CAS NO: | 198419-91-9 |
包装 | 价格(元) |
10mg | 电议 |
50mg | 电议 |
Cas No. | 198419-91-9 |
化学名 | (S)-4-(amino(carboxy)methyl)-3-methylbenzoic acid |
Canonical SMILES | OC([C@H](C1=CC=C(C(O)=O)C=C1C)N)=O |
分子式 | C10H11NO4 |
分子量 | 209.2 |
溶解度 | <20.92mg/ml in 1.1eq. NaOH |
储存条件 | Desiccate at RT |
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 | IC50: 8.8 μM LY 367385 is a selective mGlu1a receptor antagonist for blockade of quisqualate-induced phosphoinositide hydrolysis. The mGlu family of G-protein-linked glutamate receptors currently comprises eight members by 3,5-dihydroxyphenylglycine can activate specifically Group I mGlu receptors, which have been found to regulate multiple effects in the vertebrate brain. In vitro: Compared with the activity of LY367385, the novel compound LY367366 antagonizes both mGlu1a and -5 receptors at low micromolar concentrations, but also recruits other subtypes at higher concentrations. LY367366 possessing neuroprotective ability was in general less efficacious than LY357385. This fact suggested that inhibitors of mGlu1 receptors is a potential agent to confer significant neuroprotection [1]. In vivo: LY 367385 and AIDA have been administered intracerebroventricularly (i.c.v.) to lethargic mice and DBAr2 mice, and focally into the inferior colliculus of GEPR. In lethargic mice both compounds significantly decrease the incidence of spontaneous spike and wave discharges on the electroencephalogram, after the administration of LY 367385, 250 nmol, i.c.v. LY 367385, 50 nmol, inhibites spontaneous spike and wave discharges from 30 to 60 min. In DBAr2 mice both compounds produce a rapid, transient suppression of sound-induced clonic seizures. In genetically epilepsy prone rats, both compounds decreases sound-induced clonic seizures. The results suggestes that antagonists of mGlu1 receptors are potential anticonvulsant tools and that activation of mGlu1 receptors likely contributes to a variety of epilepticsyndromes [2]. Clinical trial: So far, no clinical study has been conducted. References: |