Brimonidine

Brimonidine

Systematic (IUPAC) name
5-Bromo-N-(4,5-dihydro-1H-imidazol-2-yl) quinoxalin-6-amine
Clinical data
Trade names	Alphagan, Mirvaso
AHFS/Drugs.com
MedlinePlus
Pregnancy category	US: B (No risk in non-human studies)
Legal status	US: ℞-only
Routes of administration	Ocular (eye drops), topical (gel)
Pharmacokinetic data
Metabolism	Primarily liver
Biological half-life	3 hours ocular 12 hours topical
Identifiers
CAS Registry Number	Y
ATC code	D11 S01
PubChem	CID:
IUPHAR/BPS
DrugBank	Y
ChemSpider	Y
UNII	Y
KEGG	Y
ChEBI	Y
ChEMBL	Y
Chemical data
Formula	C11H10BrN5
Molecular mass	292.135 g/mol
SMILES Brc2c1nccnc1ccc2N/C3=N/CCN3
InChI InChI=1S/C11H10BrN5/c12-9-7(17-11-15-5-6-16-11)1-2-8-10(9)14-4-3-13-8/h1-4H,5-6H2,(H2,15,16,17) Y Key:XYLJNLCSTIOKRM-UHFFFAOYSA-N Y
Y

Brimonidine (bri-MOE-ni-deen) 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 rosacea (facial erythema).

It acts via decreasing synthesis of aqueous humor, and increasing the amount that drains from the eye through uveoscleral outflow. In treating erythema, it acts by vasoconstriction (narrowing of blood vessels).

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% (Mirvaso) for facial erythema or rosacea.

Mechanism of action

Brimonidine is an α₂ adrenergic agonist.

Alpha 2 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 alpha 2 agonist activity results in vasoconstriction of blood vessels (as opposed to central alpha 2 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 alpha adrenergic stimulation. This may lead to relaxed ciliary muscle and increased uveoscleral outflow.^[2]

References

• Mosby's Drug Guide for Nurses (7th edition; Skidmore) 2007.

External links

• Alphagan P product website
• Alphagan P prescribing information