Tremelimumab 300mg/15ml solution for infusion vials
Requires a prescription from a doctor or prescriber
Tremelimumab, formerly known as ticilimumab, is a fully human IgG2 monoclonal antibody directed against cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4).
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Suspected adverse reactions reported for Tremelimumab
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Imjudo 300mg/15ml concentrate for solution for infusion vials
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.
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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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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: 12 · Randomised trials: 18 · 2009–2026
Showing the 50 most relevant studies, sorted by most relevant.
Naiyer A. Rizvi, Byoung Chul Cho, Niels Reinmuth, et al.
JAMA Oncology, 2020
- Antineoplastic Agents, Immunological
- Antibodies, Monoclonal
- Antineoplastic Combined Chemotherapy Protocols
J. Goldman, M. Dvorkin, Yuanbin Chen, et al.
The Lancet. Oncology, 2020
T. Powles, M. S. van der Heijden, D. Castellano, et al.
The Lancet. Oncology, 2020
Eileen Mary O'Reilly, Do‐Youn Oh, Neesha C. Dhani, et al.
JAMA Oncology, 2019
Michele Maio, Arnaud Scherpereel, Luana Calabrò, et al.
The Lancet Oncology, 2017
J. Schoenfeld, A. Giobbie-Hurder, S. Ranasinghe, et al.
The Lancet. Oncology, 2022
Antoni Ribas, Richard F. Kefford, Margaret A Marshall, et al.
Journal of Clinical Oncology, 2013
- Ipilimumab
- Antibodies, Monoclonal
- Antineoplastic Agents
Xiao Han, Hai-Dong Zhang, K. Sun, et al.
Frontiers in Immunology, 2024
Li W, Xiong H, Peng H, et al.
2025
BackgroundCTLA-4 inhibitors, such as tremelimumab and ipilimumab, are increasingly used in the treatment of non-small cell lung cancer (NSCLC). This meta-analysis aims to evaluate the incidence of pneumonitis associated with these inhibitors and explore potential differences between individual agents.MethodsA systematic search across three online databases identified 911 records. After screening for duplicates and irrelevant articles, nine studies with a total of 4,164 patients were included. Risk of bias was assessed using the Cochrane "Risk of Bias" tool. Pneumonitis incidence was analyzed using a random-effects model.ResultsThe overall incidence of any-grade pneumonitis was 4.0% [95% CI (2.2%, 5.8%)]. High-grade pneumonitis occurred in 1.6% [95% CI (0.5%, 2.6%)]. Subgroup analysis revealed that tremelimumab was associated with a higher incidence of both any-grade (8.0% vs. 2.0%) and high-grade (3.0% vs. 1.0%) pneumonitis compared to ipilimumab. In a comparison with a control group, patients receiving CTLA-4 inhibitors had a significantly higher incidence of any-grade pneumonitis [OR = 3.00, 95% CI (1.60, 5.64), p p = 0.14].ConclusionThis meta-analysis indicates that CTLA-4 inhibitors are associated with a higher incidence of pneumonitis in NSCLC patients, particularly with tremelimumab. These findings underline the importance of close monitoring for pneumonitis in patients receiving CTLA-4 inhibitors, especially tremelimumab, and suggest the need for further research into prevention and management strategies.
Abstract licence: CC BY
Magashi MA, Danbala IA, Shaibu Z, et al.
2025
- Pancreatic Neoplasms
- Radiosurgery
- Immune Checkpoint Inhibitors
This study aims to evaluate the efficacy and toxicity of stereotactic body radiotherapy (SBRT) in advanced pancreatic cancer (APC) patients, comparing SBRT alone to SBRT combined with immunotherapy. A systematic review was conducted following the PRISMA guidelines. Electronic databases, including Google Scholar, Medline, Embase, Cochrane, and PubMed, were searched up to October 23, 2024. Studies evaluating SBRT alone or in combination with immunotherapy for APC were included. Key outcomes assessed were overall survival (OS), progression-free survival (PFS), objective response rate (ORR), disease control rate (DCR), and grade 3/4 treatment-related adverse events (TRAEs). Data were analyzed and presented as percentages. The study is registered with PROSPERO under the registration number CRD420250655873. The 1-year OS rate was 44% for SBRT alone, compared to 8% for nivolumab + ipilimumab + SBRT, 80% for durvalumab + SBRT, and 2% for durvalumab + tremelimumab + SBRT. The 1-year PFS rate was 46% for SBRT alone, versus 43%, 4%, and 3% for the respective combinations. Grade 3/4 TRAEs were lower for SBRT alone (21.5%) compared to combination therapies: 79.1% for nivolumab + ipilimumab + SBRT, 73.2% for nivolumab + SBRT, 33.3% for durvalumab + SBRT, and 61.1% for durvalumab + tremelimumab + SBRT. SBRT is an effective treatment option for APC, with a 1-year OS rate of 44% and relatively low TRAEs. The combination of durvalumab + SBRT demonstrated a promising 1-year OS rate of 80%, highlighting its potential for further investigation.
Abstract licence: CC BY-NC-ND
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
16.9 days
Mechanism
T cell activation is influenced by several processes.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 mg/k
Half-life
16.9 days
[L43652]
Volume of distribution
24%
Clearance
0.286 L
[L43652]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Tremelimumab was first approved by the FDA in October 2022 to be used in combination with [durvalumab] to treat hepatocellular carcinoma.[L43652] It is also being investigated in other cancers, such as colon cancer, pancreatic cancer, non-small cell lung cancer (NSCLC), and malignant melanoma.[A253717][A253722] After receiving an EMA Committee for Medicinal Products for Human Use (CHMP) recommendation in December 2022, tremelimumab was approved for combined use with [durvalumab].[L46188]
[L43652][L46188]
It is also indicated in combination with durvalumab and platinum-based chemotherapy for the treatment of adult patients with metastatic non-small cell lung cancer (NSCLC) with no sensitizing epidermal growth factor receptor (EGFR) mutation or anaplastic lymphoma kinase (ALK) genomic tumor aberrations.
[L44126][L46188]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 417 interactions
[L43662]
Immune checkpoints are proteins that control the intensity and duration of T cell activation and response. CD28 and CTLA-4 are homologous receptors expressed on CD4+ and CD8+ T cell surface.[A253727] These immune checkpoints have opposing regulatory functions on T cell activity: CD28 is a positive regulator of T cell activity, while CTLA-4 is a negative regulator suppressing T cell activation and proliferation, as well as IL-2 gene transcription.[A253712][A218731] B7 molecules act as ligands to both of these receptors,[A253727] and the balance between CD28 and CTLA-4 expression and signalling influence the extent of T cell activation. In cancer immunotherapy, CTLA-4 has been investigated as a therapeutic target as blocking this receptor can enhance the activation of tumour-specific T cells, allowing them to exert cytotoxic effects on tumour cells.[A253712]
Tremelimumab is an antibody directed against CTLA-4. By binding to CTLA-4, tremelimumab blocks the interaction of CTLA-4 with its ligands, CD80 and CD86, limiting its negative regulatory effect on T cell activation. Inhibition of CTLA-4 leads to increased proliferation of T cells in tumours and promotes T cell-mediated cytotoxicity.[L43652]
In vitro, there was no evidence of nonspecific cytokine release induced by tremelimumab or drug binding to Fc receptors.[A253737][A218731]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L43652]
[L43652]
[L43652]
[L43652]
Proteins and enzymes this drug interacts with in the body
ATC L01FX20
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)
Tremelimumab
Additional database identifiers
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