目录号 | 产品详情 | 靶点 | |
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T61120 | |||
Carbonic Anhydrase Inhibitor2 (compound 7c) 是一种针对 Carbonic Anhydrase II 抑制剂,有效降低青光眼兔眼压。 | |||
T37956 | |||
Tafluprost ethyl amide 是一种前列腺素衍生物。Tafluprost ethyl amide 能降低眼压 (IOP),影响睫毛生长。Tafluprost ethyl amide 可用于抗青光眼眼药及化妆品。 | |||
T36145 | |||
Biosynthesis of 12(R)-HETE in invertebrates is via lipoxygenation of arachidonic acid . In mammals, 12(R)-HETE can be produced by 12(R)-LOs and also by CYP450 oxidation. The activity of 12(R)-HETE in mammals is predominantly proinflammatory. 12(R)-HETE exhibits dose-dependent leukocyte chemotaxis at concentrations as low as 100 nM, and lowers intraocular pressure in rabbits. | |||
T60350 | |||
Apraclonidine (ALO 2145) 是一种选择性α2和弱 α1 受体激动剂,可有效降低人眼的眼内压。Apraclonidine 也是一种局部滴眼液。 | |||
T70735 | |||
Verosudil, also known as AR-12286, is a potent and selective Rho kinase inhibitor. AR-12286 was well tolerated and provided statistically significant reduction in IOP (intraocular pressure) in patients with XFS (exfoliation syndrome) and OHT (ocular hypertension) or XFG (exfoliative glaucoma). This drug may represent an additional therapeutic paradigm for the treatment of XFG. | |||
T61180 | |||
GAT564 (Compound 15d) is a highly effective allosteric modulator of cannabinoid 1 receptor (CB1R), having EC50 values of 87 nM and 320 nM for cAMP and β-arrestin2, respectively. It significantly enhances the binding of orthosteric ligands to hCB1R. Moreover, GAT564 exhibits remarkable efficacy as a topical agent, resulting in a significant reduction of intraocular pressure (IOP) in an ocular normotensive murine model of glaucoma [1]. | |||
T62036 | |||
Sovesudil (PHP-201) 是有效的、ATP 竞争性局部作用 Rho 激酶(ROCK)抑制剂。Sovesudil 抑制 ROCK I 和 ROCK II 的IC50分别为 3.7 和 2.3 nM。Sovesudil 可以降低眼压而不引起充血。 | |||
T38194 | |||
Prostaglandin E3 (PGE3) is formed via the cyclooxygenase (COX) metabolism of eicosapentaenoic acid. [1] In human ocular tissue, it comprises 2.4% of the COX products formed. [1] When applied to the eyes of a rabbit, a 1 µg dose of PGE3 decreases intraocular pressure from 21 mmHg to about 17 mmHg.[2] | |||
T64241 | |||
Brinzolamide (AL-4862) hydrochloride 是一种碳酸酐酶 II(carbonic anhydrase II)的选择性抑制剂 (IC50: 3.2 nM)。Brinzolamide hydrochloride 能够抑制睫状体 CA-II,减少房水分泌,进而降低眼压 (IOP)。Brinzolamide hydrochloride 能够用于研究青光眼疾病。 | |||
T74736 | |||
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。 |
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-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-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-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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