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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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 Nepafenac
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1 branded products available
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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: 15 · 2007–2026
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
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
Ari Djatikusumo, Andi Arus Victor, Rina La Distia Nora, et al.
Journal of Retina-Vitreous, 2026
C. Campa, Giulia Salsini, P. Perri
Current Eye Research, 2018
Atsushi Kawahara, Tsugiaki Utsunomiya, Yuji Kato, et al.
Clinical Ophthalmology, 2016
Atsushi Kawahara,1–3 Tsugiaki Utsunomiya,4 Yuji Kato,2 Yoshinori Takayanagi3 1Department of Ophthalmology, Sapporo Tokushukai Hospital, Sapporo, Hokkaido, Japan; 2Sapporo Kato Eye Clinic, Sapporo, Hokkaido, Japan; 3Takayanagi Clinic, Kushiro, Hokkaido, Japan; 4Department of Ophthalmology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan Background: The aim of this study was to compare the effects of nepafenac ophthalmic suspension 0.1% (Nevanac) and diclofenac sodium ophthalmic solution 0.1% (Diclod) on the cornea, tear film, and ocular surface after cataract surgery. Methods: A total of 60 eyes (60 patients) were selected for this study, with no ocular diseases other than cataract (scheduled for cataract surgery by one surgeon). Patients were randomly enrolled to receive nepafenac or diclofenac in the perioperative period, and cataract surgery was performed using torsional microcoaxial phacoemulsification and aspiration with intraocular lens implantation via a transconjunctival single-plane sclerocorneal incision at the 12 o’clock position. We compared intra- and intergroup differences preoperatively and postoperatively in conjunctival and corneal fluorescein staining scores, tear film breakup times, Schirmer’s tests, the Dry Eye Related Quality of Life Scores, and tear meniscus areas using anterior segment optical coherence tomography. Results: The diclofenac group had significantly higher conjunctival and corneal fluorescein staining scores at 4 weeks postoperatively compared with the nepafenac group (P<0.001). Within the diclofenac group, significantly higher conjunctival and corneal fluorescein staining scores were noted at 4 weeks postoperatively than those seen preoperatively (P<0.001) and at 1 week postoperatively (P<0.001). No statistically significant differences were found in any other items. Conclusions: Nepafenac ophthalmic suspension 0.1% is considered safe for the corneal epithelium after cataract surgery. Keywords: nepafenac, diclofenac, cornea, tear film, ocular surface, cataract surgery
Abstract licence: CC BY-NC 3.0
Alexander Aaronson, A. Achiron, R. Tuuminen
Journal of Clinical Medicine, 2020
Abstract Background: To evaluate the clinical course of pseudophakic cystoid macular edema (PCME) treated with topical non-steroidal anti-inflammatory drugs (NSAIDs). Methods: An analysis of the clinical course of PCME consisting of 536 eyes of 536 patients from five consecutive randomized clinical trials aimed at the optimization of anti-inflammatory medication in patients undergoing routine cataract surgery. PCME was classified as (i) grade 0a; no macular thickening, (ii) grade 0b; macular thickening (central subfield macular thickness (CSMT) increase of at least 10%) without signs of macular edema, (iii) grade I; subclinical PCME, (iv) grade II; acute PCME, (v) grade III; long-standing PCME. Eyes with PCME classification from grade I onwards were treated with nepafenac 1 mg/mL t.i.d. for two months. Results: CSMT increase of at least 10% at any postoperative timepoint with cystoid changes—a criterion for PCME—was found in 19 of 536 eyes (total incidence 3.5%). Of these 19 eyes, 13 eyes (total incidence 2.4%) had clinically significant PCME. PCME was considered clinically significant when both of the following visual acuity criteria were fulfilled. At any timepoint after the cataract surgery both the corrected distance visual acuity (CDVA) gain was less than 0.4 decimals from that of preoperative CDVA, and the absolute CDVA level remained below 0.8 decimals. Only one of the 19 eyes with criteria for PCME (total incidence 0.2%, incidence of PCME eyes 5.3%) showed no macular edema resolution within 2 months after topical nepafenac administration. Conclusions: PCME in most cases is self-limiting using topical nepafenac without any further need for intravitreal treatment.
Abstract licence: CC BY 4.0
E. Mandelcorn, Mohammed Alfalah, Lei Zhao, et al.
Acta Ophthalmologica, 2021
Richard I Kaplan, Owen J. Drinkwater, Rachel H. Lee, et al.
Ophthalmology. Retina, 2019
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