Tropicamide (Ro 1-7683) is a synthetic muscarinic antagonist with anticholinergic properties similar to atropine. Upon ocular administration, it binds to and blocks muscarinic receptors in the sphincter and ciliary muscles, inhibiting cholinergic responses and causing pupil dilation and ciliary muscle paralysis. Tropicamide is used as a diagnostic agent to induce short-duration mydriasis and cycloplegia.

M4 mAChR:8 nM

At a concentration of 0.5%, Nepafenac significantly inhibits (46%) the breakdown of the blood-retinal barrier, leading to a 65% reduction in retinal edema, and almost completely suppresses PGE2 synthesis (96%). Nepafenac's bioavailability in ocular tissue is notably higher. Its inhibitory action on COX-1 is weaker (IC50: 64.3 μM). In rabbits, Nepafenac inhibits prostaglandin synthesis within the retina/choroid (55%) and in the iris/ciliary body (85-95%). Compared to control mice, Nepafenac substantially reduces choroidal neovascularization and ischemia-induced retinal neovascularization and also slows the increase in ischemia-induced retinal VEGF mRNA expression. In ocular and metastatic animal models, Nepafenac delays the progression of malignant tumors and decreases the weight of choroidal melanoma. In retinal microvessels of diabetic rats with insulin deficiency, Nepafenac markedly suppresses retinal prostaglandin E (2), superoxide, cyclooxygenase-2, and leukostasis, but does not affect vascular endothelial growth factor and nitric oxide. In diabetic rats, the compound significantly inhibits the number of dUTP nick end labeling (TUNEL) positive capillary cells, pericytes, and acellular capillaries mediated by transferase.