Brimonidine 3mg/g gel
Requires a prescription from a doctor or prescriber
Safety information for pregnancy and breastfeeding
Pregnancy
Nonclinical Toxicology
At oral doses of up to 2.5 and 5 mg/kg/day in pregnant rats and rabbits, brimonidine was not shown to be teratogenic during gestation days 6 through 18.
Breastfeeding
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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Safety monitoring data
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 Brimonidine
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1 branded products available
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Mirvaso 3mg/g gel
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)
Facial erythema of rosacea: brimonidine tartrate gel (ESNM43)
Latanoprost–netarsudil for previously treated primary open-angle glaucoma or ocular hypertension (TA1009)
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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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 the 50 most relevant studies.
Reviews & meta-analyses: 10 · Randomised trials: 23 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Gao X, Xiang W
2025
- Rosacea
- Dermatologic Agents
- Dicarboxylic Acids
Topical interventions for rosacea are often used to relieve local symptoms. However, currently, there are few articles to systematically analyze the efficacy profile of topical drugs for rosacea. This study aimed to investigate the efficacy profile of widely used topical drugs. To acquire appropriate information from related literature, we looked into 4 databases. Efficacy was appraised with the Investigator Global Assessment, Clinician's Erythema Assessment, Patient's Self-Assessment and Subject Self-Assessment of Rosacea Facial Redness scales. Treatment-emergent adverse events and dermal tolerability were also recorded. According to 21 randomized controlled trials included, a total of 6 topical drugs including minocycline, ivermectin, azelaic acid, metronidazole, brimonidine and oxymetazoline were reported. These drugs are well-tolerated and safe. Ivermectin is more effective than azelaic acid and metronidazole. Azelaic acid has a better efficacy profile than metronidazole according to included studies. Minocycline turned out to be effective improving the symptoms of rosacea. Brimonidine and oxymetazoline both have significant effects on reducing facial redness.
Abstract licence: CC BY-NC-ND
D. Scuteri, G. Bagetta, C. Nucci, et al.
Progress in brain research, 2020
Hidenobu Tanihara, Tetsuya Yamamoto, Makoto Aihara, et al.
American Journal of Ophthalmology, 2023
K. Kim, C. Lee, Jonghoon Shin, et al.
Scientific Reports, 2023
Kim M, Lee CK, Shin J, et al.
2025
The objectives of the study were to compare the efficacy and safety using ocular surface assessment between preserved and preservative-free brimonidine/timolol fixed-combination eye drops in glaucoma or ocular hypertension patients. Methods: This study was designed as a prospective, multicenter (three institutions), investigator-masked, parallel-grouped randomized clinical trial. The primary outcomes were corneal and conjunctival staining score, ocular surface disease index (OSDI) score, drug tolerance, and adherence rates at 12-week visits. The secondary outcomes were corneal and conjunctival staining score, OSDI score at 4-week visits and intraocular pressure (IOP), tear-film break-up time (TBUT), and bulbar/limbal hyperemia score at the 4- and 12-week visits. For safety assessment, best-corrected visual acuity (BCVA), systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and physical examination at 4 and 12 weeks and adverse events during the whole study period were analyzed. Results: Overall, 59 patients were enrolled and randomized into each group (29 preserved and 30 preservative-free). At the endpoint, 5 patients in the preserved group and 2 patients in the preservative-free group dropped out, leaving 24 and 28 patients in the preserved and preservative-free groups, respectively. Baseline characteristics showed no significant difference between the groups including age and sex. At the 12-week visit, intra-group change of OSDI scores did not change significantly compared to the baseline scores in both preserved and preservative-free groups (p = 0.791, 0.478, respectively). On the contrary, the corneal staining score and the conjunctival staining score showed a significant increase compared to the baseline score in the preserved group (p = 0.015, 0.009, respectively). Regarding drug satisfaction, higher proportions of patients in the preservative-free group reported convenience of installation (p = 0.002). Also, stinging and burning sensations in drug tolerance showed better results in the preservative-free group with a significant difference (p = 0.011). Safety assessment regarding systemic side effects such as SBP, DBP, and HR showed similar results between the preserved and preservative-free groups (p = 0.711, 0.232, 0.666, respectively). Conclusions: Preservative-free brimonidine/timolol showed comparable efficacy and safety, better corneal and conjunctival staining score with convenience of installation, and lower stinging and burning sensation. It is expected to be a proper treatment option for patients with glaucoma or ocular hypertension.
Abstract licence: CC BY
Soomsawasdi P, Rojananuangnit K, Arayangkoon E, et al.
