Latanoprost 50micrograms/ml eye drops
Requires a prescription from a doctor or prescriber
Latanoprost is a prodrug analog of prostaglandin F2 alpha that is used to treat elevated intraocular pressure (IOP).
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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 Latanoprost
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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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Latanoprost
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
28 branded products available
MHRA licensed products
View all licensed products for Latanoprost on the MHRA register
Xalatan 50micrograms/ml eye drops
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Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/ml eye drops
Latanoprost 50micrograms/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.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Latanoprost–netarsudil for previously treated primary open-angle glaucoma or ocular hypertension (TA1009)
Glaucoma: diagnosis and management (NG81)
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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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
Browse tools
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: 20 · Randomised trials: 21 · 1998–2026
Showing the 50 most relevant studies, sorted by most relevant.
D. Garway-Heath, D. Crabb, C. Bunce, et al.
Lancet, 2015
Robert S. Noecker, Monte S. Dirks, Neil T. Choplin, et al.
American Journal of Ophthalmology, 2003
Peng J, Huang W, Duan J
2025
ObjectiveTo evaluate and compare the effectiveness and safety of latanoprost, bimatoprost, travoprost, and tafluprost in lowering intraocular pressure (IOP) in individuals with glaucoma or ocular hypertension.MethodsWe searched PubMed, Embase, Web of Science, and the Cochrane Library for randomized controlled trials (RCTs) published up to April 2025 comparing latanoprost, bimatoprost, travoprost, and tafluprost in adults with glaucoma or ocular hypertension. Primary outcomes were IOP reduction and conjunctival hyperemia. We assessed study quality using the Cochrane Risk of Bias 2.0 tool. Evidence certainty was evaluated with the CINeMA framework. A Bayesian network meta-analysis was conducted in RStudio. This review is registered with PROSPERO (CRD420251034803).Results25 RCTs published between 2001 and 2024, involving 4,045 participants, were included. All studies compared monotherapy with latanoprost, bimatoprost, travoprost, or tafluprost. Among these, bimatoprost showed the most effective reduction in intraocular pressure compared to latanoprost [mean difference (MD) 0.69; 95%confidence interval (CI) 0.28-1.1; SUCRA 95.6%; moderate confidence]. It also performed significantly better than travoprost (MD 0.64; 0.14-1.09; 39.2%; low confidence). No other comparisons showed statistically significant differences. Overall, the quality of evidence for this outcome ranged from low to moderate. In terms of safety, 16 trials, including 3,119 participants, reported on conjunctival hyperemia. Both bimatoprost [odds ratio (OR) 3.3; 2.5-4.5; 18.4%, high confidence] and travoprost (0.46; 0.33-0.63; 55%, high confidence) were associated with a higher risk of hyperemia compared to latanoprost. Bimatoprost also posed a significantly greater risk than travoprost (1.51; 1.06-2.16, high confidence).ConclusionBimatoprost provided the greatest IOP reduction but carried a higher risk of conjunctival hyperemia. Latanoprost and tafluprost offered balanced efficacy with better tolerability, making them suitable for patients with mild disease.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251034803.
Abstract licence: CC BY
H. Uusitalo, Evgeniy N. Egorov, K. Kaarniranta, et al.
Clinical Ophthalmology (Auckland, N.Z.), 2016
Alfatih M, Wunardi C, Amaral DC, et al.
