目录号 | 产品详情 | 靶点 | |
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T3174 | Prostaglandin Receptor | ||
Taprenepag (CP-544326) 是一种有效的选择性前列腺素 E2 受体激动剂,EC50为 2.8 nM,可用于研究开角治疗高眼压和青光眼的试验。 | |||
T12670 | Others | ||
(Rac)-MGV354 (MGV354) 是 MGV354 的外消旋体,MGV354 是可溶性鸟苷酸环化酶活化剂,在 GTM-3E 和 CHO 细胞中 EC50分别为 5 nM 和小于 0.5 nM。 | |||
T0142 | Carbonic Anhydrase | ||
Brinzolamide (AL-4862) 是一种碳酸酐酶(carbonic anhydrase)II 抑制剂(IC50:3.19 nM)。 | |||
T0106 | Carbonic Anhydrase | ||
Methazolamide (CL 8490) 是一种磺胺衍生物,用作碳酸酐酶 (carbonic anhydrase) 抑制剂,对人 carbonic anhydrase II 的 Ki=为 14 nM。它是降低眼压的药物,能够抑制由青光眼及其他眼病引起的眼压升高的作用。 | |||
T60924 | ROCK | ||
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。 | |||
T1071L | Adrenergic Receptor | ||
DL-Adrenaline Hydrochloride 是天然存在的拟交感神经胺的盐酸盐,具有收缩血管、降低眼内压的活性。 | |||
T10358 | ROCK | ||
Netarsudil Dihydrochloride (AR-13324 Dihydrochloride) 是 Rho 相关蛋白激酶 (ROCK) 和去甲肾上腺素转运蛋白 (NET) 的抑制剂,可有效降低眼压 (IOP)。 | |||
T6422 | Adrenergic Receptor | ||
Brimonidine Tartrate (AGN190342 tartrate) 是一种 alpha2 Adrenergic Receptor (alpha2-AR) 受体激动剂。 | |||
T19870 | AChR | ||
Aceclidine (1-azabicyclo[2.2.2]octan-3-yl acetate) 是M3 mAChR 的调节剂,可用于有关通过降低眼内压治疗青光眼的研究。 | |||
T21371 | Adrenergic Receptor | ||
Apraclonidine hydrochloride (ALO 2145) 是一种 α2-肾上腺素能激动剂和弱的 α-1 肾上腺素能受体激动剂。 Apaclonidine hydrochloride 可降低人眼的眼内压,可用于青光眼治疗的研究。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-05435 | ANGPT1/Angiopoietin-1 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
The angiopoietin (ANGPT)-TIE2/TEK signaling pathway is essential for blood and lymphatic vascular homeostasis. ANGPT1 is a potent TIE2 activator, whereas ANGPT2 functions as a context-dependent agonist/antagonist. In disease, ANGPT2-mediated inhibition of TIE2 in blood vessels is linked to vascular leak, inflammation, and metastasis. Primary congenital glaucoma (PCG) is a leading cause of blindness in children worldwide and is caused by developmental defects in 2 aqueous humor outflow structures, Schlemm's canal (SC) and the trabecular meshwork. We previously identified loss-of-function mutations in the angiopoietin (ANGPT) receptor TEK in families with PCG and showed that ANGPT/TEK signaling is essential for SC development. A role for the major ANGPT ligands in the development of the aqueous outflow pathway. We determined that ANGPT1 is essential for SC development, and that Angpt1-knockout mice form a severely hypomorphic canal with elevated intraocular pressure. By linking ANGPT1 with PCG, these results highlight the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target for therapeutic development.