2025
IntroductionIntravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents are a primary management option for retinal diseases. Acute elevation of intraocular pressure (IOP) is a complication associated with these injections that should be considered. This study investigated and compared the prophylactic effects of fixed combination anti-glaucoma medication on IOP spikes following intravitreal anti-VEGF injections.MethodsThis randomized double-blind clinical trial included one eye of each participant indicated for treatment with intravitreal injection of anti-VEGF agents (bevacizumab, aflibercept, and ranibizumab) and randomly allocated to one of the three prophylactic anti-glaucoma medications, with each drug further divided into one- and two-drop regimens before intravitreal injection. Participants with allergies or contraindications to medications were excluded from the pretreatment groups and were invited to participate in the control group.ResultsThe study involved 308 participants: 89 in the dorzolamide/timolol group, 86 in the brimonidine/timolol group, 101 in the brinzolamide/brimonidine group, and 32 in the control group. Baseline characteristics and IOP were comparable across all groups. In the prophylactic premedication groups, mean IOP at 30 min were within 21 mmHg and returned to their baseline at 1 h. Mean IOP measurements between baseline and 30 min in the brimonidine/timolol two-drop regimen were not significantly different: 13.72 ± 4.63 vs 15.11 ± 4.39 mmHg, p = 0.096. In the control group, IOP significantly increased from baseline at 30 min and 1 h post-injection: 14.31 ± 4.10, 22.15 ± 8.64, and 18.36 ± 7.52 mmHg, respectively, p ConclusionTopical fixed combination anti-glaucoma medication used as a prophylactic treatment before intravitreal anti-VEGF injections significantly prevented IOP spikes post-injection, with a comparable effect among three medications. Prophylactic treatment of IOP spikes should be considered as standard care to prevent further damage in patients with compromised retinal vascular and optic nerve perfusion.Trial registrationTCTR20241005001, retrospectively registered.
Abstract licence: CC BY-NC
Mohamed EA, Obaid ZM, Fouda I
2025
Zakeri P, Akhavanakbari G, Ojaghi H, et al.
2026
- Dexmedetomidine
- Intraocular Pressure
- Posterior Capsulotomy
Posterior capsule opacification (PCO) is a common post-cataract surgery complication treated with Nd:YAG laser posterior capsulotomy, which may cause intraocular pressure (IOP) spikes and threaten vision. Brimonidine and apraclonidine are widely used to prevent such elevations. This prospective, double-masked, randomized clinical trial evaluated the efficacy of topical dexmedetomidine, a novel ophthalmic drop, in preventing IOP rise after Nd:YAG laser treatment. A total of 111 eyes from 89 pseudophakic patients were randomized to receive dexmedetomidine 0.008% or brimonidine 0.2% one h before the procedure. Patients with glaucoma, baseline IOP > 24 mmHg, keratoconus, corneal edema, prior refractive/corneal surgery, or unstable cardiovascular disease were excluded. IOP was measured with air-puff tonometry at baseline, 30 min, 4 h, and 24 h post-laser. Baseline characteristics were comparable. In the dexmedetomidine group, mean IOP values were 16.3 ± 3.6, 14.8 ± 4.7, 17.1 ± 6.2, and 16.7 ± 4.5 mmHg, while in the brimonidine group, they were 16.7 ± 2.9, 13.3 ± 3.9, 13.2 ± 5.5, and 14.2 ± 3.9 mmHg, respectively. At 30 min, brimonidine significantly reduced IOP (p = 0.000), whereas dexmedetomidine did not (p = 0.116). At 4 and 24 h, IOP increased above baseline with dexmedetomidine but decreased with brimonidine (p = 0.001 and p = 0.004). Dexmedetomidine was associated with more IOP spikes > 10 mmHg (9% vs. 2%, p = 0.035) and IOP > 30 mmHg (7% vs. 2%, p = 0.09). No systemic or ocular side effects occurred. Although dexmedetomidine prevented acute IOP surges, its efficacy was inferior to brimonidine. Further studies should explore optimal dosing, formulations, and long-term safety to clarify its prophylactic potential.
Abstract licence: CC BY
Abid MA, Abid MH, Afzal MD
2026
Presbyopia is a progressive, irreversible age-related decline in ocular accommodation caused by reduced lens elasticity, resulting in impaired near vision and a significant impact on daily activities and quality of life. Globally, presbyopia affects approximately 1.8 billion individuals, with projections rising to 2.1 billion by 2030. Current management options include spectacles, contact lenses, pharmacologic agents such as pilocarpine, and surgical interventions; however, each approach carries limitations related to convenience, adaptability, or visual compromise. Yuvezzi™ (carbachol 2.75% and brimonidine tartrate 0.1%) is a recently U.S. Food and Drug Administration (FDA)-approved dual-agent ophthalmic solution designed to improve near vision through pharmacologically induced miosis. Carbachol, a parasympathomimetic agent, stimulates muscarinic receptors to produce sustained pupillary constriction, while brimonidine, an α2-adrenergic agonist, inhibits iris dilator activity and prolongs the miotic effect, enhancing tolerability. Its approval was based on two Phase 3 randomized controlled trials, BRIO-I and BRIO-II, which demonstrated significant improvement in binocular uncorrected near visual acuity without compromising distance vision. Common adverse effects included ocular discomfort, irritation, visual disturbances, and headache. Yuvezzi™ offers a noninvasive, reversible alternative for presbyopia management; however, long-term safety and sustained efficacy require further evaluation.
