Rimexolone 10mg/ml eye drops
Rimexolone is a 1% eye drop solution is a glucocorticoid steroid.
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Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Rimexolone
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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.
EudraVigilance
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Suspected adverse reactions reported for Rimexolone
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8 branded products available
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
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Supply & safety information
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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
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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 all 38 studies.
Randomised trials: 1 · Trials: 2 · 1980–2026
Showing all 38 studies, sorted by most relevant.
Pleyer U, Ursell PG, Rama P
2013
The efficacy of topical corticosteroids as ocular anti-inflammatory agents following cataract surgery is well-documented. They also help to prevent a number of complications associated with post-operative ocular inflammation, including corneal edema and cystoid macular edema. However, topical corticosteroids are associated with side effects, such as increased intraocular pressure (IOP). Indeed, corticosteroid-induced ocular hypertension and the potential for steroid-induced glaucoma remain the leading drawbacks of topical corticosteroid therapy. Some individuals are known to experience a high degree of IOP elevation with low doses or short durations of treatment with topical corticosteroids. Careful monitoring of IOP in such individuals is essential. Few randomized, controlled studies are available on the comparative safety and efficacy of common topical corticosteroids in the treatment of post-operative ocular inflammation. Furthermore, the lack of consistent reporting criteria for clinically significant IOP increases across clinical studies makes meaningful comparisons among corticosteroids difficult. This review aims to examine data from available published studies, including studies in steroid responders, to determine whether topical corticosteroids are the same in terms of their effect on IOP. Early generation corticosteroids, such as dexamethasone and prednisolone, are more likely to result in clinically significant increases in IOP. Newer corticosteroids, such as rimexolone and the retro-metabolically designed corticosteroid, loteprednol etabonate, offer similar anti-inflammatory efficacy to older corticosteroids with less effect on IOP. However, randomized controlled trials of newer corticosteroids are needed. The proportion of patients exhibiting an increase of ≥10 mmHg IOP in clinical studies has emerged as the most clinically relevant parameter for ophthalmologists to consider when deciding on which topical corticosteroid to use.
Abstract licence: CC BY-NC
Gao TL, Geng S, Chen J, et al.
2026
Alzheimer's disease (AD) is a multifactorial neurodegenerative condition in which accumulating genetic and molecular evidence implicates dysregulation of peripheral immune processes in disease pathogenesis. Nevertheless, the contribution of distinct peripheral immune cell subsets and associated gene regulatory landscapes to AD risk remains incompletely defined. To address this gap, we integrated single-cell expression quantitative trait loci (sc‑eQTL) data from the OneK1K cohort with AD GWAS summary statistics. We systematically interrogated immune cell-specific genes for their contributions to AD risk by integrating genetic causal inference with Bayesian colocalization analyses, and identified 24 eGenes that passed both the MR significance threshold (P 0.8). Notable candidates included GATS, HLA-DOB, HLA-DQA1, PM20D1, and others, with each gene demonstrating a cell-type-specific association restricted to its corresponding immune cell type, such as monocytes, CD8 + T cells, or B cells. Independent peripheral blood single-cell transcriptomic data further supported disease-associated shifts in cell-type-specific expression patterns in AD. Phenome-wide association studies (PheWAS) indicated limited associations with off-target traits, indicating a favorable safety profile for therapeutic intervention, with the exceptions of B4GALNT3, PM20D1, and CNN2. Integration of immune gene targets with pharmacological databases yielded three candidate compound, including NSC321521 (targeting HLA-DQA1), phenoxybenzamine (targeting GSTP1), and rimexolone (targeting BIN1). Among these compounds, Predicted blood-brain barrier permeability was observed only for phenoxybenzamine and rimexolone, with docking studies indicating stable interactions, such as those between NSC321521 and HLA-DQA1, phenoxybenzamine and GSTP1, and rimexolone and BIN1. This integrative approach highlights key immune‑cell‑specific genes involved in AD and proposes repurposable drugs with central nervous system potential, paving the way for more targeted immunomodulatory strategies in AD.
Abstract licence: CC BY
C. STEPHEN FOSTER, GEORGE ALTER, L. RAYMOND DEBARGE, et al.
American Journal of Ophthalmology, 1996
Howard M. Leibowitz
Archives of Ophthalmology, 1996
Chen YH, Gepstein R, Sharief L, et al.
2020
- Visual Acuity
- Glaucoma
- Uveitis, Anterior
Reactions Weekly, 2020
Mohamed Karim Sidky, Ahmed Mohamed Sherif, Nancy Maher Lotfy
Cataract and Cornea Journal of the Egyptian Society of Cataract and Corneal Diseases, 2017
Abeer T. Al Hanaineh, Dina H. Hassanein, Sameh H. Abdelbaky, et al.
Journal of American Association for Pediatric Ophthalmology and Strabismus, 2017
Dorothy S. P. Fan
Archives of Ophthalmology, 2003
- Strabismus
- Ocular Hypertension
- Inflammation
Kerry K. Assil, Guy Massry, Robert Lehmann, et al.
Journal of Cataract and Refractive Surgery, 1997
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
1-2 hours
Mechanism
Rimexolone is a glucocorticoid receptor agonist.
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
1-2 hours
Metabolism
80%
Elimination
80%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 264 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:27120390 PMID:37478846
Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors .
PMID:28139699
Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Involved in chromatin remodeling .
PMID:9590696
Plays a role in rapid mRNA degradation by binding to the 5' UTR of target mRNAs and interacting with PNRC2 in a ligand-dependent manner which recruits the RNA helicase UPF1 and the mRNA-decapping enzyme DCP1A, leading to RNA decay .
PMID:25775514
Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth (By similarity)
Requires dimerization and the coactivator, PGC-1A, for full activity. The ERRalpha/PGC1alpha complex is a regulator of energy metabolism. Induces the expression of PERM1 in the skeletal muscle
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
ATC H02AB12
ATC S01BA13
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)
Rimexolone
Additional database identifiers
Drugs Product Database (DPD)
187
ChemSpider
4470902
BindingDB
50103606
ZINC
ZINC000003945984
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7978
GenAtlas
NR3C1
GeneCards
NR3C1
GenBank Gene Database
X03225
GenBank Protein Database
31680
Guide to Pharmacology
625
UniProt Accession
GCR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3471
GeneCards
ESRRA
GenBank Gene Database
X51416
GenBank Protein Database
36609
Guide to Pharmacology
622
UniProt Accession
ERR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1540
GenAtlas
SERPINA6
GeneCards
SERPINA6
GenBank Gene Database
J02943
GenBank Protein Database
179971
UniProt Accession
CBG_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