Indications
Travoprost is prescribed for lowering elevated intraocular pressure in individuals diagnosed with open-angle glaucoma or ocular hypertension. It is also suitable for pediatric patients aged from two months to under 18 years. This broad age range highlights its versatility and effectiveness in managing conditions related to increased intraocular pressure.
Pharmacodynamics
Travoprost functions by selectively and fully activating the prostaglandin FP receptor, demonstrating its action in the nanomolar range. Importantly, travoprost does not exhibit significant affinity for other prostanoid or non-prostanoid receptors. The reduction in intraocular pressure typically occurs approximately two hours post-administration, reaching peak effectiveness around 12 hours. A single dose can maintain significant intraocular pressure reduction for over 24 hours, showcasing its long-lasting effects.
Absorption
When administered ophthalmically, travoprost is absorbed through the cornea. In various multiple-dose pharmacokinetic studies, the plasma concentrations of travoprost's free acid were often below 0.01 ng/mL, the lower limit of quantification for the assay. The mean maximum plasma concentration (Cmax) recorded was 0.018 ± 0.007 ng/mL, with a range of 0.01 to 0.052 ng/mL, and the time to reach peak concentration (Tmax) was approximately 30 minutes.
Metabolism
Travoprost is an isopropyl ester prodrug that undergoes hydrolysis by esterases within the cornea to become its active free acid form. Systemically, this free acid is further metabolized into inactive forms. This occurs through beta-oxidation of the alpha carboxylic acid chain into 1,2-dinor and 1,2,3,4-tetranor analogs, oxidation of the 15-hydroxyl moiety, and reduction of the 13, 14 double bond, ensuring the drug's effects are moderated post-activity.
Mechanism of Action
Travoprost functions as a prodrug that, following administration, is absorbed through the cornea and subsequently hydrolyzed to its active metabolite, travoprost free acid. This transformation is facilitated by the ester moiety of the free acid, which enhances its penetration into the aqueous humour. Although the precise mechanism of action of travoprost is not fully understood, it is believed to operate through its full agonist activity at the prostaglandin FP receptor. By binding to this receptor, travoprost free acid promotes the increased outflow of aqueous humour through both the trabecular meshwork and uveoscleral pathways, effectively reducing intraocular pressure.
