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RA

ranibizumab (RTPR 024 / RTPR024 / RanizuRel)

✓ Approved

Reliance Life Sciences Private Limited · VEGFA · Monoclonal Antibodies

What is ranibizumab?

ranibizumab is a monoclonal antibodies developed by Reliance Life Sciences Private Limited. It is approved for therapeutic indications via injectable (others) or intraocular injection.

Drug Profile

Brand NamesRTPR 024, RTPR024, RanizuRel
CompanyReliance Life Sciences Private Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetVEGFA
RouteInjectable (Others), Intraocular Injection
StatusApproved
Sources: ClinicalTrials.gov, Reliance Life Sciences Private Limited

Mechanism of Action

Molecular Targets

ranibizumab acts on 1 molecular target:

VEGFAvascular endothelial growth factor A (VPF, MVCD1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

ranibizumab is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Eye disordersNeovascular age-related macular degeneration✓ Approved

Related Research Articles

PubMedClinical ophthalmology (Auckland, N.Z.)2026-09-20

Real-World Analysis of Switching Between Ranibizumab Biosimilars: Safety and Results - a Multicenter Retrospective Observational Study.

Chakraborty Debdulal D, Sinha Tushar Kanti TK, Biswas Rupak Kanti RK, Maiti Aniruddha A et al.

To describe disease-specific visual, anatomical, treatment-exposure, and documented safety outcomes over 24 weeks among eyes undergoing availability-driven switching between ranibizumab biosimilars in routine retinal practice in India. This multicenter retrospective observational cohort study reviewed records from January to December 2024. Baseline was the index-switch visit, before administration of the substituted ranibizumab biosimilar. Only one eye per patient was included; when both eyes were eligible, the right eye was selected by convention. Eligible eyes had at least one documented availability-driven biosimilar-to-biosimilar switch and complete 24-week follow-up. Outcomes were summarized descriptively because there was no non-switch comparator group. Of 742 screened eyes, 595 eyes from 595 patients met the inclusion criteria and received 1625 intravitreal ranibizumab biosimilar injections over 24 weeks (mean, 2.73 injections per eye). One switch was recorded in 466 eyes (78.3%) and two switches in 129 eyes (21.7%). Mean BCVA improved from 0.57 logMAR at baseline to 0.26 at 12 weeks and 0.32 at 24 weeks; the early visual improvement therefore attenuated modestly by week 24 but remained better than baseline. Mean central macular thickness decreased from 490.4 micrometers at baseline to 273.6 micrometers at 24 weeks. At final follow-up, 369 eyes (62.0%) gained at least two lines and 488 eyes (82.0%) maintained or improved vision. No endophthalmitis, retinal detachment, or treatment-related systemic adverse event was documented in the available clinical records. Eyes exposed to availability-driven switching between ranibizumab biosimilars showed favorable short-term visual and anatomical outcomes over 24 weeks. Because this retrospective study lacked a non-switch comparator and protocol-mandated safety or immunogenicity surveillance, it cannot establish an effect attributable to switching, comparative safety, equivalence, or formal interchangeability.

PMID 42763736
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PubMedJournal of medicine and life2026-09-17

Understanding anti-vascular endothelial growth factor medications: chemical properties, costs, and side effects.

Makhdoum Hanan H, Alharbi Abeer A, Alhazmi Shaden S, Alrehaili Ahlam A et al.

Vascular endothelial growth factor (VEGF) is an important driver of abnormal retinal neovascularization and increased vascular permeability. VEGF overexpression is associated with a number of retinal conditions, such as diabetic macular edema (DME), and neovascular age-related macular degeneration (nAMD). Anti-VEGF treatments have been the most common for these conditions and have improved vision by reducing abnormal blood vessel formation and leakage. This narrative review addressed the fact that the pharmacological properties, safety profiles, and cost-effectiveness of the currently marketed anti-VEGF intravitreal agents (i.e. bevacizumab, ranibizumab, aflibercept, brolucizumab, pegaptanib, and recently faricimab) differ and therefore, each of these agents, have their own unique molecular structure, target specificity, duration of action in the eye, and systemic circulation, each of which will affect the dosing intervals and treatment burden as well as the safety and adverse events associated with each drug. Aflibercept is a high-binding-affinity decoy receptor and is therefore distinct from faricimab, which is a dual-action (VEGF-A and angiopoietin-2) inhibitor. By contrast, ranibizumab, bevacizumab, brolucizumab, and pegaptanib are anti-angiogenic agents with different VEGF blockade profiles, which ultimately lead to distinct clinical outcomes and pharmacokinetic profiles. While anti-VEGF therapies are highly effective, the outcomes regarding safety, efficacy, and cost depend heavily on the study design and reflect the actual treatment paradigm and continuum of care within the healthcare system. The various attributes of agents should help personalize a patient's treatment approach while also addressing potential challenges related to the safety, efficacy, and longevity of treatment for retinal diseases.

