＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

卢非酰胺；CGP 33101；E 2080；RUF 331

白色粉末

DMSO : 47 mg/mL (197.32 mM), warmed

Sodium channel

Rufinamide is extensively metabolised by non-CYP450 systems with a half-life of 8-12 hours. Rufinamide’s mechanism of action is thought to be inhibition of sodium-dependent action potentials in neurons, with possible membrane-stabilising effects. Rufinamide hydrolysis is mediated primarily by human carboxylesterase (hCE) 1 and is nonsaturable up to 500 μM.

Rufinamide given orally at 20 mg/kg every 12 h in healthy dogs should result in a plasma concentration and half-life sufficient to achieve the therapeutic level extrapolated from humans without short-term adverse effects in adult dogs. Rufinamide alleviates injury-induced mechanical allodynia for 4 hours. Rufinamide reduces peak current and stabilizes the inactivated state of voltage-gated sodium channel Nav1.7, with similar effects in dorsal root ganglion neurons in the Spared Nerve Injury neuropathic pain model in mice. Rufinamide suppresses pentylenetetrazol-induced seizures in mice (ED(50) 45.8 mg/kg) but not rats, and is active against MES-induced tonic seizures in mice (ED(50) 23.9 mg/kg) and rats (ED(50) 6.1 mg/kg). Rufinamide suppresses pentylenetetrazol-, bicuculline-, and picrotoxin-induced clonus in mice (ED(50) 54.0, 50.5, and 76.3 mg/kg, respectively). Rufinamide is partially effective in the mouse strychnine test.