Travoprost 40micrograms/ml eye drops
Requires a prescription from a doctor or prescriber
Travoprost is a synthetic isopropyl ester prodrug of a prostaglandin F2alpha (F2α) analogue and selective FP prostanoid receptor agonist.
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MHRA alerts for Travoprost
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 Travoprost
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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 Travoprost
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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.
21 branded products available
MHRA licensed products
View all licensed products for Travoprost on the MHRA register
Travatan 40micrograms/ml eye drops
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Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/ml eye drops
Travoprost 40micrograms/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.
WHO defined daily dose (DDD)
100 microlitre
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). 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)
The SENSIMED Triggerfish contact lens sensor for continuous 24-hour recording of ocular dimensional changes in people with or at risk of developing glaucoma (MIB14)
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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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
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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 the 50 most relevant studies.
Reviews & meta-analyses: 13 · Randomised trials: 10 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Nagstrup AH
2023
- Glaucoma
- Prostaglandins F, Synthetic
- Goblet Cells
English summaryGlaucoma is a leading cause of the global prevalence of irreversible blindness. The pathogenesis of glaucoma is not entirely known, but the major risk factors include advancing age, genetic predisposition, and increased intraocular pressure (IOP). The only evidence-based treatment is a lowering of IOP through the use of eye drops, laser procedures, or surgical interventions. Although laser treatment is gaining recognition as a first-choice treatment option, the most common approach for managing glaucoma is IOP-lowering eye drops. A major challenge in the treatment is the occurrence of adverse events and poor adherence. In this context, the ocular surface is an area of great concern, as most glaucoma patients have dry eye disease (DED), which is largely caused by eye drops. Preservation with benzalkonium chloride (BAK) is a controversial topic due to its potential role as a significant cause of DED. A systematic review and meta-analyses investigate potential differences in efficacy and safety between BAK-preserved and BAK-free anti-glaucomatous eye drops (I). Many of the included studies report on ocular surface damage caused by the application of BAK-preserved eye drops. However, the meta-analyses addressing hyperemia, number of ocular adverse events, and tear break-up time did not identify any significant differences. The latter is likely due to varying measurement methods, different endpoints, and study durations. It is, therefore, possible that the large variations between the studies conceal differences in the safety profiles. The efficacy meta-analysis finds that there are no differences in the IOP-lowering effect between BAK-preserved and BAK-free eye drops, indicating that BAK is not necessary for the effectiveness of eye drops. To promote more homogeneous choices of endpoints and methods when evaluating BAK-preserved and BAK-free glaucoma treatments, a Delphi consensus statement was performed. In this study, glaucoma experts and ocular surface disease experts reached consensus on the key factors to consider when designing such studies (II). The hope is to have more studies with comparable endpoints that can systematically show the potentially adverse effects of BAK. The preclinical studies in the current Ph.D. research focus on conjunctival goblet cells (GCs). GCs are important for the ocular surface because they release the mucin MUC5AC, which is an essential component of the inner layer of the tear film. BAK preservation may damage the GCs and result in a low GC density, leading to an unstable tear film and DED. The most commonly used IOP-lowering drugs are prostaglandin analogs (PGAs). Thus, the conducted studies investigate the effect of PGAs preserved in different ways on GCs. BAK-preserved latanoprost is cytotoxic to primary cultured human conjunctival GCs and results in a scattered expression of MUC5AC, in contrast to negative controls, where MUC5AC is localized around the cell nucleus (III). Preservative-free (PF) latanoprost is not cytotoxic and does not affect the MUC5AC expression pattern. Furthermore, BAK-preserved travoprost is found to be cytotoxic in a time-dependent manner, while Polyquad®-preserved travoprost does not affect GC survival at any measured time point (IV). Both Polyquad and BAK induce scattered expression of MUC5AC. The cytotoxicity of BAK-preserved PGA eye drops is higher compared to the safer profile of PF and Polyquad-preserved PGA eye drops (V). Additionally, PF latanoprost does not increase the release of the inflammatory markers interleukin (IL)-6 and IL-8, unlike BAK-preserved latanoprost. A review highlights the active and inactive components of IOP-lowering eye drops (VI). Several preclinical and clinical studies have identified adverse effects of BAK. Although other components, such as the active drug and phosphates, can also cause adverse events, the review clearly states that BAK alone is a major source of decreased tolerability. The conclusion of this thesis is that BAK preservation is unnecessary and harmful to the ocular surface. The preclinical studies demonstrate that GCs die when exposed to BAK. Furthermore, they find that BAK induces a pro-inflammatory response. The review included in the thesis concludes that BAK should be phased out of eye drops for chronic use. Overall, the inclusion of BAK poses a risk of developing DED and poor adherence, which can ultimately lead to disease progression and blindness.
