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Travoprost
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Travoprost is a synthetic lipophilic cloprostenol derivative. It is a prodrug of the active compound travoprost free acid, a prostaglandin F2α-analog with anti-glaucoma property. Upon administration, travoprost is hydrolyzed to the free acid by corneal esterases. It then selectively stimulates the prostaglandin F receptor, thereby increasing the uveoscleral outflow which leads to a reduction in intra-ocular pressure. Travoprost ophthalmic solution is indicated for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension (1).
Headaches related to latanoprost in open-angle glaucoma
Published in Clinical and Experimental Optometry, 2021
Henrietta Wang, Katherine Masselos, Michael Kalloniatis, Jack Phu
Glaucoma is a significant cause of irreversible blindness across the world.1 Currently, the treatment of glaucoma is through methods of reducing intraocular pressure. Across national and professional guidelines,2–5 it is now widely recognised that treatment of uncomplicated primary open-angle glaucoma typically begins with medical therapy, of which the first-line option is a prostaglandin analogue (PGA).6,7 PGA medications lower intraocular pressure by increasing aqueous outflow via the unconventional (uveoscleral) pathway, though more recent evidence8 has suggested additional action through the conventional (trabecular) pathway as well.9 Ophthalmic PGAs act on the prostaglandin F2α receptor to produce these effects. In comparison to other topical anti-glaucoma therapies, such as β-blockers and α2-agonists, PGAs offer a range of advantages as a therapeutic agent for chronic primary open-angle glaucoma: it has a convenient once-daily dosing regimen; it produces a significant decrease in intraocular pressure; it provides consistent diurnal control of intraocular pressure; and it has minimal systemic adverse effects.7,10,11
Selexipag for the treatment of pulmonary arterial hypertension
Published in Expert Review of Respiratory Medicine, 2021
Léon Genecand, Julie Wacker, Maurice Beghetti, Frédéric Lador
Cyclooxygenase metabolizes arachidonic acid (AA) into PGI2,Prostaglandin D2, prostaglandin E2, prostaglandin G2a, and thromboxane, regrouped under the term ‘prostanoids’ [7]. Prostanoids act via their receptors including prostaglandin D receptor, prostaglandin E receptor (1–4), prostaglandin F receptor, and PGI2 receptor (IP receptor). Vascular endothelial cells are the main producers of PGI2, which act mainly via the IP receptor leading to vasodilatation, antiplatelet and antiproliferative actions [7]. Reductions of PGI2 urinary metabolites and of PGI2 synthase expression in the pulmonary arteries have been shown in PAH patients [8]. Nonspecific binding of PGI2 to prostaglandin receptors in the gastric mucosa has been described and could explain some side effects [9].
Investigational drugs targeting prostaglandin receptors for the treatment of glaucoma
Published in Expert Opinion on Investigational Drugs, 2018
Artemis Matsou, Eleftherios Anastasopoulos
Up to 15% of glaucoma patients may not respond to prostaglandins F2a, likely due to the presence of specific single nucleotide polymorphisms (SNPs)of genes coding matrix metalloproteinases and the prostaglandin F2a receptor gene [11,76]. In addition to this, more than 30% of glaucoma patients on PGA treatment, will need additional medical treatment a few years down the line. Combination of multiple glaucoma medications can clearly augment the ocular hypertensive effect. However, by adding more medications, patients bear the burden of increased cost of treatment and risk for adverse reactions. As a direct consequence, compliance and adherence decline. This further highlights the need for more potent, more efficacious and more tolerable drugs to existing therapeutics options.