Nepafenac 3mg/ml eye drops
Requires a prescription from a doctor or prescriber
Nepafenac is a non-steroidal anti-inflammatory prodrug (NSAID) usually sold as a prescription eye drop.
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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 Nepafenac
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Nevanac 3mg/ml eye drops
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. 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.
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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: 11 · Randomised trials: 21 · 2000–2026
Showing the 50 most relevant studies, sorted by most relevant.
Almasri M, Ismaiel A, Gavris I, et al.
2024
- Anti-Inflammatory Agents, Non-Steroidal
- Phacoemulsification
- Visual Acuity
The aim of this Network Meta-analysis was to compare the efficacy of the different topical Nonsteroidal anti-inflammatory drugs (NSAIDs) when added or not to topical steroids in preventing the thickening of the macula and their impact on visual acuity and intraocular pressure after phacoemulsification. Five electronic databases were searched, including PubMed, Embase, Scopus, Cochrane Library, and ClinicalTrials.gov. Our primary outcome was one-month post-surgery visual outcome. We also considered change in Foveal thickness (FT) and Intraocular pressure (IOP) at one-month post-surgery. We summarized our analyses by calculating the mean differences (MD) with associated 95% confidence intervals (CI) using restricted maximum likelihood in random effects models for continuous outcomes. The methodological quality of the studies was assessed with Cochrane Collaboration's tool. The network meta-analysis was conducted using frequentist approach considering Nepafenac 0.1% as a reference medication. Eleven Randomized controlled trials (RCTs) including 2175 subjects were selected for quantitative analysis. At one-month post-surgery, Bromfenac had statistically significant better visual acuity compared to Nepafenac 0.1% (p < 0.001), regarding FT, Nepafenac 0.3% had the least increase in FT compared to Nepafenac 0.1% (p = 0.09), regarding IOP, Diclofenac had the lowest IOP. No significant results regarding FT and IOP. Interestingly Ketorolac had the worst results regarding BCVA and IOP, and came last but one for FT. Overall, our network meta-analysis demonstrated that Bromfenac was associated with a significant improvement in visual acuity compared to Nepafenac 0.1% at one-month following cataract surgery, while Nepafenac 0.3% was associated with the least increase in foveal thickness.
Abstract licence: CC BY
Xinyu Zhao, Song Xia, E. Wang, et al.
PLoS ONE, 2017
As a new ophthalmic non-steroidal anti-inflammatory drug (NSAID) with prodrug structure, Nepafenac was supposed to have a better efficacy than conventional NSAIDs both in patients’ tolerability and ocular inflammation associated with cataract surgery. However, many current studies reached contradictory conclusions on the superiority of Nepafenac over Ketorolac. The objective of our study is to evaluate the efficacy and patients’ tolerability of Nepafenac and Ketorolac following cataract surgery. To clarify this, we conducted a meta-analysis of randomized controlled trials. Eleven articles were included in this study. The dataset consisted of 1165 patients, including 1175 cataract surgeries. Among them, 574 patients were in the Nepafenac group and 591 in the Ketorolac group. Our analysis indicated that these two drugs were equally effective in controlling post cataract surgery ocular inflammation, reducing macular edema, achieving a better visual ability and maintaining intraoperative mydriasis during cataract surgery. However, Nepafenac was more effective than Ketorolac in reducing the incidence of postoperative conjunctival hyperemia and ocular discomfort. This meta-analysis indicated that topical Nepafenac is superior to Ketorolac in patients’ tolerability following cataract surgery. However, these two drugs are equally desirable in the management of anterior chamber inflammation, visual rehabilitation and intraoperative mydriasis. Given the limitations in our study, more researches with larger sample sizes and focused on more specific indicators such as peak aqueous concentrations of drugs or PEG2 levels are required to reach a firmer conclusion.
Abstract licence: CC BY 4.0
Ibrahim RMM, Abdelkadous SG, Macky TA, et al.
2024
- Macula Lutea
- Benzeneacetamides
- Phenylacetates
Ben Klinghoffer, Asaf Achiron, Elad Eilon, et al.
Journal of refractive surgery, 2026
- Benzeneacetamides
- Phenylacetates
- Cyclopentolate
A. Djatikusumo, A. Victor, Rina La Distia Nora, et al.
Journal of Retina-Vitreous, 2026
Burgos MSM, Mendoza JCR, Burgos LCM, et al.
2026
Abstract Background Retinopathy of prematurity (ROP) is a leading cause of preventable childhood blindness worldwide. Although timely screening and treatment remain the cornerstone of management, specialist shortages, referral delays, geographic barriers, and unreliable follow-up continue to compromise care delivery in many settings. In response to these challenges, some clinicians have adopted off-label topical nonsteroidal anti-inflammatory drug prophylaxis for early-stage disease despite limited supporting evidence. This study compared real-world clinical outcomes associated with topical ketorolac or nepafenac prophylaxis for stage 1–2 ROP with those associated with standard screening and historical surveillance-only care. Methods This multicenter retrospective cohort study included preterm infants screened for ROP at 14 institutions in Colombia. Infants receiving ketorolac or nepafenac prophylaxis (2019–2025) were analyzed separately compared with a historical cohort managed with surveillance only (2011–2018). The same consulting retina specialist performed all examinations and made all treatment decisions. The primary outcome was progression to treatment-requiring ROP by 60 weeks postmenstrual age. Secondary outcomes included time to progression, time to regression without rescue treatment, retreatment, and number of ophthalmic follow-up visits. Results The final analysis cohort included 192 infants: 98 in the nepafenac group, 48 in the ketorolac group, and 46 in the historical comparison group. Progression to treatment-requiring ROP occurred in 20.83% of ketorolac-treated infants and 22.45% of nepafenac-treated infants, compared with 45.65% in the historical cohort (relative risk 0.46 [95% CI 0.24–0.86] and 0.49 [0.30–0.80], respectively; number needed to treat 4 for both). Both agents were associated with fewer follow-up visits and faster regression. After adjustment, ketorolac remained associated with lower odds of progression (odds ratio 0.28 [95% CI 0.09–0.87]). No major prophylaxis-related adverse effects were reported. Conclusions Prophylaxis showed a clinically relevant real-world signal in early-stage ROP, but the adjusted findings were more internally coherent for ketorolac. Randomized controlled trials are needed to determine efficacy, safety, and economic value.
Abstract licence: CC BY
Muhammad Ahmed, Shujah ur Rehman, Muhammad Ali
Insights – Journal of Health and Rehabilitation, 2025
Cansu Özcan Pehlivan, Esra Arıcan, Burak Turgut, et al.
Annals of Clinical and Analytical Medicine, 2026
Ayala Pollack, Giovanni Staurenghi, Dana Sager, et al.
British Journal of Ophthalmology, 2016
Claudio Campa, Giulia Salsini, P. Perri
Current Eye Research, 2018
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
4 found
Half-life
Not available
Mechanism
Nepafenac is a prodrug.
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Protein binding
95.4%
Metabolism
Elimination
85%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 156 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:7947975
Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells (Probable).
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity)
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
ATC S01BC10
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)
Nepafenac
Additional database identifiers
Drugs Product Database (DPD)
20215
ChemSpider
133160
BindingDB
50228731
ZINC
ZINC000005162311
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9604
GenAtlas
PTGS1
GeneCards
PTGS1
GenBank Gene Database
M31822
GenBank Protein Database
387018
Guide to Pharmacology
1375
UniProt Accession
PGH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_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