Travoprost is a synthetic ester prodrug of a prostaglandin F2α analogue that inhibits IKir6.2/Sur2a ion channel with an IC50 value of 3μM [1]. Travoprost is hydrolyzed into the active FP prostaglandin receptor agonist by the cornea and sclera, improving trabecular outflow facility[2].Travoprost has been widely used as an eye drop to reduce intraocular pressure in vivo experiments[3].
In vitro, Travoprost treatment at 20µg/ml for 20min significantly inhibited the viability of primary human limbal epithelial cells (LECs) and inhibited cell proliferation[4]. 35µg/ml Travoprost treatment for 72 hours significantly inhibited CD31 and CD54 expression in conjunctiva-derived epithelial cells[5]. Aniridia limbal stromal cells (AN-LSCs) were treated with 0.313μg/ml Travoprost for 20 minutes, resulting in an increase in the MMP-9 protein level of the cells, and an elevation in the mRNA levels of PTGFR and JNK[6].
References:
[1] Friesacher T, Houtman M J C, Chen X, et al. Development of IKatp ion channel blockers targeting sulfonylurea resitant mutant KIR6. 2 based channels for treating DEND syndrome[J]. Biophysical Journal, 2022, 121(3): 388a.
[2] Toris C B, Zhan G, Fan S, et al. Effects of travoprost on aqueous humor dynamics in patients with elevated intraocular pressure[J]. Journal of glaucoma, 2007, 16(2): 189-195.
[3] Lim K S, Nau C B, O'Byrne M M, et al. Mechanism of action of Bimatoprost, Latanoprost, and Travoprost in healthy subjects: a crossover study[J]. Ophthalmology, 2008, 115(5): 790-795. e4.
[4] Li S, Stachon T, Liu S, et al. The effect of travoprost on primary human limbal epithelial cells and the siRNA-based aniridia limbal epithelial cell model, in vitro[J]. Plos one, 2025, 20(8): e0330492.
[5] Guenoun J M, Baudouin C, Rat P, et al. In vitro study of inflammatory potential and toxicity profile of latanoprost, travoprost, and bimatoprost in conjunctiva-derived epithelial cells[J]. Investigative ophthalmology & visual science, 2005, 46(7): 2444-2450.
[6] Li S, Stachon T, Liu S, et al. Increased sensitivity of primary aniridia limbal stromal cells to travoprost, leading to elevated migration and MMP-9 protein levels, in vitro[J]. PloS one, 2025, 20(6): e0326967.
Travoprost是一种前列腺素F2α类似物的合成酯类前药，可抑制IKir6.2/Sur2a离子通道，IC50值为3μM[1]。Travoprost在角膜和巩膜中水解为具有活性的FP前列腺素受体激动剂，从而改善小梁网途径的房水流出易度[2]。Travoprost在体内实验中已被广泛用作滴眼剂以降低眼压[3]。
在体外，使用20µg/ml的Travoprost处理20分钟，显著抑制了原代人角膜缘上皮细胞（LECs）的活力并抑制了细胞增殖[4]。使用35µg/ml的Travoprost处理72小时，显著抑制了结膜来源上皮细胞中CD31和CD54的表达[5]。使用0.313µg/ml的Travoprost处理无虹膜角膜缘基质细胞（AN-LSCs）20分钟，导致细胞中MMP-9蛋白水平升高，以及PTGFR和JNK的mRNA水平上升[6]。