PMID 42751623
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PubMedActa ophthalmologica2026-09-16

Safety of intravitreally applied epidermal growth factor receptor antibody panitumumab.

Bikbov Mukharram M MM, Kazakbaeva Gyulli M GM, Gilemzianova Leisan I LI, Panda-Jonas Songhomitra S et al.

To examine the safety of the epidermal growth factor (EGF) receptor antibody panitumumab intravitreally applied in patients with myopic macular degeneration (MMD) or neovascular age-related macular degeneration (AMD). Patients with MMD stage 4 underwent repeated intravitreal panitumumab injections in escalating doses, and patients with neovascular AMD received combined intravitreal ranibizumab/panitumumab injections, with single ranibizumab injections applied in between. The study included 28 patients. In the first cohort, 11 highly myopic patients with MMD stage 4 (age: 66.8 ± 6.3 years) received intravitreal panitumumab injections in doses of 0.6 mg (4 eyes; 1 × 1 injection, 3 × 2 Injections), 1.2 mg (4 eyes; 1 × 1 injection; 2 × 2 injections; 1 × 3 injections) and 1.8 mg (3 eyes; 1 × 1 injection, 2 × 2 injections), respectively, in intervals of 3.6 ± 1.8 months (first to second injection), and 4.7 months (second to third injection). At 3.7 ± 0.4 years (median: 3.6 years; range: 3.5-4.7 years) after the first injection, ten patients were re-examined, with no change in axial length (30.6 ± 1.0 vs. 30.7 ± 1.3; p = 0.66). A second cohort included 17 eyes with neovascular AMD and receiving bimonthly combined panitumumab/ranibizumab (1.2 mg/0.5 mg) injections (mean: 2.4 ± 0.5 injections). The mean follow-up period was 11.0 ± 1.0 months (median: 11 months; range: 6-14 months). In none of the eyes of the first and second cohort, treatment-related systemic or intraocular adverse events were noted. Ocular side effects were hyposphagmata at the injection sites. Signs of intraocular inflammation were not detected in any eye. The morphology of the optic nerve head did not change significantly, nor did the IOP (14.5 ± 4.3 mmHg vs. 13.5 ± 1.5 mmHg; p = 0.30). Repeated intravitreal panitumumab applications in various doses, single or combined with ranibizumab, were not associated with severe ocular or systemic side effects.

PMID 42747171
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PubMedJournal of clinical medicine2026-09-15

Comparative Histopathological Effects of Intra-Articular Bevacizumab, Ranibizumab, and Aflibercept in Experimental Osteoarthritis.

Dalaslan Raşit Emin RE, Arıcan Mehmet M, Karaduman Zekeriya Okan ZO, Yücel Mücahid Osman MO et al.

Background: Vascular endothelial growth factor (VEGF) has emerged as a potential therapeutic target in osteoarthritis (OA). Although several anti-VEGF agents are widely used in clinical practice, their comparative effects on osteoarthritic cartilage remain unclear. This study compared the histopathological effects of intra-articular bevacizumab, ranibizumab, and aflibercept in an experimental rat model of OA. Methods: Experimental OA was induced in 36 rats using anterior cruciate ligament transection. One month later, animals received two intra-articular injections of bevacizumab (2 mg/kg), ranibizumab (0.5 mg/kg), aflibercept (3.2 mg/kg), or saline at 3-week intervals. Histopathological evaluation was performed using the Osteoarthritis Research Society International (OARSI) grading and staging system by two blinded pathologists. The primary outcome was the total OARSI score. Group comparisons were performed using the Kruskal-Wallis test followed by Dunn-Holm post hoc analysis. Results: Three animals were lost during anesthesia and surgical induction of OA before treatment allocation, leaving 33 rats for analysis. Significant overall differences were observed among the groups for the primary outcome of total OARSI score (p = 0.026) and the secondary outcomes of OARSI grade (p = 0.042) and OARSI stage (p = 0.019). Ranibizumab demonstrated numerically lower OARSI grade and total scores than the control group, whereas both groups had the same median OARSI stage score. Bevacizumab showed numerically lower OARSI grade and total scores than the control group but a slightly higher median stage score. Pairwise analysis showed significantly lower OARSI stage and total OARSI scores in the ranibizumab group than in the aflibercept group, whereas no significant differences were observed between any treatment group and the control group after correction for multiple comparisons. Conclusions: Anti-VEGF agents demonstrated differential histopathological responses in experimental OA. Although no treatment significantly improved histopathological outcomes compared with the control group after adjustment for multiple comparisons, ranibizumab showed lower OARSI stage and total scores than aflibercept. These findings indicate that the evaluated anti-VEGF agents may not exert equivalent biological effects and warrant further investigation in adequately powered experimental studies.

