Certolizumab pegol 200mg/1ml solution for injection cartridges
Requires a prescription from a doctor or prescriber
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1 branded products available
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Cimzia 200mg/1ml solution for injection in a dose-dispenser cartridge
WHO defined daily dose (DDD)
14 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 BNF/ATC 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)
Certolizumab pegol for treating moderate to severe plaque psoriasis (TA574)
Certolizumab pegol for treating rheumatoid arthritis after inadequate response to a TNF-alpha inhibitor (TA415)
Certolizumab pegol and secukinumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA445)
Adalimumab, etanercept, infliximab, certolizumab pegol, golimumab, tocilizumab and abatacept for rheumatoid arthritis not previously treated with DMARDs or after conventional DMARDs only have failed (TA375)
Golimumab for treating active non-radiographic axial spondyloarthritis (TA497)
Upadacitinib for treating severe rheumatoid arthritis (TA665)
TNF-alpha inhibitors for treating active ankylosing spondylitis and non-radiographic axial spondyloarthritis (TA383)
Sarilumab for moderate to severe rheumatoid arthritis (TA485)
Spondyloarthritis in over 16s: diagnosis and management (NG65)
Ixekizumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA537)
Tofacitinib for moderate to severe rheumatoid arthritis (TA480)
Tofacitinib for treating active psoriatic arthritis after inadequate response to DMARDs (TA543)
Filgotinib for treating moderate to severe rheumatoid arthritis (TA676)
Tocilizumab for the treatment of rheumatoid arthritis (TA247)
Adalimumab, etanercept, infliximab and abatacept for treating moderate rheumatoid arthritis after conventional DMARDs have failed (TA715)
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. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 30 studies.
Reviews & meta-analyses: 6 · Randomised trials: 1 · 2022–2026
Showing all 30 studies, sorted by most relevant.
Xiuying Lv, Xiuying Lv, Xiuying Lv, et al.
Frontiers in Immunology, 2026
- Tumor Necrosis Factor Inhibitors
- Immune System Diseases
- Inflammation
Background: Tumor necrosis factor-α inhibitors (TNFi) are established to increase the risk of tuberculosis (TB). However, the comparative risk across different TNFi agents remains poorly defined due to a lack of head-to-head comparative studies. This network meta-analysis (NMA) aimed to evaluate and compare the risk of TB infection associated with various TNFi therapies in patients with immune-mediated inflammatory diseases (IMIDs) based on real-world, long-term cohort studies. Methods: We conducted a systematic search of PubMed, EMBASE, Cochrane Library, and Web of Science from inception to May 30, 2025, for cohort studies reporting TB events in patients with IMIDs treated with TNFi. Study selection, data extraction, and risk of bias assessment were performed by three independent reviewers using the Newcastle-Ottawa Scale. A Bayesian arm-based NMA with random-effects models was used to estimate log risk ratio (logRR) and 95% credible intervals (CrIs) for TB infection across different TNFi agents compared with TNFi-naive. Results: A total of 19 cohort studies involving 396, 044 patients were included. Compared to TNFi-naive, infliximab (IFX) was associated with the highest risk of TB (logRR = 2.32, 95% CrI: 1.12-3.32), followed by adalimumab (ADA) (logRR = 1.72, 95% CI: 0.42-2.65) and etanercept (ETN) (logRR = 1.39, 95% CI: 0.33-2.42). Certolizumab pegol (CZP) was associated with the lowest risk among TNFi agents. Conclusion: TNFi treatment in patients with IMIDs is associated with a significantly increased risk of TB infection. Among the TNFi agents, IFX was associated with the highest risk, while ETN and CZP demonstrated lower risks. These findings can inform clinical decision-making, suggesting that ETN or CZP may be preferable in patients with high TB risk, while emphasizing that vigilant TB monitoring remains paramount regardless of the chosen agent. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42022331674.
Abstract licence: CC BY
M. Østergaard, R. V. van Vollenhoven, A. Rudin, et al.
Annals of the Rheumatic Diseases, 2023
- Arthritis, Rheumatoid
- Antirheumatic Agents
- Certolizumab Pegol
Michio Tokuyama, T. Mabuchi
Immunotherapy, 2024
- Psoriasis
- Tumor Necrosis Factor-alpha
- Certolizumab Pegol
Elizabeth Anderson, Secia Beier, J. Desmarais
Immunotherapy, 2024
Amirhossein Heidari, Yekta Ghane, Nazila Heidari, et al.
Therapeutic Advances in Chronic Disease, 2024
I. E. van der Horst-Bruinsma, P. Robinson, E. Favalli, et al.
Rheumatology and Therapy, 2022
BACKGROUND: Acute anterior uveitis (AAU) affects up to 40% of patients with axial spondyloarthritis (axSpA). An effective treatment for patients with axSpA that reduces the risk of AAU flares while also targeting axial symptoms is therefore highly desirable. Tumor necrosis factor inhibitors (TNFis) have been shown effective for treatment of axSpA and AAU occurrence, with guidelines conditionally recommending treating patients with axSpA and associated AAU with TNFi monoclonal antibodies. To date, most available data on the impact of TNFis on AAU in axSpA are from observational, open-label studies without parallel comparator arms. However, there is a growing body of evidence describing the impact of the TNFi certolizumab pegol (CZP) on the incidence of axSpA-associated AAU. OBJECTIVE: Our objective was to collate data pertaining to the impact of CZP in axSpA-associated AAU in patients across the full axSpA spectrum. METHODS: Data were obtained from four industry-supported phase 3 and 4 clinical trials (C-VIEW, C-axSpAnd, C-OPTIMISE, and RAPID-axSpA). To supplement these data, a targeted literature review was performed through searches of MEDLINE, Embase, and reference lists. RESULTS: Available data from 1467 patients from the C-VIEW, C-axSpAnd, C-OPTIMISE, and RAPID-axSpA trials show CZP to be effective in AAU in patients across the full axSpA spectrum, reducing AAU flares when compared with placebo or pretreatment period. No differences in AAU outcomes were reported when stratified by axSpA subgroup age or sex. The targeted literature review identified six further studies of CZP in spondyloarthritis-associated AAU, only one of which was specific to axSpA. CONCLUSION: CZP was effective in reducing AAU incidence in clinical trials with patients with axSpA. The targeted literature review, however, highlighted that there remains a paucity of data beyond these trials. Data from comparative studies would further enhance the body of evidence on the effects of CZP in patients with axSpA who develop AAU.
