Brolucizumab 19.8mg/0.165ml solution for injection pre-filled syringes
Requires a prescription from a doctor or prescriber
Brolucizumab, also known as RTH258 or ESBA1008,[A187211] is a monoclonal antibody indicated to treat neovascular age related macular degeneration.[L9089] Brolucizumab was granted FDA approval in October 2019.[L9089]
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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 Brolucizumab
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1 branded products available
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Beovu 19.8mg/0.165ml solution for injection pre-filled syringes
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)
Brolucizumab for treating diabetic macular oedema (TA820)
Brolucizumab for treating wet age-related macular degeneration (TA672)
Diabetic retinopathy: management and monitoring (NG242)
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: 29 · Randomised trials: 4 · 2019–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Monés, S. Srivastava, G. Jaffe, et al.
Ophthalmology, 2020
L. Justino, G. B. Justino, Fabrissio Graffunder, et al.
Clinical Ophthalmology (Auckland, N.Z.), 2024
Bellucci C, Virgili M, Romano A, et al.
2025
Background: Laser Speckle Flowgraphy (LSFG) is a non-invasive imaging technology that quantitatively evaluates retinal and choroidal blood flow by analyzing speckle patterns generated by laser light scattering. This systematic review summarizes the application of LSFG in two major degenerative retinal diseases: age-related macular degeneration (AMD) and diabetic retinopathy (DR). Methods: A comprehensive literature search (2010-2025) was conducted in PubMed, Cochrane Library and EMBASE according to PRISMA guidelines. Twenty-three studies including a total of 974 eyes (191 AMD, 783 DR) were analyzed. Results: In AMD, LSFG detected baseline reductions in choroidal and retinal perfusion in non-exudative disease, often extending beyond atrophic regions. Anti-VEGF injections produced acute reductions in MBR, particularly with brolucizumab, with partial recovery over time; drug-specific differences suggest a potential impact on geographic atrophy progression. In DR, LSFG revealed early microvascular dysfunction even in asymptomatic eyes. Retinal and choroidal MBR and blowout score correlated with HbA1c, DR severity, and inflammatory mediators. Intravitreal anti-VEGF therapy consistently reduced retinal and choroidal MBR and RFV, while conventional panretinal photocoagulation decreased choroidal flow and vascular caliber more robustly than patterned laser, reflecting oxygenation-driven VEGF modulation. Low baseline MBR predicted higher central macular thickness and reduced therapeutic response in diabetic macular edema. Conclusions: LSFG provides reproducible, rapid, and non-invasive quantitative insights into ocular hemodynamics across degenerative retinal diseases. Its integration into multimodal imaging may facilitate early diagnosis, support personalized management, and assist in the prognostic assessment of retinal and choroidal vascular disorders.
Abstract licence: CC BY
Chen KY, Chan HC, Chan CM
2026
- Macular Degeneration
- Angiogenesis Inhibitors
- Vascular Endothelial Growth Factor A
IntroductionNeovascular age-related macular degeneration (nAMD) is a leading cause of irreversible vision loss in older adults. Intravitreal anti-vascular endothelial growth factor (VEGF) agents-including Aflibercept, Ranibizumab, Bevacizumab, Brolucizumab, and Faricimab-are the mainstay of therapy. However, their comparative efficacy and safety remain uncertain. This study aimed to compare the visual and systemic outcomes of these agents to inform clinical decision-making.MethodsA systematic search of PubMed, Embase, Scopus, and Web of Science from inception to September 2025 identified randomized controlled trials (RCTs) and observational studies comparing at least two anti-VEGF agents in nAMD. Eligible studies reported outcomes of best-corrected visual acuity (BCVA) change, visual gain ≥ 15 letters, mortality, or arteriothrombotic events. Risk of bias was assessed using Cochrane Risk of Bias 2 (RoB 2) and Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I) tools. A frequentist network meta-analysis estimated mean differences (MD) and odds ratios (OR) with 95 % confidence interval (CI). The protocol was registered in PROSPERO (CRD42025631298).ResultsSixteen studies involving 6758 participants (follow-up 3-24 months) met the inclusion criteria. For BCVA improvement, Aflibercept had the highest surface under the cumulative ranking curve (SUCRA) ranking (0.80), although all agents showed similar mean differences that were not statistically significant: aflibercept (MD 0.80; 95 % CI -1.20-2.80), Ranibizumab (0.64; -1.87-3.15), Bevacizumab (0.60; -2.02-3.22), Faricimab (2.20; -0.69-5.09), and Brolucizumab (4.20; -5.97-14.36). The larger point estimate for Brolucizumab reflects imprecision rather than superior visual efficacy. Mortality was lowest with Aflibercept (risk ratio (RR) 0.76; 95% CI 0.41-1.55). For arteriothrombotic events, no statistically significant differences were observed between anti-VEGF agents. Comparisons between Aflibercept and Bevacizumab (RR 1.11; 95% CI 0.60-2.07), aflibercept and Ranibizumab (RR 0.77; 95% CI 0.49-1.21), and Bevacizumab and Ranibizumab (RR 0.88; 95% CI 0.60-1.30) showed wide confidence intervals, reflecting substantial imprecision. Certainty of evidence (GRADE) ranged from moderate to low.ConclusionAll anti-VEGF agents stabilize or improve vision in nAMD. Aflibercept may provide the most favorable efficacy-safety balance, Faricimab offers promising durability, and Brolucizumab demonstrates large visual gains with potential safety concerns. Further head-to-head and long-term real-world studies are needed to optimize individualized treatment strategies.
Abstract licence: CC BY
Paneerselvam GS, Ng JW, Lim JS, et al.
