Belatacept 250mg powder for solution for infusion vials
Requires a prescription from a doctor or prescriber
Belatacept is a soluble fusion protein, which links the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) to the modified Fc (hinge, CH2, and CH3 domains) portion of human immunoglobulin G1 (IgG1).
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Yellow Card reports
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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 Belatacept
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Nulojix 250mg powder for concentrate for solution for infusion vials
WHO defined daily dose (DDD)
12.5 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(3)
Immunosuppressive therapy for kidney transplant in adults (TA481)
Immunosuppressive therapy for kidney transplant in children and young people (TA482)
Prevention of recurrence of C3 glomerulopathy post-transplant: eculizumab (ESUOM44)
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
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. 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: 20 · Randomised trials: 10 · 2015–2026
Showing the 50 most relevant studies, sorted by most relevant.
Juliana Schilsky, R. H. Dvorai, Christine Yang, et al.
Transplant immunology, 2024
Xuchuan Wang, Dandan Song, Shufu Hou, et al.
Frontiers in Immunology, 2026
- Diabetes Mellitus
- Postoperative Complications
- Immunosuppressive Agents
Background The novel immunosuppressant belatacept demonstrates a unique mechanism of action that significantly improves renal function and reduces metabolic complications. However, systematic evidence comparing the risk of post-transplant diabetes mellitus (PTDM) and overall safety profiles between belatacept-based regimens and calcineurin inhibitor (CNI)-based protocols remains limited. This meta-analysis aims to synthesize high-quality evidence to determine the comparative efficacy of these two regimens in PTDM prevention and safety outcomes, thereby providing robust guidance for clinical decision-making. Methods We systematically searched PubMed, Cochrane Library, CNKI, and EMBASE for studies published until November 30, 2024, comparing belatacept versus calcineurin inhibitors (CNIs) regarding PTDM risk in kidney transplant recipients. The primary outcome was PTDM incidence. Following data extraction and quality assessment, we performed pairwise meta-analyses to compare PTDM risk between belatacept (either less intensive(LI) or more intensive (MI) regimen) and CNIs. Bayesian network meta-analysis (WinBUGS 1.4.3) was then conducted for indirect comparison between belatacept LI and MI regimens. Results The initial search yielded 3,206 records. After deduplication, title/abstract screening, and full-text evaluation, 6 studies involving 1,737 kidney transplant recipients were included in the final analysis. Compared with CNIs, belatacept demonstrated significant reductions in PTDM risk for both the LI (RR = 0.65, 95% CI 0.52-0.81, p<0.001; I²=30%) and MI (RR = 0.65, 95% CI 0.52-0.81, p<0.001; I²=30%) regimens. Bayesian network meta-analysis revealed no statistically significant difference between the LI and MI regimens. Conclusions This meta-analysis demonstrates that belatacept significantly reduces PTDM risk compared to CNIs, a finding consistent with previous studies. Notably, both LI and MI dosing regimens showed protective effects, suggesting that even low-intensity belatacept therapy could serve as a viable alternative to CNIs, particularly for patients requiring reduced immunosuppressive toxicity. Systematic review registration https://inplasy.com/, identifier INPLASY202540041.
Abstract licence: CC BY
Alissa M Krek, Miro E Raeber, Onur Boyman
2024
Ibrahim Tawhari, Fatma Yamani, Manal Alotaibi, et al.
BMC Nephrology, 2026
- BK Virus
- Cytomegalovirus Infections
- Polyomavirus Infections
Paraskevas T, Kanta A, Perdiki P, et al.
2026
BackgroundPrimary focal segmental glomerulosclerosis (FSGS) frequently recurs after kidney transplantation and remains a major cause of premature allograft failure. Despite multiple proposed preventive strategies, no standardized approach has been established. This review aimed to systematically evaluate and compare the efficacy and safety of prophylactic interventions for preventing recurrent FSGS following kidney transplantation.MethodsWe performed a systematic review and network meta-analysis of randomized and nonrandomized studies including patients with primary FSGS undergoing kidney transplantation. PubMed and Embase were searched through July 2025. Any intervention administered prior to FSGS recurrence-either before or shortly after transplantation-was eligible for inclusion. The primary outcome was posttransplant FSGS recurrence; secondary outcomes included proteinuria, time to recurrence, and treatment-related adverse events.ResultsTwenty-five unique studies evaluating six interventions were included in the systematic review. None of the prophylactic strategies significantly reduced recurrence compared with control. The combination of rituximab and plasma exchange yielded lower effect estimates than either intervention alone, but this difference did not reach statistical significance. Evidence for belatacept and bleselumab was limited to single studies; however, their findings warrant further investigation. Adverse events were infrequently reported.ConclusionsCurrent evidence does not support a definitive prophylactic strategy to prevent recurrent FSGS after kidney transplantation. These findings remain inconclusive, and confirmation of potential benefit-or lack thereof-requires adequately powered randomized trials. Future multicenter studies should standardize recurrence definitions, timing of prophylaxis, and safety reporting.