Abstract licence: CC BY-NC
Shinji Okabayashi, H. Yamazaki, Ryohei Yamamoto, et al.
The Cochrane database of systematic reviews, 2022
- Certolizumab Pegol
- Crohn Disease
- Inflammation
D. Branch, Mimi Kim, Marta M. Guerra, et al.
Annals of the rheumatic diseases, 2025
- Immunosuppressive Agents
- Polyethylene Glycols
- Pregnancy Complications
Dexiao Wang, Jie Zhao, Jingyu Zhang, et al.
International immunopharmacology, 2024
- Certolizumab Pegol
- Anti-Inflammatory Agents
- Blood-Brain Barrier
J. Smolen, Peter C. Taylor, Yoshiya Tanaka, et al.
Rheumatology (Oxford, England), 2024
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
14 days
Mechanism
Certolizumab targets the activation of TNF-alpha with high affinity (KD 90 pM and IC90 0.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
171 hours
[A176606]…
Half-life
14 days
[A176606]
Protein binding
Volume of distribution
4-8 L
[A176666]…
Metabolism
Elimination
Clearance
9-14 ml
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Certolizumab does not require glycosylation for active function and hence, its production is significantly more affordable when compared to other existing TNF-alpha therapies as it can be done directly in bacterial hosts such as E. coli.[A176606] It was developed and manufactured by UCB Pharma, first FDA approved in 2008[L45018] and updated for a new indication on March 28, 2019.[L5819]
- Symptomatic management of Chron's disease patients and for the maintenance of clinical response in patients with moderate to severe disease with inadequate response to conventional therapy.
- Treatment of adult patients with moderate to severely active rheumatoid arthritis.
- Treatment of adult patients with active psoriatic arthritis.
- Treatment of adult patients with active ankylosing spondylitis.
- Treatment of adult patients with moderate-to-severe plaque psoriasis that are candidates for systemic therapy or phototherapy.[FDA label]
- Treatment of adult patients with active non-radiographic axial spondyloarthritis with objective signs of inflammation.
[L5819]
In Canada, certolizumab pegol is additionally approved in combination with [methotrexate] for the symptomatic treatment, including major clinical response, and for the reduction of joint damage in adult patients with moderately to severely active rheumatoid arthritis and psoriatic arthritis.
[L5825]
Inflammation is a biological response against a potential threat. This response can be normal but in certain conditions, the immune system can attack the body's normal cells or tissues which causes an abnormal inflammation.
[L5840]
TNF-alpha has been identified as a key regulator of the inflammatory response. The signaling cascades of this inflammatory mediator can produce a wide range of reactions including cell death, survival, differentiation, proliferation and migration.
[A176660]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1890 interactions
Certolizumab pegol does not present mutagenic potential nor presents effects in fertility and reproductive performance. On the other hand, carcinogenicity studies have not been performed.[FDA label]
One additional feature od certolizumab pegol is that, due to the presence of the PEGylation, it is more significantly distributed into inflamed tissues when compared to other TNF-alpha inhibitors such as [infliximab] and [adalimumab].[A176606]
In vitro studies with certolizumab pegol in human tissue did not show any unexpected binding at 3 mcg/ml nor at 10 mcg/ml. Due to the drug class, certolizumab pegol is not expected to present adverse effects on the major vital systems.F4232
In phase III clinical trials in psoriatic arthritis patients, certolizumab pegol was reported to generate improvements in skin disease, joint involvement, dactylitis, enthesitis and general life quality. The clinical effect of certolizumab was paired to a comparable safety profile to other TNF-alpha inhibitors.[A176606]
The clinical effectiveness of certolizumab pegol was mainly studied in six randomized controlled trials that compared its effect versus placebo. In a comparative study, the efficacy for certolizumab pegol registered ranged from 30-65% while in placebo ranged from 4-25%.[A176612] However, in other additional trials, certolizumab was proven to present a similar clinical efficacy to other disease-modifying antirheumatic drugs in patients with inadequate response to TNF inhibitors.[A176603]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A176606]
Certolizumab presents a linear pharmacokinetic profile with a peak plasma concentration of 43-49 mcg/ml.F4232
[A176606]
[A176666]
It is known to have a very good distribution in the joints when compared to other TNF-alpha inhibitors.
[A176645]
[A31470]
On the other hand, the PEG section is processed normally by the action of the alcohol dehydrogenase to the formation of carboxylic acid.
[A176672]
[A176606]
Proteins and enzymes this drug interacts with in the body
Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective .
PMID:23396208
Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line .
PMID:16829952 PMID:22517918 PMID:23396208
Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity).
Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 .
PMID:12794819
Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC L04AB05
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)
Certolizumab pegol
Additional database identifiers
Drugs Product Database (DPD)
20513
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11892
GenAtlas
TNF
GeneCards
TNF
GenBank Gene Database
M16441
GenBank Protein Database
339741
UniProt Accession
TNFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:380
GeneCards
AKR1A1
GenBank Gene Database
J04794
GenBank Protein Database
178481
UniProt Accession
AK1A1_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q412909), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.