Indications
Latanoprost is prescribed to lower elevated intraocular pressure in individuals diagnosed with open-angle glaucoma or ocular hypertension. It can be utilized as a standalone treatment or in a combination therapy with either netarsudil or timolol. In Canada, latanoprost is also indicated for treating elevated intraocular pressure resulting from angle-closure glaucoma, provided that a peripheral iridotomy or laser iridoplasty has been performed.
Pharmacodynamics
Latanoprost functions by effectively reducing intraocular pressure through the enhancement of uveoscleral outflow. The decrease in pressure can be observed within 3 to 4 hours following administration, reaching its peak reduction between 8 and 12 hours, and remaining effective for up to 24 hours. It should be noted that between 3% to 10% of patients may experience changes in iris pigmentation after approximately 3 to 4 months of use. This risk should be communicated to patients prior to starting treatment. Other ocular effects reported include occasional conjunctival hyperemia, changes in periocular tissue pigmentation, changes to eyelashes, and mild ocular irritation.
Absorption
Latanoprost is swiftly absorbed in the cornea as an isopropyl ester prodrug, which is then activated through hydrolysis. A minor fraction of the drug is absorbed systemically. The maximum concentration (Cmax) of latanoprost in systemic circulation occurs within 5 minutes and is approximately 53 pg/mL. In the aqueous humor, Cmax is reached within 2 hours after administration, measured to be between 15 and 30 ng/mL.
Metabolism
Following corneal absorption, latanoprost is hydrolyzed by esterases into its pharmacologically active form. The small proportion that enters circulation undergoes hepatic metabolism, resulting in the formation of the metabolites 1,2-dinor and 1,2,3,4-tetranor through fatty acid beta-oxidation.
Mechanism of Action
Latanoprost functions by selectively stimulating the prostaglandin F2 alpha receptor, effectively reducing intraocular pressure (IOP) through enhanced outflow of aqueous humor. This mechanism is critical in managing elevated intraocular pressure, which is a significant risk factor for glaucomatous damage to the optic nerve and subsequent visual field loss. The drug may facilitate increased outflow of aqueous humor by promoting the remodeling of the extracellular matrix and regulating matrix metalloproteinases. These processes potentially increase tissue permeability along the humor outflow pathways, thereby altering outflow resistance and rates.