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TMPY-04245 | ANGPT1/Angiopoietin-1 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
The angiopoietin (ANGPT)-TIE2/TEK signaling pathway is essential for blood and lymphatic vascular homeostasis. ANGPT1 is a potent TIE2 activator, whereas ANGPT2 functions as a context-dependent agonist/antagonist. In disease, ANGPT2-mediated inhibition of TIE2 in blood vessels is linked to vascular leak, inflammation, and metastasis. Primary congenital glaucoma (PCG) is a leading cause of blindness in children worldwide and is caused by developmental defects in 2 aqueous humor outflow structures, Schlemm's canal (SC) and the trabecular meshwork. We previously identified loss-of-function mutations in the angiopoietin (ANGPT) receptor TEK in families with PCG and showed that ANGPT/TEK signaling is essential for SC development. A role for the major ANGPT ligands in the development of the aqueous outflow pathway. We determined that ANGPT1 is essential for SC development, and that Angpt1-knockout mice form a severely hypomorphic canal with elevated intraocular pressure. By linking ANGPT1 with PCG, these results highlight the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target for therapeutic development.
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TMPY-05351 | ANGPT1/Angiopoietin-1 Protein, Cynomolgus, Recombinant (hFc) | Cynomolgus | HEK293 | ||
The angiopoietin (ANGPT)-TIE2/TEK signaling pathway is essential for blood and lymphatic vascular homeostasis. ANGPT1 is a potent TIE2 activator, whereas ANGPT2 functions as a context-dependent agonist/antagonist. In disease, ANGPT2-mediated inhibition of TIE2 in blood vessels is linked to vascular leak, inflammation, and metastasis. Primary congenital glaucoma (PCG) is a leading cause of blindness in children worldwide and is caused by developmental defects in 2 aqueous humor outflow structures, Schlemm's canal (SC) and the trabecular meshwork. We previously identified loss-of-function mutations in the angiopoietin (ANGPT) receptor TEK in families with PCG and showed that ANGPT/TEK signaling is essential for SC development. A role for the major ANGPT ligands in the development of the aqueous outflow pathway. We determined that ANGPT1 is essential for SC development, and that Angpt1-knockout mice form a severely hypomorphic canal with elevated intraocular pressure. By linking ANGPT1 with PCG, these results highlight the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target for therapeutic development.
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TMPY-00366 | ANGPT1/Angiopoietin-1 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
The angiopoietin (ANGPT)-TIE2/TEK signaling pathway is essential for blood and lymphatic vascular homeostasis. ANGPT1 is a potent TIE2 activator, whereas ANGPT2 functions as a context-dependent agonist/antagonist. In disease, ANGPT2-mediated inhibition of TIE2 in blood vessels is linked to vascular leak, inflammation, and metastasis. Primary congenital glaucoma (PCG) is a leading cause of blindness in children worldwide and is caused by developmental defects in 2 aqueous humor outflow structures, Schlemm's canal (SC) and the trabecular meshwork. We previously identified loss-of-function mutations in the angiopoietin (ANGPT) receptor TEK in families with PCG and showed that ANGPT/TEK signaling is essential for SC development. A role for the major ANGPT ligands in the development of the aqueous outflow pathway. We determined that ANGPT1 is essential for SC development, and that Angpt1-knockout mice form a severely hypomorphic canal with elevated intraocular pressure. By linking ANGPT1 with PCG, these results highlight the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target for therapeutic development.
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TMPY-02248 | Myocilin Protein, Human, Recombinant (His) | Human | HEK293 | ||
Myocilin, also known as Trabecular meshwork-induced glucocorticoid response protein, MYOC, and GLC1A, is a protein that contains one olfactomedin-like domain. Myocilin / MYOC may participate in the obstruction of fluid outflow in the trabecular meshwork. Myocilin / MYOC is expressed in large amounts in various types of muscle, ciliary body, papillary sphincter, skeletal muscle, heart, and other tissues. Myocilin / MYOC is expressed predominantly in the retina. In normal eyes, it is found in the inner uveal meshwork region and the anterior portion of the meshwork. In contrast, in many glaucomatous eyes, it is found in more regions of the meshwork and appeared more intensively than in normal eyes, regardless of the type of clinical severity of glaucoma. Defects in Myocilin / MYOC may contribute to primary congenital glaucoma type 3A (GLC3A). Defects in MYOC may also contribute to this phenotype via digenic inheritance. GLC3A is an autosomal recessive form of primary congenital glaucoma (PCG). PCG is characterized by a marked increase of intraocular pressure at birth or early childhood, large ocular globes (buphthalmos), and corneal edema.
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