CAS NO: | 1240514-89-9 |
包装 | 价格(元) |
1mg | 电议 |
5mg | 电议 |
10mg | 电议 |
25mg | 电议 |
Cas No. | 1240514-89-9 |
化学名 | (3R)-3-[(2-methylbenzoyl)amino]-[1,4'-bipiperidine]-1'-carboxylic acid, ethyl ester, 2,2,2-trifluoroacetate |
Canonical SMILES | CC1=C(C(N[C@@H]2CCCN(C3CCN(C(OCC)=O)CC3)C2)=O)C=CC=C1.OC(C(F)(F)F)=O |
分子式 | C21H31N3O3o CF3COOH |
分子量 | 487.5 |
溶解度 | ≤25mg/ml in ethanol;14mg/ml in DMSO;16mg/ml in dimethyl formamide |
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 | IC50: 477 ± 172 nM VU0364572 is a M1 agonist. Alzheimer's disease (AD) is the leading cause of dementia worldwide, and no disease-modifying therapy is availables. Selective M1 muscarinic acetylcholine receptor activation is an attractive mechanism for AD therapy since M1 mediates key effects on cognition, memory, and behavior and has potential for disease-modifying effects on Aβ formation and tau phosphorylation. In vitro: Previous study found that VU0364572 could completely displace [(3)H]-NMS binding to the orthosteric site of M(1)-M(5) receptors at high concentrations. Moreover, consistent with previous studies suggesting actions at a site that is distinct from the orthosteric binding site, VU0364572 was able to slow the rate of [(3)H]-NMS dissociation from CHO-rM(1) membranes [1]. In vivo: To validate M1 as a neuroprotective treatment target for AD, VU0364572 was chronically dosed to 5XFAD mice from a young age preceding Aβ pathology to an age where these mice are known to display memory impairments. Results showed that VU0364572 could significantly decrease oligomeric (oAβ) levels in the cortex, demonstrating one mechanism whereby VU0364572 might exert its neuroprotective effects by reducing the available oAβ pool in the brain. These findings suggested that chronic M1 activation has neuroprotective potential for preventing memory impairments and reducing neuropathology in AD [2]. Clinical trial: So far, no clinical study has been conducted. References: |