text articles, were independently screened by two reviewers, with any disagreements being resolved by a third reviewer. Certainty of evidence was evaluated via the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Network meta-analyses for the Psoriasis Area and Severity Index (PASI) 90 and PASI100 outcomes were performed. The risk ratio (RR) of relapse was ranked using the surface under the cumulative ranking curve (SUCRA) metric.ResultsA total of 7444 records were retrieved, 54 of which included data from 18 different trials. The data revealed a total of 2995 patients who were subjected to anti-IL withdrawal regimens that were eligible for comparison with anti-IL maintenance. For the PASI90 outcome, the network meta-regression, adjusted for a post-withdrawal follow-up duration of 40-48 weeks, indicated that bimekizumab demonstrated a RR for relapse (RR 5.36; 95% confidence interval (CI) 3.45-8.34; SUCRA 0.685) comparable to that of guselkumab (RR 7.45; 95% CI 4.97-11.19; SUCRA 0.412) and lower than that of ixekizumab (RR 17.45; 95% CI 10.22-29.80; SUCRA 0.006). No significant difference in adverse event rates was observed between the anti-IL withdrawal and maintenance groups.ConclusionsCompared with continued treatment, planned withdrawal of anti-IL therapy is associated with a largely superior risk of relapse, without any reduction in the incidence of adverse events. Moreover, bimekizumab withdrawal demonstrated better outcomes than ixekizumab withdrawal did according to the PASI90 outcome.Study registrationThis study was prospectively registered on PROSPERO (identification number CRD420251118724).
Abstract licence: CC BY-NC
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
13 days
Mechanism
Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
160 mg
Half-life
13 days
Volume of distribution
7.11 L
Metabolism
Clearance
0.39 L
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ixekizumab is produced by recombinant DNA technology in a recombinant mammalian cell line and purified using standard technology for bioprocessing. Ixekizumab is comprised of two identical light chain polypeptides of 219 amino acids each and two identical heavy chain polypeptides of 445 amino acids each, and has a molecular weight of 146,158 Daltons for the protein backbone of the molecule. It is indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.
[L40953]
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: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)
ATC L04AC13
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)
Ixekizumab
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