{'fraction_non_alphanumeric': 0.023687580025608196, 'fraction_numerical': 0.027528809218950064, 'mean_word_length': 5.737068965517241, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Bimatoprost, a novel efficacious ocular hypotensive drug now recognized as a member of a new class of agents called prostamides

Pursuit of a new FP‐agonist prodrug led to the identification of an interesting series of neutral C1‐substituted prostaglandin F2α analogues. Although these initial analogues were devoid of any inherent pharmacological activity at the FP‐receptor, two compounds AGN‐190910 and AGN‐191129, were found to have pronounced effects in lowering intraocular pressure (IOP) in normotensive dogs and monkeys. The cat iris sphincter assay was quickly developed as a primary screen for these analogues, leading to rapid identification of AGN‐192024 (17‐phenyl PGF2α ethyl amide, bimatoprost). While bimatoprost is structurally similar to naturally occurring mammalian hormones of the prostanoid family, surprisingly it demonstrates no significant activity at any of the known prostanoid receptors. Furthermore, results of considerable additional pharmacological studies provide evidence that it may indeed act through a unique receptor yet to be identified. The effect of Bimatoprost on lowering IOP has also been found to be unique in comparison to prostanoids. Bimatoprost reduces human IOP by increasing aqueous humor outflow through a dual mechanism of action where it improves both pressure‐dependent and pressure‐independent outflow pathways. First introduced to the market in 2002, bimatoprost is currently the most potent single therapy available for control of ocular hypertension. Drug Dev Res 68:147–155, 2007. ©2007 Wiley‐Liss, Inc.