Clinical data
Pronunciation bri-MOE-ni-deen
Trade names Alphagan, Mirvaso
AHFS/ Consumer Drug Information
MedlinePlus a601232
  • US: B (No risk in non-human studies)
Routes of
topical (ophthalmic solution, gel)
ATC code D11AX21 (WHO) S01EA05 (WHO)
Legal status
Legal status
Pharmacokinetic data
Metabolism Primarily liver
Biological half-life 3 hours (ocular), 12 hours (topical)
CAS Number 59803-98-4 YesY
PubChem (CID) 2435
DrugBank DB00484 YesY
ChemSpider 2341 YesY
KEGG D07540 YesY
ECHA InfoCard 100.149.042
Chemical and physical data
Formula C11H10BrN5
Molar mass 292.135 g/mol
3D model (Jmol) Interactive image
Melting point 252 °C (486 °F)

Brimonidine is a drug used as eye drops under the brand names Alphagan and Alphagan-P to treat open-angle glaucoma or ocular hypertension, and as a gel, Mirvaso, for facial skin redness in rosacea.

It acts via decreasing synthesis of aqueous humor, and increasing the amount that drains from the eye through uveoscleral outflow; brimonidine treats reddened skin (erythema) by causing narrowing of blood vessels (vasoconstriction).

Clinical uses

Brimonidine is indicated for the lowering of intraocular pressure in patients with open-angle glaucoma or ocular hypertension. It is also the active ingredient of Combigan along with timolol maleate.

A Cochrane Systematic Review compared the effect of brimonidine and timolol in slowing the progression of open angle glaucoma in adult participants.[1]

In 2013, the FDA approved topical application of brimonidine 0.33% gel (Mirvaso) for persistent facial redness of rosacea.

Mechanism of action

Brimonidine is an α2 adrenergic agonist.

α2 agonists, through the activation of a G protein-coupled receptor, inhibit the activity of adenylate cyclase. This reduces cAMP and hence aqueous humour production by the ciliary body.

Peripheral α2 agonist activity results in vasoconstriction of blood vessels (as opposed to central α2 agonist activity that decreases sympathetic tone, as can be seen by the medication clonidine). This vasoconstriction may explain the acute reduction in aqueous humor flow. The increased uveoscleral outflow from prolonged use may be explained by increased prostaglandin release due to α adrenergic stimulation. This may lead to relaxed ciliary muscle and increased uveoscleral outflow.[2]


  1. Sena DF, Lindsley K (2013). "Neuroprotection for treatment of glaucoma in adults". Cochrane Database Syst Rev. 2: CD006539. doi:10.1002/14651858.CD006539.pub3. PMC 4261923Freely accessible. PMID 23450569.
  2. Toris, C.; Camras, C.; Yablonski, M. (1999). "Acute versus chronic effects of brimonidine on aqueous humor dynamics in ocular hypertensive patients". American journal of ophthalmology. 128 (1): 8–14. doi:10.1016/s0002-9394(99)00076-8. PMID 10482088.
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