目录号 | 产品详情 | 靶点 | |
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T15719 | Others | ||
Latanoprostene bunod (LBN) 是一氧化氮 (NO) 供体前列腺素 F2a 类似物,有用于开角型青光眼或高眼压 (OHT) 患者降低眼压 (IOP) 的局部眼科的研究潜力。 | |||
T67746 | Others | ||
IMS2186 是一种抗脉络膜新生血管 (CNV) 试剂, 可以使癌细胞周期阻滞在 G2/M 期,由此产生抗增殖和抗血管生成作用。IMS2186 能够减少眼睛渗漏和病变细胞的数量,并且无眼内毒性。 | |||
T22029 | 5-HT Receptor Adrenergic Receptor | ||
AL 34662 是一种具有选择性和高效性的 5-HT2A 受体激动剂,对大鼠和人 5-HT2 受体的IC50 分别为 0.77 nM 和 1.5 nM。AL 34662 还是一种亲和力较低的 α-1D 肾上腺素能激动剂,EC50 值为 0.4 μM。AL 34662 可用于降低眼压。 | |||
T2403 | COX | ||
Bromfenac sodium hydrate (Bromfenac monosodium salt sesquihydrate) 是一种可口服的 COX 抑制剂,抑制 COX-1和COX-2的IC50值分别为 5.56 和 7.45 nM。它是一种溴化非甾体类抗炎药,有用于白内障的术后炎症和疼痛以及假晶状体囊状黄斑水肿的研究。 | |||
T25483 | |||
H-0106 Dihydrochloride is an inhibitor of ROCK that acts by applying strong intraocular pressure (IOP)-lowering effects into the eyes of monkeys. | |||
T25482 | |||
H-0104 Dihydrochloride is an inhibitor of ROCK that acts by applying potent intraocular pressure (IOP)-lowering effects into the eyes of monkeys. | |||
T13955 | Others | ||
Unoprostone is a prostaglandin F2α analogs (PGAs), and reduces intraocular pressure and is used topically for glaucoma or ocular hypertension. | |||
T10358L2 | Others | ||
Netarsudil mesylate is an inhibitor of Rho-associated protein kinase (ROCK) and norepinephrine transporter (NET) with effective in intraocular pressure (IOP) reduction. | |||
T11821 | Others | ||
Latanoprost lactone diol is an important intermediate compound in the synthesis of Latanoprost. Latanoprost, classified as a prostaglandin F2α analogue, functions as an agonist for the FP prostanoid receptor, resulting in a reduction in intraocular pressure (IOP). | |||
T28126 | |||
Nabitan hydrochloride is a synthetic cannabinoid analog with antiemetic and analgesic effects. It may bind to and activate the CB1 and CB2 cannabinoid receptors. It also reduces intraocular pressure and may be useful in treating glaucoma. |
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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