Abstract licence: CC BY
Suzuki M, Arimura S, Iwasaki K, et al.
2026
Background/Objectives: Rho-associated protein kinase inhibitors reduce intraocular pressure (IOP) by enhancing aqueous humor outflow through the trabecular meshwork-Schlemm's canal pathway. However, it remains unclear whether the fixed-dose combination of ripasudil hydrochloride hydrate and brimonidine tartrate (GLAALPHA) enhances conventional aqueous outflow in vivo. Methods: This single-center randomized clinical trial included healthy adult volunteers who received GLAALPHA, a brimonidine tartrate-brinzolamide fixed-dose combination (Ailamide), or brimonidine tartrate monotherapy (Aiphagan) in a crossover sequence. The aqueous column width in the episcleral veins was assessed at baseline and at 2 h (primary outcome) and 8 h using hemoglobin video imaging. Results: Among 24 participants, analyses included 23 GLAALPHA-treated eyes, 21 Ailamide-treated eyes, and 22 Aiphagan-treated eyes. Two hours after instillation, the aqueous column width significantly increased from baseline only in the GLAALPHA group (p = 0.002). The percent increase in the aqueous column width at 2 h was significantly greater with GLAALPHA than with Ailamide (p = 0.039) and not significantly different between GLAALPHA and Aiphagan (p = 0.114). At 8 h, the aqueous column width did not differ from the baseline in any groups. Conclusions: In healthy adult eyes, GLAALPHA significantly increased the aqueous column width in the episcleral veins 2 h after instillation, indicating enhanced conventional aqueous outflow. These findings provide evidence that GLAALPHA promotes trabecular outflow beyond the effects of brimonidine tartrate-containing comparators and offer mechanistic insights into its action.
Abstract licence: CC BY
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
11 found
Half-life
3 hours
Mechanism
In the eye, alpha-1 adrenoceptors play a role in vasoconstriction, mydriasis, ey…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.2%
Half-life
0.2%
Protein binding
Volume of distribution
Metabolism
Elimination
74%
Clearance
87%
[A36674]
…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ophthalmically, brimonidine is used to lower intraocular pressure by reducing aqueous humor production and increasing uveoscleral outflow. Because it is oxidately stable, brimonidine is associated with fewer reports of ocular allergic reactions compared to other alpha-2 adrenergic agonists.[A178969] The ophthalmic solution of brimonidine was first approved by the FDA in 1996 as Alphagan [label] and brimonidine is the only selective alpha-adrenergic receptor agonist approved for chronic treatment in glaucoma.[A36674] Brimonidine is also found in ophthalmic solutions in combination with [brinzolamide] under the market name Simbrinza for the reduction in intraocular pressure. Unlike nonselective beta-blockers used in ocular hypertension, brimonidine is not associated with significantly adverse cardiopulmonary side effects.[A178945] Thus brimonidine is an effective and safe alternative to beta-blockers, in patients with, or at high risk for, cardiopulmonary disease.[A178948] The topical form of brimonidine was approved by the FDA in August 2013 for the symptomatic treatment of persistent facial erythema of rosacea in adults. It is marketed under the brand name Mirvaso.[L6535] Brimonidine is the first topical treatment approved for facial erythema of rosacea.[A178978]
Indicated for lowering intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension [label] as monotherapy or combination product with [brinzolamide].
Topical
Indicated for the treatment of persistent (non-transient) facial erythema of rosacea in adults 18 years of age or older.
[L6535]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 835 interactions
Oral LD50 is 50 mg/kg in mice and 100 mg/kg in rats.MSDS While there is limited clinial data on brimonidine overdose in adults, some common symptoms from oral overdoses of alpha-2 adrenergic agonists include hypotension, asthenia, vomiting, lethargy, sedation, bradycardia, arrhythmias, miosis, apnoea, hypotonia, hypothermia, respiratory depression and seizure.
[L6544]
Treatment of an oral overdose includes supportive and symptomatic therapy. Cases of brimonidine overdose have been reported in neonates, infants, and pediatric patients receiving brimonidine tartrate as part of medical treatment of congenital glaucoma or by accidental oral ingestion. In these cases, children experienced symptoms consistent with previously reported oral overdoses of alpha-2 adrenergic agonists in young children.
