推荐产品
产品名称
美金胺 盐酸盐, ≥98% (GC)
质量水平
方案
≥98% (GC)
表单
powder
创始人
Forest Labs
SMILES字符串
Cl.C[C@]12CC3C[C@](C)(C1)CC(N)(C3)C2
InChI
1S/C12H21N.ClH/c1-10-3-9-4-11(2,6-10)8-12(13,5-9)7-10;/h9H,3-8,13H2,1-2H3;1H/t9-,10+,11-,12-;
InChI key
LDDHMLJTFXJGPI-VXMZOEJHSA-N
基因信息
human ... DRD1(1812) , DRD2(1813) , DRD3(1814) , DRD4(1815) , DRD5(1816)
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应用
盐酸美金刚用作：
- 培养基的补充剂，作为对照，在N-甲基-D-天冬氨酸受体诱导毒性的条件下，研究促红细胞生成素的神经保护作用
- 腹腔注射实验动物，研究其对创伤的影响
- 作为试验化合物，确定穿透视网膜色素上皮组织的动态范围和选择性
生化/生理作用
低亲和力 NMDA 谷氨酸受体拮抗剂；刺激多巴胺释放。
美金刚对阿尔茨海默氏病和帕金森氏病有效。 也可用于治疗癫痫、运动神经元疾病和创伤。
特点和优势
该化合物是受体分类及信号转导手册上谷氨酸受体（离子通道家族）页面上的特色化合物。想要浏览手册的其他页面， 请单击此处。
该化合物由森林实验室(Forest Labs)开发。要浏览其他药物开发化合物和批准的药物/候选药物列表，单击此处。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Anton N Shuvaev et al.
Brain sciences, 12(4) (2022-04-22)
Memantine is an FDA approved drug for the treatment of Alzheimer's disease. It reduces neurodegeneration in the hippocampus and cerebral cortex through the inhibition of extrasynaptic NMDA receptors in patients and mouse models. Potentially, it could prevent neurodegeneration in other
Ye-Eun Yoo et al.
Frontiers in molecular neuroscience, 14, 712576-712576 (2021-10-02)
Shank2 is an excitatory postsynaptic scaffolding protein strongly implicated in autism spectrum disorders (ASDs). Shank2-mutant mice with a homozygous deletion of exons 6 and 7 (Shank2-KO mice) show decreased NMDA receptor (NMDAR) function and autistic-like behaviors at juvenile [∼postnatal day
Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine
Kelestemur T, et al.
Neuroscience Letters, 612(1), 92-97 (2016)
Dementia of Alzheimer?s disease and other neurodegenerative disorders-memantine, a new hope
Sonkusare SK, et al.
Pharmacological Research, 51(1), 1-17 (2005)
Anton N Shuvaev et al.
International journal of molecular sciences, 22(15) (2021-08-08)
Spinocerebellar ataxias are a family of fatal inherited diseases affecting the brain. Although specific mutated proteins are different, they may have a common pathogenetic mechanism, such as insufficient glutamate clearance. This function fails in reactive glia, leading to excitotoxicity and
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