Abstract licence: CC BY-NC
Pourriyahi H, Hosseini NS, Nooshabadi MP, et al.
2024
- Vitiligo
- Prostaglandins, Synthetic
- Phosphodiesterase Inhibitors
BackgroundThe treatment of vitiligo is a persistent challenge in dermatology. New treatments are being offered and studied in this field for those resistant to or intolerant of classical therapies.AimsIn this systematic review, we study the use of prostaglandin analogues (PGAs) and phosphodiesterase inhibitors (PDEIs) in the treatment of vitiligo, as they are known for their pigmentation inducing effects through activating melanocytes.MethodsWe searched four main online databases with the keywords "Vitiligo", "Prostaglandin analogue" and "Phosphodiesterase inhibitor".ResultsA total of 42 articles were included, with 1027 cases, studying drugs like bimatoprost, latanoprost, travoprost, dinoprostone, apremilast, crisaborole, etc. Among the included studies, the treatment regimens are commonly once or twice daily for 12-48 weeks, with a mean of 20.61 weeks, and the routes of administration are mainly topical gels or ophthalmic solutions and oral tablets. Side effects are mild and tolerable, namely erythema, itching or burning sensations at application site for topicals, or gastrointestinal problems with apremilast. Repigmentation results are significant in both adult and pediatric patients and progressive or stable vitiligo. PGAs and PDEIs outperform many classical therapies, for example, narrowband ultraviolet B phototherapy (NB-UVB), tacrolimus, mometasone or methylprednisolone mini-pulse. PGAs or PDEIs are usually used in combination therapies to either cause synergism or increase drug delivery, and almost always enhance repigmentation, for example, with NB-UVB, fractional CO2 laser, microneedling, and mometasone.ConclusionMonotherapy or add-on PGAs and PDEIs can be considered effective treatments for vitiligo and promising last resorts for those resistant to other therapies.
Abstract licence: CC BY
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
S. Sarkisian, R. Ang, Andy M. Lee, et al.
Ophthalmology and Therapy, 2024
S. Sarkisian, R. Ang, Andy M. Lee, et al.
Ophthalmology, 2024
- Ocular Hypertension
- Glaucoma, Open-Angle
- Antihypertensive Agents
Xiu-Li Zhang, Li Qin
Medicine, 2019
Abstract Background: This study will evaluate the efficacy of travoprost for patients with glaucoma systematically. Methods: A comprehensive literature search will be carried from following literature sources from inception to the present: Cochrane Library, MEDLINE, EMBASE, Web of Science, Google scholar, Chinese Biomedical Literature Database, and China National Knowledge Infrastructure. We will only consider randomized controlled trials on assessing the efficacy and safety of travoprost for glaucoma for inclusion. We will use Cochrane risk of bias tool for the methodological quality assessment for each qualified study. If it is possible, we will pool the outcome data, and will perform meta-analysis. Results: This study will systematically evaluate the efficacy and safety of travoprost for glaucoma. Primary outcomes include intraocular pressure (IOP), mean IOP, and mean reduction of IOP. Secondary outcomes consist of diastolic ocular perfusion pressure, central corneal thickness, and quality of life, as measured by 36-Item Short Form Health Survey, and treatment-related adverse events included hyperemia, eye pain, and eye pruritus. Conclusion: The findings of the present study will summarize the updated evidence of travoprost for patients with glaucoma. PROSPERO registration number: PROSPERO CRD42019126956.
Abstract licence: CC BY 4.0
H. Barnebey, A. Robin
American journal of ophthalmology, 2017
de Almeida RCMC, Lindenmeyer RL, Lavinsky F, et al.