2026
- Ocular Hypertension
- Glaucoma
- Antihypertensive Agents
Chen KY, Chan HC, Chan CM
2026
This study systematically evaluates the efficacy, safety, tolerability, and contemporary clinical positioning of topical pilocarpine in the management of glaucoma and ocular hypertension. This systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. PubMed/MEDLINE, EMBASE, Cochrane CENTRAL via the Cochrane Library, Scopus, Web of Science Core Collection, and Google Scholar were searched from inception to 1 May 2026 without language restrictions. Randomized controlled trials and controlled observational studies in adults with glaucoma or ocular hypertension were eligible when topical pilocarpine, used alone or in combination, was compared with placebo, no treatment, laser trabeculoplasty, or other intraocular pressure (IOP)-lowering therapies. The primary outcome was mean change in IOP, and secondary outcomes included responder outcomes, ocular adverse events, discontinuation, visual field outcomes, medication burden, post-laser pressure spikes, and postoperative outcomes. Risk of bias was assessed with the Cochrane Risk of Bias 2.0 tool (RoB 2.0) for randomized studies and the Risk of Bias in Nonrandomized Studies of Interventions (ROBINS-I) tool for nonrandomized studies. We performed random-effects meta-analysis using raw mean difference in mmHg for continuous outcomes and risk ratio (RR) for binary safety outcomes, each reported with a 95% confidence interval (CI); certainty of evidence was assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Of the 38 studies that met the inclusion criteria, 34 contributed data to the quantitative meta-analysis. In the primary analysis, pilocarpine-containing regimens reduced IOP by an additional 1.16 mmHg compared to all comparators (95% CI 0.84 to 1.47; P 2 = 50.7%). Subgroup analyses suggested larger pooled effects in placebo/no-treatment comparisons, ocular hypertension, primary open-angle glaucoma, and monotherapy studies; however, comparisons with beta-blockers and prostaglandin analogs require cautious interpretation because several large individual trials favored timolol or latanoprost for daily clinical use, tolerability, or dosing convenience. Pilocarpine was associated with a sevenfold higher risk of blurred vision (RR 7.33; 95% CI 3.30 to 16.29) and a sixfold higher risk of discontinuation due to adverse events (RR 6.07; 95% CI 3.69 to 10.00). Egger's test pointed to funnel plot asymmetry (P = 0.003), although the trim and fill method did not impute any missing studies. Pilocarpine lowers IOP effectively, but its modern role is limited by frequent dosing, miosis, blurred vision, accommodative symptoms, brow ache, and higher discontinuation. In current glaucoma care, prostaglandin analogs and selective laser trabeculoplasty are generally more consistent with first-line open-angle glaucoma management, whereas pilocarpine is better positioned for selected clinical scenarios, including angle-closure mechanisms, post-laser pressure-spike prophylaxis, selected postoperative angle-surgery settings, intolerance or nonresponse to other drug classes, and resource-limited settings where newer therapies are unavailable or unaffordable.
Abstract licence: CC BY
W Y Zhang
British Journal of Ophthalmology, 2001
H. Tanihara, Toshihiro Inoue, Tetsuya Yamamoto, et al.
JAMA ophthalmology, 2015
S. Asrani, A. Robin, J. Serle, et al.
American journal of ophthalmology, 2019
Jong-wook Lee, Hyeon-Soo Ahn, Jin-Ho Chang, et al.
Korean Journal of Ophthalmology : KJO, 2022
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
17 minutes
Mechanism
Elevated intraocular pressure leads to an increased risk of glaucomatous visual field loss.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
5 minutes
Half-life
17 minutes
[A184493][L8357]
…
Protein binding
90%
[L8402]
Volume of distribution
0.02 L/kg
Metabolism
Elimination
88%
Clearance
7 mL/min/kg
[L8357]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L8357][L8402][L44401]
It is available as monotherapy or in a combination product with [netarsudil] [L8369] or [timolol].
[L15217]
In Canada, latanoprost is also indicated to treat elevated intraocular pressure due to angle-closure glaucoma that has been treated with peripheral iridotomy or laser iridoplasty.
[L8402]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 113 interactions
[L8360]
An overdose of latanoprost is not expected to result in dangerous patient outcomes, however, conjunctival or episcleral hyperemia may occur.
[L8357]
An intravenous infusion of 3 μg/kg of latanoprost in healthy volunteers led to mean plasma concentrations 200 times higher than a normally administered therapeutic dose and no adverse effects were noted.
[L8357]
One study suggested that an overdose of latanoprost leads to cystoid macular edema after a large, unintended overdose. This resolved within 4 weeks after 4 weeks following treatment with nepafenac 0.3% eye drops in addition to oral acetazolamide.
[A184538]
Contact the local poison control center for updated guidance on managing a latanoprost overdose.
A note on eye and periorbital changes
Between 3 to 10% of patients taking latanoprost have experienced iris pigmentation after about 3-4 months of latanoprost use.[A982][A184490] Patients should be notified of this risk before initiating treatment. It may occur in both patients with light-colored irides (green-brown or blue/grey-brown) or dark-colored (brown) irides, but is less pronounced in the latter group.[A982] This drug may also cause other ocular effects including infrequent conjunctival hyperemia, pigmentation of periocular tissues, eyelash changes, hypertrichosis, and ocular irritation.[A184493][L8357]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A184490]
The Cmax of latanoprost in the systemic circulation is reached after 5 minutes and is measured to be 53 pg/mL. The Cmax in the aqueous humor is attained within 2 hours after administration.
[A184493][L8357]
and has been estimated to be 15-30 ng/mL.
[A184493]
[A184493][L8357]
The elimination half-life of latanoprost from the eye is estimated at 2–3 hours.
[A184493]
[L8402]
[L8357]
This drug is more lipophilic than its parent prostaglandin and easily penetrates the cornea.
[A184490]
It has been shown to cross the placenta in rats.
[L8402]
[A184490][A184493][L8357]
[A184490][L8357]
About 15% of a dose is reported to be excreted in the feces.
