Disorat

Disorat Uses, Dosage, Side Effects, Food Interaction and all others data.

A beta-adrenergic antagonist effective for both beta-1 and beta-2 receptors. It is used as an antiarrhythmic, antihypertensive, and antiglaucoma agent.

Disorat is a beta1 and beta2 (non-selective) adrenergic receptor-blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Disorat is indicated in the treatment of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. Disorat, when applied topically to the eye, has the action of reducing elevated, as well as normal, intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. Disorat reduces intraocular pressure with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce.

Disorat
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Trade Name	Disorat
Availability	Prescription only
Generic	Metipranolol
Metipranolol Other Names	Metipranolol, Metipranololum
Related Drugs	epinephrine ophthalmic, latanoprost ophthalmic, timolol ophthalmic, brimonidine ophthalmic, pilocarpine ophthalmic, Xalatan, Lumigan
Type
Formula	C₁₇H₂₇NO₄
Weight	Average: 309.4006 Monoisotopic: 309.194008357
Groups	Approved
Therapeutic Class
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Available Country
Last Updated:	September 19, 2023 at 7:00 am

Uses

Disorat is a beta-adrenergic antagonist used for the reduction of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma.

Indicated in the treatment of elevated intraocular pressure in patients with ocular hypertension or open angle glaucoma.

Disorat is also used to associated treatment for these conditions: Ocular Hypertension, Open Angle Glaucoma (OAG)

How Disorat works

Although it is known that metipranolol binds the beta1 and beta2 adrenergic receptors, the mechanism of metipranolol's action is not known. It has no significant intrinsic sympathomimetic activity, and has only weak local anesthetic (membrane-stabilizing) and myocardial depressant activity. It appears that the ophthalmic beta-adrenergic blocking agents reduce aqueous humor production, as demonstrated by tonography and fluorophotometry. A slight increase in aqueous humor outflow may be an additional mechanism.