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161230-88-2

中文名稱 3-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸
英文名稱 (Z)-2-CARBOXY-4,6-DICHLOROINDOLE-3-(2'-PHENYL-2'-CARBOXY)-ENE
CAS 161230-88-2
分子式 C18H11Cl2NO4
分子量 376.19
MOL 文件 161230-88-2.mol
更新日期 2024/12/03 15:40:32
161230-88-2 結構式 161230-88-2 結構式

基本信息

中文別名
3-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸
英文別名
MDL-105212
MDL 105,519
MDL 105,519 >=98% (HPLC), solid
(Z)-2-CARBOXY-4,6-DICHLOROINDOLE-3-(2'-PHENYL-2'-CARBOXY)-ENE
3-[(1E)-2-Carboxy-2-phenylethenyl]-4,6-dichloro-1H-indole-2-carboxylic acid
1H-Indole-2-carboxylic acid, 3-[(1E)-2-carboxy-2-phenylethenyl]-4,6-dichloro-
所屬類別
生物化工:激動劑抑制劑

物理化學性質

沸點601.3±55.0 °C(Predicted)
密度1.594±0.06 g/cm3(Predicted)
儲存條件-20°C儲存
溶解度DMSO: 5 mg/mL
酸度系數(pKa)3.20±0.19(Predicted)
形態(tài)solid
顏色white

安全數據

WGK Germany3
3-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸價格(試劑級)
報價日期產品編號產品名稱CAS號包裝價格
2024/11/08HY-150853-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸
MDL 105519
161230-88-25mg1000元
2024/11/08HY-150853-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸
MDL 105519
161230-88-210mM * 1mLin DMSO1100元
2024/11/08HY-150853-[(1E)-2-羧基-2-苯乙烯基]-4,6-二氯-1H-吲哚-2-羧酸
MDL 105519
161230-88-210mg1700元

常見問題列表

生物活性
MDL 105519是有效和選擇性的甘氨酸與 NMDA 受體結合的拮抗劑。
體外研究

MDL 105519 is a potent and selective ligand for the glycine recognition site that completely inhibit the binding of [ 3 H]glycine to rat brain membranes with a K i value of 10.9 nM. MDL 105519 is approximately 10,000-fold selective for the glycine recognition site relative to the other receptor types investigated. MDL 105519 inhibits NMDA-dependent responses, such as elevations of [ 3 H]TCP binding in brain membranes, cyclic GMP accumulation in brain slices, and alterations in cytosolic Ca 2+ and Na + -Ca 2+ currents in cultured neurons. Inhibition is non-competitive with respect to NMDA and could be nullified with D-serine.

體內研究

MDL 105519 is an NMDA receptor antagonist in vivo . Intravenously administration of MDL 105519 prevents harmaline-stimulated increases in cerebellar cyclic GMP content, providing biochemical evidence of NMDA receptor antagonism in vivo . This antagonism is associated with anticonvulsant activity in genetically based, chemically induced, and electrically mediated seizure models. Anxiolytic activity is observed in the rat separation-induced vocalization model, but muscle-relaxant activity is apparent at lower doses. Higher doses impair rotorod performance, but are without effect on mesolimbic dopamine turnover or prepulse inhibition of the startle reflex.

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