2026
- Angiogenesis Inhibitors
- Vascular Endothelial Growth Factor A
- Cost-Benefit Analysis
ObjectivesTo evaluate the cost-effectiveness of VEGF inhibitors, ranibizumab, aflibercept, bevacizumab, brolucizumab, pegaptanib, and conbercept for wAMD treatment.MethodsA systematic search was conducted in PubMed, Cochrane, and SpringerLink databases to identify cost-effectiveness analyses and cost-utility analyses related to wAMD treatment. Eligible studies were assessed using Drummond's 10-point checklist to evaluate methodological quality. The extracted data included intervention costs, quality-adjusted life-years, and incremental cost-effectiveness ratios.ResultsTwenty-two studies met the inclusion criteria. Bevacizumab and brolucizumab were frequently reported as cost-effective alternatives, offering comparable or superior visual outcomes at lower costs than ranibizumab or aflibercept. Pegaptanib was consistently less cost-effective. Findings for ranibizumab versus aflibercept varied by treatment regimen and analytic assumptions. Across studies, cost-effectiveness estimates were influenced by model perspective, time horizon, exclusion of adverse events, and single-eye modeling. A further limitation is that in contexts of non-inferior efficacy, small incremental quality-adjusted life-years differences may artificially inflate incremental cost-effectiveness ratios, potentially overstating the costs relative to benefits.ConclusionsDecision making in wAMD treatment requires more thorough economic evaluations that incorporate standardized methodologies and lengthy cost assessments.
Abstract licence: CC BY
Krishnan B V, Kauser N, Priya G, et al.
2026
Diabetic macular edema (DME) is a leading cause of vision loss, with anti-vascular endothelial growth factor (VEGF) agents as standard therapy. However, comparative efficacy and safety remain debated. To evaluate anti-VEGF agents' efficacy/safety in DME by drug class, dosing, and baseline severity. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)-compliant meta-analysis of 21 studies (2010-2024) was conducted. Random-effects models pooled mean differences (MD) for visual acuity (VA) and central retinal thickness. Subgroup analyses assessed anti-VEGF types, dosing regimens, and baseline severity. Aflibercept showed superior VA gains in severe DME (+8.2 letters; 95% CI: 6.1-10.3) compared with bevacizumab (+3.7 letters). Faricimab demonstrated non-inferiority to ranibizumab with extended dosing (every 16 weeks; +10.1 letters). Bevacizumab biosimilars were cost-effective but required more injections. Brolucizumab was associated with a higher risk of intraocular inflammation (RR = 2.1, 95% CI: 1.6-2.6). Monthly regimens outperformed PRN (MD: +2.5 letters, p < 0.001). Aflibercept remains optimal for severe DME, while faricimab reduces treatment burden. Safety and cost considerations favor individualized therapy. Heterogeneity was extremely high (I² = 97.19%), indicating substantial variability in treatment effects across studies, only partially explained by differences in drug class, dosing regimens, and baseline severity. This high heterogeneity underscores the need for personalized treatment approaches and cautious interpretation of pooled estimates.
Abstract licence: CC BY
Christof Hänsli, Christin Schild, Isabel Pfister, et al.
Life, 2023
Ran Dou, Jian Jiang
PeerJ, 2024
Background To evaluate the efficacy and safety of Brolucizumab for neovascular age-related macular degeneration (n-AMD) through a systematic review and meta-analysis. Materials and Methods Cochrane, PubMed, Embase, and Web of Science databases were comprehensively searched for relevant studies. Stata and RevMan5.4 were applied for meta-analysis and risk of bias assessment. Data on the best-corrected visual acuity (BCVA), central subfield thickness (CSFT), presence of intraretinal fluid (IRF) and/or subretinal fluid (SRF), participants with ≥1 serious adverse events, and participants with ≥1 adverse events were analyzed. Results Six studies were finally included. Meta-analysis showed statistical differences in BCVA [SMD = −0.65, 95% CI [−0.17 to −0.23], P 0.05] or the safety of participants with ≥1 adverse events [RR = 1.07, 95% CI [0.97–1.17], P > 0.05]. Conclusions Compared to other anti-VEGF drugs such as Aflibercept and Ranibizumab, intravitreal injection of 6 mg Brolucizumab is more effective and safer for n-AMD, especially in the presence of IRF and/or SRF, and for participants with ≥1 serious adverse events.
Abstract licence: CC BY 4.0
Sørensen, Torben Lykke, Becher, Anja, Sébastien Balez, et al.
2023
Schild, Christin, Isabel B. Pfister, Pfister, Isabel B, et al.
2023
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
2.0 days
Mechanism
Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which targ…
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
3mg
Half-life
2.0 days
[L9089]
The elimination half life is 108h for a 3mg dose and 103h for a 6mg dose.
[L9104]
Protein binding
[A31470]
Volume of distribution
[L9089]
Metabolism
[A31470]
Elimination
[L9089]
…
Clearance
[L9089]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Brolucizumab was granted FDA approval in October 2019.[L9089]
[A187208][L9089]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 388 interactions
[L9089]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L9104]
A 6mg dose of brolucizumab reaches a Cmax of 77.6ng/mL with a Tmax of 17.4h and an AUC of 9169ng\*h/mL.
[L9104]
[L9089]
The elimination half life is 108h for a 3mg dose and 103h for a 6mg dose.
[L9104]
[A31470]
[L9089]
[A31470]
[L9089]
Monoclonal antibodies are generally not eliminated in the urine, and only a small amount is excreted in bile.
[A40006]
[L9089]
Proteins and enzymes this drug interacts with in the body
PMID:35455969
Involved in protecting cells from hypoxia-mediated cell death (By similarity)
ATC S01LA06
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)
Brolucizumab
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