Abstract licence: CC BY-NC
K. Budde, R. Prashar, H. Haller, et al.
JASN, 2021
F. Vincenti, L. Rostaing, J. Grinyo, et al.
The New England journal of medicine, 2016
Halawa A., Reccia I., Virdis F., et al.
2021
N. Lange, Kristen L. King, S. Husain, et al.
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2024
O. Bredewold, W. Moest, J. W. Fijter, et al.
Journal of Medical Virology, 2024
- Immunosuppressive Agents
- Kidney Transplantation
- Viral Load
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
9.8 days
Mechanism
Belatacept is a fusion protein in which the Fc portion of human IgG1 is attached…
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10 mg/k
Half-life
10 mg/k
10 mg/kg, kidney transplant recipients= 9.8 days;
5 mg/kg, kidney transplant recipient = 8.2 days
Volume of distribution
10 mg/k
Vd, steady state, transplant patients, 5 mg/kg = 0.12 L/kg
Metabolism
Clearance
10 mg/k
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 359 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Cmax, 10 mg/kg = 247 µg/mL;
Cmax, 5 mg/kg = 139 µg/mL;
AUC, 10 mg/kg = 22,252 µg · h/mL;
AUC, 5 mg/kg = 14,090 µg · h/mL;
Belatacept had linear and dose-dependent pharmacokinetic profile.
10 mg/kg, kidney transplant recipients= 9.8 days;
5 mg/kg, kidney transplant recipient = 8.2 days
Vd, steady state, transplant patients, 5 mg/kg = 0.12 L/kg
Mean systemic clearance:
10 mg/kg, kidney transplant recipients= 0.49 mL/h/kg;
5 mg/kg, kidney transplant recipient = 0.51 mL/h/kg.
Proteins and enzymes this drug interacts with in the body
PMID:12196291
May play a critical role in the early events of T-cell activation and costimulation of naive T-cells, such as deciding between immunity and anergy that is made by T-cells within 24 hours after activation .
PMID:7527824
Also involved in the regulation of B cells function, plays a role in regulating the level of IgG(1) produced. Upon CD40 engagement, activates NF-kappa-B signaling pathway via phospholipase C and protein kinase C activation (By similarity)
PMID:38467718
Acts as the primary auxiliary signal augmenting the MHC/TCR signal in naive T-cells together with the CD28 receptor which is constitutively expressed on the cell surface of T-cells .
PMID:12196291
In turn, activates different signaling pathways such as NF-kappa-B or MAPK leading to the production of different cytokines .
PMID:10438913
In addition, CD28/CD80 costimulatory signal stimulates glucose metabolism and ATP synthesis of T-cells by activating the PI3K/Akt signaling pathway .
PMID:12121659
Also acts as a regulator of PDL1/PDCD1 interactions to limit excess engagement of PDL1 and its inhibitory role in immune responses .
PMID:36727298
Expressed on B-cells, plays a critical role in regulating interactions between B-cells and T-cells in both early and late germinal center responses, which are crucial for the generation of effective humoral immune responses (By similarity)
PMID:1650475 PMID:7568038
Functions not only as an amplifier of TCR signals but delivers unique signals that control intracellular biochemical events that alter the gene expression program of T-cells .
PMID:24665965
Stimulation upon engagement of its cognate ligands CD80 or CD86 increases proliferation and expression of various cytokines in particular IL2 production in both CD4(+) and CD8(+) T-cell subsets .
PMID:1650475 PMID:35397202
Mechanistically, ligation induces recruitment of protein kinase C-theta/PRKCQ and GRB2 leading to NF-kappa-B activation via both PI3K/Akt-dependent and -independent pathways .
PMID:21964608 PMID:24665965 PMID:7568038
In conjunction with TCR/CD3 ligation and CD40L costimulation, enhances the production of IL4 and IL10 in T-cells PMID:8617933
ATC L04AA28
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)
Belatacept
Additional database identifiers
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1705
GenAtlas
CD86
GeneCards
CD86
GenBank Gene Database
L25259
GenBank Protein Database
439839
Guide to Pharmacology
2745
UniProt Accession
CD86_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1700
GenAtlas
CD80
GeneCards
CD80
GenBank Gene Database
M27533
GenBank Protein Database
306916
Guide to Pharmacology
2744
UniProt Accession
CD80_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1653
GeneCards
CD28
Guide to Pharmacology
2863
UniProt Accession
CD28_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