CPPHA 是 mGluR5 和 mGluR1（代谢型谷氨酸受体）的有效和选择性正变构调节剂 (PAM)。
| Cas No. | 693288-97-0 |
| 别名 | N-[4-氯-2-[(1,3-二氢-1,3-二氧代-2H-异吲哚-2-基)甲基]苯基]-2-羟基苯甲酰胺 |
| 化学名 | N-(4-chloro-2-((1,3-dioxoisoindolin-2-yl)methyl)phenyl)-2-hydroxybenzamide |
| Canonical SMILES | O=C(N1CC2=C(NC(C3=CC=CC=C3O)=O)C=CC(Cl)=C2)C4=CC=CC=C4C1=O |
| 分子式 | C22H15ClN2O4 |
| 分子量 | 406.82 |
| 溶解度 | DMSO: 100mM |
| 储存条件 | Store at -20℃ |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request |
| 产品描述 | Description:
IC50 Value: N/A
CPPHA is a selective positive allosteric modulator of mGluR5 receptor. It has no agonist activity alone, but reduces threshold response and shifts dose-response curves to glutamate, quisqualate, and DHPG by 4- to 7-fold to the left in recombinant CHO cells expressing human or rat mGluR5.
in vitro: The selective mGlu5 receptor positive allosteric modulator, N-{4-chloro-2-[(1,3-dioxo-1,3-dihydro-2H-isoindol-2yl)-methyl]phenyl}-2-hydrobenzamide (CPPHA) potentiated the response to a subthreshold concentration of 3,5-dihydroxy-phenylglycine (DHPG) on extracellular signal-regulated protein kinase (ERK) and cyclic-AMP responsive element-binding protein (CREB) activity, as well as N-methyl d-aspartate (NMDA) receptor subunit NR1 phosphorylation in cortical and hippocampal slices [1]. CPPHA potentiated threshold responses to glutamate in fluorometric Ca(2+) assays 7- to 8-fold with EC(50) values in the 400 to 800 nM range, and at 10 microM shifted mGluR5 agonist concentration-response curves to glutamate, quisqualate, and (R,S)-3,5-dihydroxyphenylglycine (DHPG) 4- to 7-fold to the left. CPPHA (10 microM) potentiated NMDA receptor currents in hippocampal slices induced by threshold levels of DHPG, whereas having no effect on these currents by itself. Similarly, 10 microM CPPHA also potentiated mGluR5-mediated DHPG-induced depolarization of rat subthalamic nucleus neurons [2]. CPPHA induced an increase in basal mGluR5-mediated ERK1/2 phosphorylation and potentiated the effect of low concentrations of agonists. In contrast, CPPHA significantly decreased ERK1/2 phosphorylation induced by high concentrations of agonists [3].
in vivo: N/A
Toxicity: N/A
Clinical trial: N/A |
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