2026
- Ocular Hypertension
- Glaucoma, Open-Angle
- Antihypertensive Agents
AimsTo compare the effectiveness of PSLT and the use of topical prostaglandin eye drops in the treatment of ocular hypertensive (OHT) or open-angle glaucoma patients (POAG) in reducing intraocular pressure (IOP) and peak IOP.MethodsThis is a non-inferiority randomized clinical trial, after washout, both patients eyes were randomized, one eye treated with PSLT (intervention group) and the contralateral eye treated with travoprost eye drops (controls). IOP, peak IOP by water drinking test (WDT), visual field (VF) and OCT were performed at baseline and at 7 days, 2, 6, 9 and 12 months after treatment. The primary outcome measure was to assess if the impact of PSLT on IOP and peak IOP is not inferior to that of the standard treatment (travoprost eye drops) by a margin not greater than the predefined threshold of 1.5 mmHg.ResultsA total of 30 patients participated in this trial. The mean baseline IOP was similar in both groups, 18.8 ± 4.0 mmHg and 18.8 ± 4.2 mmHg, intervention and control respectively. At 2, 6 and 9 months of treatment no significant difference in IOP was found between the two groups. At 12 months of follow-up the PSLT group showed lower average IOP (13.5 ± 2.3 mmHg versus 14.9 ± 2.7 and p ConclusionPSLT was as effective as prostaglandin eye drops in reducing IOP and IOP peak in POAG and OHT patients. These findings are especially important as interest grows in minimally invasive glaucoma treatments and reducing reliance on topical medications.Trial registrationClinicaltrials.gov NCT05241938.
Abstract licence: CC BY
Leivas L, Procianoy F, Almeida RC, et al.
2026
- Cloprostenol
- Antihypertensive Agents
- Trabeculectomy
PurposeTo assess the one-year impact of prostaglandin analog (travoprost) on periorbital appearance and lower eyelid horizontal tension, compared with the contralateral eye treated with Pascal selective laser trabeculoplasty.MethodsThis nested case-control study was derived from a non-inferiority randomized clinical trial comparing Pascal selective laser trabeculoplasty efficacy with travoprost in fellow eyes over 12 months. One eye received daily travoprost, while the contralateral eye underwent Pascal selective laser trabeculoplasty. Lower eyelid horizontal tension was measured using a validated digital imaging method, and prostaglandin-associated periorbitopathy signs were graded by masked observers. Statistical analyses included generalized estimating equations and the Mann-Whitney U test for nonparametric data, with pResultsTen patients met the inclusion criteria for this subanalysis. Travoprost-treated eyes had significantly lower mean lower eyelid distension compared with Pascal selective laser trabeculoplasty-treated eyes (4.32 mm vs. 5.02 mm; mean difference: 0.70 mm; pConclusionsChronic use of prostaglandin analogs is associated with notable periorbital changes and increased lower eyelid tension, potentially affecting aesthetics and ocular function. Pascal selective laser trabeculoplasty may offer a safer profile for preserving periorbital anatomy while maintaining effective intraocular pressure control. Laser trabeculoplasty should be considered as an initial treatment when appropriate to minimize cosmetic and functional changes from chronic topical therapy.
Abstract licence: CC BY
R. Feldman, G. Katz, M. McMenemy, et al.
American journal of ophthalmology, 2016
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
Travoprost is a prodrug.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.01 ng/mL
Half-life
17 minutes
[L49434]
…
Protein binding
Volume of distribution
Metabolism
Elimination
2%
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L49434][L49429][L49515]
It is also used in pediatric patients aged two months to less than 18 years.
[L5146]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 107 interactions
[L5146]
Travoprost-induced reduction of intraocular pressure is observed about two hours after administration, and the maximum effect is reached after 12 hours. Significant lowering of intraocular pressure can be maintained for periods exceeding 24 hours with a single dose.[L5146]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L49434]
[L49434]
[L5146][L49434]
[L49434]
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
ATC S01EE04
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)
Travoprost
Additional database identifiers
Drugs Product Database (DPD)
12477
ChemSpider
4445407
BindingDB
50248302
ZINC
ZINC000004474682
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
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