| CAS NO: | 202825-46-5 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 1mg | 电议 |
| 2mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
| Molecular Weight (MW) | 398.45 |
|---|---|
| Formula | C17H19FN2O2.CH4O3S |
| CAS No. | 202825-46-5; 133865-89-1 (free base); |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 80 mg/mL (200.8 mM) |
| Water: 80 mg/mL (200.8 mM) | |
| Ethanol: 13 mg/mL (32.62 mM) | |
| Solubility (In vivo) | Saline: 30 mg/mL |
| Synonyms | PNU-151774E, FCE28073; Safinamide mesylate; Xadago; NW 1015; PNU 151774E; EMD 1195686; FCE-28073; Safinamide mesilate; FCE 28073; NW1015; NW-1015; EMD-1195686; EMD1195686; PNU-151774E; Chemical Name: (S)-2-((4-((3-fluorobenzyl)oxy)benzyl)amino)propanamide methanesulfonate SMILES Code: C[C@H](NCC1=CC=C(OCC2=CC=CC(F)=C2)C=C1)C(N)=O.CS(=O)(O)=O |
| In Vitro | In vitro activity: Safinamide is a highly selective MAO-B inhibitor in rat brain mitochondria, with an IC50 of 98 nM. safinamide inhibits MAO-B in human brain with an IC50 of 9 nM. Safinamide has high affinity for the Na+ channel-binding site II in rat cortical membranes, with an IC50 of 8 μM. Safinamide inhibits the fast Na+ currents in a concentration- and state-dependent manner in rat cortical neurons. Safinamide blocks N-Type Ca2+ currents in rat cortical neurons with IC50 of 23 μM. Safinamide inhibits glutamate release induced by depolarizing conditions in rat hippocampal synaptosomes with IC50 of 9 μM. Safinamide incubated 1 hour before veratridine reduces the neuron damage with an IC50 1.4 μM through blockade of opening voltage-dependent Na+ and Ca2+ channels in rat primary cortical neurons. Safinamide binds to human MAO B with a Ki of 0.5 μM. Safinamide binds to human MAO B in an extended conformation occupying both flavin and entrance cavity. Kinase Assay: Safinamide (EMD 1195686; FCE 26743) selectively and reversibly inhibits MAO-B with IC50 of 98 nM, exhibits 5918-fold selectivity against MAO-A. Cell Assay: Safinamide has high affinity for the Na+ channel-binding site II in rat cortical membranes, with an IC50 of 8 μM. Safinamide inhibits the fast Na+currents in a concentration- and state-dependent manner in rat cortical neurons. Safinamide blocks N-Type Ca2+ currents in rat cortical neurons with IC50 of 23 μM. Safinamide inhibits glutamate release induced by depolarizing conditions in rat hippocampal synaptosomes with IC50 of 9 μM. Safinamide incubated 1 hour before veratridine reduces the neuron damage with an IC50 1.4 μM through blockade of opening voltage-dependent Na+ and Ca2+channels in rat primary cortical neurons. Safinamide binds to human MAO B with a Ki of 0.5 μM. Safinamide binds to human MAO B in an extended conformation occupying both flavin and entrance cavity. |
|---|---|
| In Vivo | Safinamide orally administrated dose-dependently inhibits mouse brain MAO-B with IC50 of 0.6 mg/kg, and MAO-B activity recovers quickly, starting from 8 hours. Safinamide significantly inhibits cell body degeneration in the substantia nigra pars compacta. Safinamide intraperitoneally administered 15 minutes before kainic acid protects against hippocampal neuron loss, starting at 10 mg/kg showing neuroprotective properties. Safinamide intraperitoneally administrated at dose of 100 mg/kg shows a relevant neurorescuing effect on hippocampal neurons when given 3 hours after ischemia. Safinamide has a high oral bioavailability (80-92%), is rapidly absorbed in plasma after reaching the peak within 0.5-2 hours declines, with a terminal half-life of about 3, 7, and 13 hours in mice, rats, and monkeys, respectively. |
| Animal model | DA-depleted C57BL mice |
| Formulation & Dosage | Dissolved in 0.9% sodium chloride solution; 20 mg/kg; i.p. injection |
| References | Neurology. 2006 Oct 10;67(7 Suppl 2):S18-23; J Med Chem. 2007 Nov 15;50(23):5848-52. |
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