[L6544]
Nonclinical Toxicology
At oral doses of up to 2.5 and 5 mg/kg/day in pregnant rats and rabbits, brimonidine was not shown to be teratogenic during gestation days 6 through 18.
Findings from various in vitro and in vivo studies, including the Ames bacterial assay, CHO cell chromosomal aberration assay, and CD-1 mice studies, did not demonstrate any mutagenic or clastogenic potential of brimonidine.[label] There were no observable adverse effects on male or female fertility when tested at oral doses of up to 1 mg/kg, which is approximately 200 times the systemic exposure following the maximum recommended ophthalmic dose of 0.5% brimonidine.[label]
Use in special populations
Due to limited clinical data on the use of brimonidine pregnant or breastfeeding female patients, the use of brimonidine in these patients is generally not recommended and the use should be only considered after taking into account the benefit-to-risk ratio of continuing the drug therapy in these patients. In nursing mothers, the decision should be made whether to discontinue the drug or discontinue breastfeeding.[label] As the systemic absorption and elimination of brimonidine are not significantly affected by age, the use of brimonidine is considered safe in geriatric patients. In contrast, the use of brimonidine in infants under the age of 2 and pediatric patients under the age of 18 is strongly not recommended due to the reports of serious adverse events following ophthalmic administration of brimonidine in infants between the age of 28 days and 3 months.
[L6544]
Brimonidine mediates vasoconstrictive effects and it was shown to exhibit anti-inflammatory properties in ex vivo human skin model and in vivo inflammation models.[A179041] In a clinial trials consisting of adults with moderate to severe facial erythema of rosacea, brimonidine was shown to improve the extent of redness at 3 hours after application, compared to placebo.[L6544] It was shown to be a potent vasoconstrictor of human subcutaneous vessels with a diameter of less than 200 µm. In in vivo mouse inflammation models, brimonidine displayed anti-inflammatory properties by inhibiting edema.[A178978] In a randomized, double-blind study, brimonidine reduced erythema for the 12 hours of the study in a dose-dependent manner.[A178978]
When adminsitered systemically, brimonidine was shown to cause cardiovascular effects by decreasing blood pressure, decreasing heart and respiratory rate, and prolonging the PR interval in the electrocardiogram. This is due to the targeting of adrenoceptors by the drug.[A178963][A178966] Although the clinical significance has not been established, there is evidence that brimonidine exhibits neuroprotective activity in experimental models of cerebral ischemia and optic nerve injury.[A178969] In vitro studies show that brimonidine mediated protective effects on neuronal cells from kainate acid insult and on cultured retinal ganglion cells from glutamate-induced cytotoxicity, which is a possible mediator of secondary neuronal degeneration in human glaucoma. Neuroprotective actions of brimonidine were also demonstrated in rat models of acute retinal ischemia and chronic IOP elevation. It has been proposed that brimonidine may exert neuroprotective effects on the retina and optic nerve by enhancing intrinsic retinal ganglion cell survival mechanisms and/or induction of neuronal survival factors, such as bFGF.[A178951] However, further investigations are needed to conclude on these possible therapeutic benefits of the drug.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A36674]
Following ocular administration of 0.2% brimonidine solution, the peak plasma concentrations were achieved within 1 to 4 hours.[label]
In a clinical study of adult subjects with facial erythema of rosacea, brimonidine was cutaneously applied on facial skin in a repeated manner. While there was no drug accumulation in plasma, the highest peak plasma concentrations (Cmax) and AUC were 46 ± 62 pg/mL and 417 ± 264 pgxhr/mL, respectively.
[L6544]
[A178951]
[A36674]
Approximately 87% of the total radioactive dose of brimonidine was shown to be eliminated within 120 hours following oral administration.[label]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC D11AX21
ATC S01EA55
ATC S01GA07
ATC S01EA05
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)
Brimonidine
Additional database identifiers
Drugs Product Database (DPD)
11710
Drugs Product Database (DPD)
22245
ChemSpider
2341
BindingDB
34572
PDB
J59
Guide to Pharmacology
520
ZINC
ZINC000021303210
HUGO Gene Nomenclature Committee (HGNC)
HGNC:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:282
GenAtlas
ADRA2B
GeneCards
ADRA2B
GenBank Gene Database
M34041
GenBank Protein Database
178198
Guide to Pharmacology
26
UniProt Accession
ADA2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:283
GenAtlas
ADRA2C
GeneCards
ADRA2C
GenBank Gene Database
J03853
GenBank Protein Database
178194
Guide to Pharmacology
27
UniProt Accession
ADA2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:553
GeneCards
AOX1
GenBank Gene Database
L11005
GenBank Protein Database
438656
Guide to Pharmacology
3186
UniProt Accession
AOXA_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