[L8402]
[L8357]
Proteins and enzymes this drug interacts with in the body
Isoforms 2 to 7 do not bind PGF2-alpha but are proposed to modulate signaling by participating in variant receptor complexes; heterodimers between isoform 1 and isoform 5 are proposed to be a receptor for prostamides including the synthetic analog bimatoprost
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11997326 PMID:26692285 PMID:8787677
PGs and thromboxanes play fundamental roles in diverse functions such as intraocular pressure, gastric acid secretion, renal salt and water transport, vascular tone, and fever .
PMID:15044627
Plays a role in the clearance of PGs from the circulation through cellular uptake, which allows cytoplasmic oxidation and PG signal termination .
PMID:8787677
PG uptake is dependent upon membrane potential and involves exchange of a monovalent anionic substrate (PGs exist physiologically as an anionic monovalent form) with a stoichiometry of 1:1 for divalent anions or of 1:2 for monovalent anions .
PMID:29204966
Uses lactate, generated by glycolysis, as a counter-substrate to mediate PGE2 influx and efflux .
PMID:11997326
Under nonglycolytic conditions, metabolites other than lactate might serve as counter-substrates .
PMID:11997326
Although the mechanism is not clear, this transporter can function in bidirectional mode .
PMID:29204966
When apically expressed in epithelial cells, it facilitates transcellular transport (also called vectorial release), extracting PG from the apical medium and facilitating transport across the cell toward the basolateral side, whereupon the PG exits the cell by simple diffusion (By similarity). In the renal collecting duct, regulates renal Na+ balance by removing PGE2 from apical medium (PGE2 EP4 receptor is likely localized to the luminal/apical membrane and stimulates Na+ resorption) and transporting it toward the basolateral membrane (where PGE2 EP1 and EP3 receptors inhibit Na+ resorption) (By similarity). Plays a role in endometrium during decidualization, increasing uptake of PGs by decidual cells .
PMID:16339169
Involved in critical events for ovulation .
PMID:27169804
Regulates extracellular PGE2 concentration for follicular development in the ovaries (By similarity).
Expressed intracellularly, may contribute to vesicular uptake of newly synthesized intracellular PGs, thereby facilitating exocytotic secretion of PGs without being metabolized (By similarity). Essential core component of the major type of large-conductance anion channel, Maxi-Cl, which plays essential roles in inorganic anion transport, cell volume regulation and release of ATP and glutamate not only in physiological processes but also in pathological processes (By similarity). May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:11669456 PMID:11907186 PMID:14675047 PMID:22108572 PMID:23832370 PMID:28534121 PMID:9950961
Mediates the uptake of OA across the basolateral side of proximal tubule epithelial cells, thereby contributing to the renal elimination of endogenous OA from the systemic circulation into the urine .
PMID:9887087
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
Transports prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) and may contribute to their renal excretion .
PMID:11907186
Also mediates the uptake of cyclic nucleotides such as cAMP and cGMP .
PMID:26377792
Involved in the transport of neuroactive tryptophan metabolites kynurenate (KYNA) and xanthurenate (XA) and may contribute to their secretion from the brain .
PMID:22108572 PMID:23832370
May transport glutamate .
PMID:26377792
Also involved in the disposition of uremic toxins and potentially toxic xenobiotics by the renal organic anion secretory pathway, helping reduce their undesired toxicological effects on the body .
PMID:11669456 PMID:14675047
Uremic toxins include the indoxyl sulfate (IS), hippurate/N-benzoylglycine (HA), indole acetate (IA), 3-carboxy-4- methyl-5-propyl-2-furanpropionate (CMPF) and urate .
PMID:14675047 PMID:26377792
Xenobiotics include the mycotoxin ochratoxin (OTA) .
PMID:11669456
May also contribute to the transport of organic compounds in testes across the blood-testis-barrier PMID:35307651
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
ATC S01EE01
ATC S01EE51
ATC S01EE52
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)
Latanoprost
Additional database identifiers
Drugs Product Database (DPD)
11458
ChemSpider
4470740
BindingDB
50240648
ZINC
ZINC000012468792
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9600
GenAtlas
PTGFR
GeneCards
PTGFR
GenBank Gene Database
L24470
GenBank Protein Database
456564
Guide to Pharmacology
344
UniProt Accession
PF2R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10955
GeneCards
SLCO2A1
GenBank Gene Database
U70867
GenBank Protein Database
1617590
UniProt Accession
SO2A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10970
GenAtlas
hROAT1
GeneCards
SLC22A6
GenBank Gene Database
AF057039
GenBank Protein Database
3831566
Guide to Pharmacology
1025
UniProt Accession
S22A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_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