Disease relevance of Lumigan

• The low toxicity of the bimatoprost solution did not reveal a possible antioxidative effect [1].
• CONCLUSIONS: Bimatoprost 0.03% once daily was safe and statistically superior to timolol 0.5% twice daily in lowering IOP in patients with ocular hypertension or glaucoma [2].
• Effect of bimatoprost on patients with primary open-angle glaucoma or ocular hypertension who are nonresponders to latanoprost [3].
• Trace-to-mild conjunctival hyperemia was recorded more often with bimatoprost phase (P = 0.035) [3].
• CONCLUSION: Bimatoprost-induced periocular hyperpigmentation is caused by increased melanogenesis [4].

High impact information on Lumigan

• Prostanoid FP receptor agonists selectively increase uveoscleral outflow and the prostamide analog bimatoprost alters trabecular and uveoscleral outflow [5].
• Because prostamide receptors are, to date, defined only at the pharmacological level, Bimatoprost effects on Cyr61 and CTGF were studied in the isolated feline iris sphincter preparation, a tissue highly responsive to prostamides [6].
• The prostamide analog Bimatoprost and an EP2-selective agonist affects only Cyr61 [6].
• Prostaglandin F2alpha formation from prostaglandin H2 by prostaglandin F synthase (PGFS): crystal structure of PGFS containing bimatoprost [7].
• PURPOSE: This study was designed to clarify the involvement of the prostanoid FP receptor in the intraocular pressure (IOP)-lowering effects of latanoprost, travoprost, bimatoprost, and unoprostone with the use of FP-receptor-deficient (FPKO) mice [8].

Chemical compound and disease context of Lumigan

• In vitro study of inflammatory potential and toxicity profile of latanoprost, travoprost, and bimatoprost in conjunctiva-derived epithelial cells [9].
• CONCLUSIONS: In individuals with glaucoma or ocular hypertension, uncontrolled on a topical beta-blocker alone, bimatoprost lowered IOP more consistently than did combined timolol and dorzolamide [10].
• PURPOSE: To evaluate the IOP-lowering efficacy of bimatoprost and travoprost for the treatment of glaucoma and ocular hypertension [11].
• CONCLUSION: Decreased vision of at least two lines caused by angiographically confirmed cystoid macula edema was noted in each of three patients started, respectively, on unoprostone, travaprost, and bimatoprost [12].
• PURPOSE: To study the effect of bimatoprost 0.03% (Lumigan) on ocular hemodynamics in patients with open-angle glaucoma or ocular hypertension [13].

Biological context of Lumigan

• Effect of bimatoprost on intraocular pressure in prostaglandin FP receptor knockout mice [14].
• Assuming that this conversion also occurs in vivo at a similar rate, this hydrolysis product may account for the reduction of intraocular pressure occurring in patients treated with bimatoprost [15].
• Retrobulbar hemodynamics by CDI, intraocular pressure by Goldmann applanation tonometer, blood pressure by cuff, and heart rate by palpation were measured at baseline and at 1 month after bimatoprost treatment [13].
• Assuming that AGN 192024 does not cause prolonged lowering of episcleral venous pressure, the results show that pressure-insensitive outflow is enhanced by 50%, whereas tonographic facility of outflow (reciprocal of resistance) was enhanced 35% [16].
• We found that cornea, sclera, iris, and ciliary body, all rapidly hydrolyzed bimatoprost to 17-phenyl-PGF(2 alpha) with linear kinetics at a rate of 6.3, 2.0, 2.8, and 1.5 pmol mg tissue(-1) hr(-1), respectively [17].

Anatomical context of Lumigan

• Tissue, aqueous humor and vitreous concentrations of bimatoprost, latanoprost, and their C-1 free acids were determined by liquid chromatography and tandem mass spectrometry [14].
• In vitro comparison of cytoprotective and antioxidative effects of latanoprost, travoprost, and bimatoprost on conjunctiva-derived epithelial cells [1].
• Results indicated that the potent responses to bimatoprost in the rabbit uterus are produced by the intact molecule and not by its putative free acid metabolite, 17-phenyl PGF(2alpha) [18].
• 4) Bimatoprost pretreatment did not attenuate PGF(2alpha)-induced Ca(2+) signals in Swiss 3T3 cells [19].
• In contrast, bimatoprost exhibited weak excitatory activity in human myometrium from pregnant and nonpregnant donors, mouse uterus, rat uterus, and endothelium-intact rabbit jugular veins, and did not stimulate DNA synthesis in mouse fibroblasts [18].

Associations of Lumigan with other chemical compounds

• Both PGF2alpha and Bimatoprost up-regulated Cyr61 mRNA expression in the cat iris tissue [6].
• The FP receptor-selective antagonist AL-8810 antagonized the (+/-)-fluprostenol-induced PI turnover in these cells (K(i) = 2.56 +/- 0.62 micro M) as well as that induced by bimatoprost and acids of latanoprost and travoprost [20].
• 5. It appears that PGF(2alpha) and Butaprost activate Nur77 transcription mechanisms through the activation of FP and EP(2) receptor-coupled signaling pathways, whereas Bimatoprost stimulates neither FP nor EP(2) receptors [21].
• PURPOSE: To compare the efficacy and safety of once-daily (QD) bimatoprost, latanoprost, and timolol gel-forming solution in providing 24-hour intraocular pressure (IOP) control [22].
• Using human and bovine corneal tissue, we investigated the in vitro metabolism of bimatoprost (17-phenyl-18,19,20-trinor-prostaglandin F(2alpha) ethyl amide, Lumigan (Allergan, Inc, Irvine, CA) [15].

Gene context of Lumigan

• Bimatoprost (nonhydrolyzed amide) also behaved as an FP agonist at the cloned human FP receptor (EC50 = 681 nM), in h-TM (EC50 = 3245 nM) and other cell types [23].
• Bimatoprost (BMP), which is a highly effective ocular hypotensive agent, is a PGF(2)(alpha) analogue that inhibits both the PGD(2) 11-ketoreductase and PGH(2) 9,11-endoperoxide reductase activities of PGFS [7].
• Bimatoprost acid exhibited functional activity at the EP1 (EC50 = 2.7 nM) and FP (EC50 = 2.8-3.8 nM in most cells) receptors [23].
• CONCLUSIONS: An intact FP receptor gene is critical to the IOP response to bimatoprost in the mouse eye [14].
• Serial IOP measurements were also performed after topical bimatoprost in a separate generation of homozygous FP-knockout mice and wild-type littermate control animals (n = 4 per group) [14].

Analytical, diagnostic and therapeutic context of Lumigan

• Tissue and aqueous humor concentrations of bimatoprost, latanoprost, and their C-1 free acids indicate that latanoprost, but not bimatoprost, is hydrolyzed in the mouse eye after topical administration [14].
• 3. Bioassay metabolism studies of bimatoprost and latanoprost (FP receptor agonist prodrug) in the rabbit uterus were conducted using recipient mouse uterus [18].
• In a 12-month extension of two identically designed 1-year, multicenter, randomized, double-masked clinical trials, patients were treated topically with bimatoprost 0.03% QD (n=167), bimatoprost 0.03% BID (n=131), or timolol 0.5% BID (n=81) [24].
• METHODS: Eyelid biopsy specimens from bimatoprost-treated patients and matched controls were examined by light microscopy and transmission electron microscopy [4].
• A Markov modelled pharmacoeconomic analysis of bimatoprost 0.03% in the treatment of glaucoma as an alternative to filtration surgery in Italy [25].

References