PMID 42739571
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PubMedInternational journal of molecular sciences2026-09-15

Molecular Determinants of Intravitreal Anti-VEGF Durability: Drug Architecture, Intraocular Pharmacokinetics, Target Biology and Treatment Resistance.

Panos Georgios D GD, Empeslidis Theo T, Amaxilati Efstratia E, Tsiropoulos Georgios N GN et al.

Intravitreal inhibition of vascular endothelial growth factor (VEGF) has transformed the management of neovascular age-related macular degeneration, diabetic macular oedema and macular oedema secondary to retinal vein occlusion, but frequent monitoring and retreatment remain major burdens. Ocular half-life is often used as shorthand for durability, although the clinical interval is produced by a wider molecular and biological system. This narrative review examines how dose, molecular format, hydrodynamic size, binding affinity, valency, ligand spectrum, target turnover, tissue distribution and delivery architecture determine the time for which an eye remains controlled. Human ocular pharmacokinetic and pharmacodynamic evidence is interpreted according to compartment, assay and model provenance, with particular attention to the distinction between drug elimination, free-ligand suppression, anatomical control and protocol-assigned treatment interval. Trial evidence for ranibizumab, aflibercept, conbercept, brolucizumab and faricimab shows that extended dosing can arise from greater starting exposure, altered binding architecture or pathway expansion without a proportionate change in intrinsic ocular half-life. Patient phenotype and retreatment rules further modify the observed interval. Refillable reservoirs, biodegradable depots and ocular gene therapy change the governing kinetics from bolus elimination to controlled release or sustained local production, thereby increasing the importance of reversibility and cumulative safety. We propose that durability be defined as a time-to-threshold phenotype integrating active target-site exposure, biological demand, anatomical recurrence, all treatment-related procedures and safety. Standardised estimands, longitudinal human ocular sampling, spatial exposure methods and externally validated mechanism-informed models are needed to make molecular durability comparable and clinically actionable.

PMID 42737684
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PubMedDiabetes, obesity & metabolism2026-09-10

Renal Safety of Intravitreal Ranibizumab and the Effects of SGLT2 Inhibition in Diabetic Macular Oedema: A Post Hoc Analysis of the COMET Trial.

Sakai Toshiki T, Ishibashi Ryoichi R, Koshizaka Masaya M, Takatsuna Yoko Y et al.

To evaluate whether intravitreal ranibizumab (IVR) frequency is associated with longitudinal renal markers in diabetic macular oedema (DMO) and whether the expected systemic renal and haematological effects of SGLT2 inhibition are reproduced. In this post hoc sub-analysis of the prospective COMET randomised controlled trial, 53 participants were analysed. The estimated glomerular filtration rate (eGFR), haematocrit (Hct), and urinary albumin-to-creatinine ratio (UACR) were assessed over 48 weeks using linear mixed-effects models with the treatment group, week, group-by-week interaction, and cumulative IVR as fixed effects. Baseline eGFR was preserved (72.2 ± 18.5 mL/min/1.73 m2) despite common albuminuria (median UACR 50.6 mg/gCr); mean cumulative IVR at week 48 was 7.00 ± 4.42. Cumulative IVR was not significantly associated with eGFR (-0.22 mL/min/1.73 m2 per injection; 95% CI -0.59 to 0.15; p = 0.25), ln(UACR), or Hct. The SGLT2 inhibitor reproduced an early eGFR dip and Hct rise. No statistically significant exposure-response association was detected between cumulative IVR and renal markers within the COMET trial cohort and dosing range. Because all participants received IVR and the sample size was modest, small cumulative renal effects cannot be excluded. University Hospital Medical Information Network Center (UMIN000057674); Japan Registry of Clinical Trials (jRCTs031180210, parent COMET trial).

PMID 42717542
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