Bimatoprost is the only representative of a novel class of
prostaglandin ethanolamide (prostamide) compounds used therapeutically as an efficacious treatment for
glaucoma. The pathways through which
bimatoprost works to improve uveoscleral outflow to relieve elevated intraocular pressure are similar to those of the conventional
prostaglandins used in
glaucoma therapy, with some evidence of a preferential action at the trabecular meshwork. The pharmacology of
bimatoprost is however, unclear. Pharmacological evidence supports a specific and distinct receptor-mediated agonist activity of
bimatoprost at 'prostamide' receptors, which is selective to the prostamides as a class. However, other studies have reported either activity of
bimatoprost at additional
prostanoid and nonprostanoid receptors, or a conversion of
bimatoprost to metabolites with agonist activity at
prostaglandin FP receptors in the human eye. The formation of endogenous prostamides has been demonstrated in vivo, by a novel pathway involving the cyclooxygenase-2-mediated conversion of endogenous
cannabinoid (
endocannabinoid) substrates. Irrespective of the pharmacology of
bimatoprost and the prostamides in general, further studies are needed to determine the
biological role and biochemical pathology of prostamides in the human eye, particularly in
glaucoma. Such studies may improve our understanding of uveoscleral flow and may offer new treatments for controlling intraocular pressure.