trabecular

CK-666 是一种肌动蛋白相关蛋白 Arp2 3 复合物的细胞渗透性抑制剂。 它与 Arp2 3 复合物结合，稳定复合物的非活性状态，阻止 Arp2 和 Arp3 亚基进入活化的丝状短节距构象。

Tetrahydrocortisol（四氢皮质醇）是一种神经类固醇和皮质醇的代谢物，是一种GABAA受体的拮抗剂，还能够降低眼压。

Poncirin (Isosakuranetin-7-neohesperidoside) 是从三叶草中分离出来的一种天然产物，具有抗炎活性。 它防止脂肪生成，增强间充质干细胞中的成骨细胞分化，增加骨矿物质密度，改善小梁微结构，可能反映 GIO 小鼠的骨形成增加和骨吸收减少。

Sphinganine-1-phosphate (d17:0) is a sphingolipid analog of sphinganine-1-phosphate (d18:0) and sphingosine-1-phosphate (d18:1) that has a 17-carbon base. Sphinganine-1-phosphate (d17:0) levels are lower in surgical and cadaver trabecular meshwork samples isolated from patients with primary open angle glaucoma compared with control samples.

C16 Sphingosine-1-phosphate (C16 S1P) is a derivative of sphingosine-1-phosphate that binds to S1P1/EDG-1, S1P3/EDG-3, and S1P2/EDG-5 receptors with affinities of 115%, 83%, and 103%, respectively, relative to S1P in CHO cells. C16 S1P was increased in postmortem primary open angle glaucoma trabecular meshwork samples.

Verosudil (AR-12286) 是一种高效的 Rho 激酶 (ROCK) 抑制剂，对 ROCK1 和 ROCK2 的 Ki 分别为 2 和 2 nM。AR-12286 可逆转类固醇诱导的小鼠眼内压，可通过增加眼房水通过小梁网流出来减缓眼压。

ROCK-IN-4 是 ROCK 的有效抑制剂，可维持 NO 释放能力。ROCK-IN-4 能够可逆地解聚 F-肌动蛋白，并阻碍人小梁网 (HTM) 细胞的线粒体呼吸。ROCK-IN-4 能够用于研究青光眼或高眼压。

KR-67607, also known as NTX-101 is novel selective 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) inhibitor. KR-67607 decreased 4-hydroxynonenal expression and increased antioxidant and mucus secretion in BAC-treated rat eyes. KR-67607 showed its protective effects against ischemia-reperfusion-induced eye injury. KR-67607 effectively reduced cortisol levels in mouse eyes and maintained the trabecular meshwork (TM) structure in the presence of transient ischemic stress. Furthermore, KR-67607 reversed the elevation of intra-ocular pressure (IOP), suggesting that the TM structure maintained by KR-67607 prevented the excessive rise in IOP that exacerbates glaucoma.

2MD是一种口服活性维生素D类似物，能刺激骨膜骨形成并减少小梁骨吸收，从而恢复小梁和皮质骨的质量与强度。在非人灵长类动物研究中，2MD还可以调节(IOP)相关基因，降低眼压。

VnP-16是一种合成肽段，对应vitronectin的氨基酸270-281，vitronectin是一种具有细胞附着、迁移和扩散等多功能作用的糖蛋白。该肽段在9.1 µg/cm2浓度下应用于细胞板时，能促进人类成骨细胞的附着和扩散，此效应可通过β1整合素的siRNA敲除被逆转。VnP-16诱导人类皮肤来源的间充质前体细胞和MC3T3-E1小鼠颅骨成骨前体细胞的成骨作用。在体内，VnP-16减少IL-1α诱导的骨质流失并减少小鼠颅骨中破骨细胞的数量。它还在卵巢切除引起的骨质疏失小鼠模型中增加骨矿物质密度并减少松质骨流失。