产品
编 号：F624915
分子式：C21H23ClFN7O
分子量：443.91
分子式：C21H23ClFN7O
分子量：443.91
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 1293284-49-7
产品详情
生物活性：
Seltorexant hydrochloride (JNJ-42847922 hydrochloride) is an orally active, high-affinity, and selective OX2R antagonist (pKi values of 8.0 and 8.1 for human and rat OX2R). Seltorexant hydrochloride crosses the blood-brain barrier and quickly occupies OX2R binding sites in the rat brain.
体内研究：
Seltorexant (JNJ-42847922) hydrochloride (3-30 mg/kg；口服) 剂量依赖性地诱导和延长雄性 Sprague-Dawley 大鼠的睡眠。 Seltorexant hydrochloride (30 mg/kg；口服每天，持续 7 天) 的延长睡眠的作用在大鼠中重复给药 7 天后得以维持。Animal Model:Male Sprague-Dawley rats (350-450 g)
Dosage:30 mg/kg
Administration:p.o.; per day for 7 days
Result:The reduced sleep onset (non–rapid eye movement (NREM) latency) and the increased NREM sleep duration were maintained upon 7-day repeated dosing with JNJ-42847922. The prolongation of NREM sleep time was due to a significant increase in NREM bout duration throughout the treatment period assessed on D1 and D7. Rapid eye movement (REM) sleep was only marginally affected on D4 of treatment, resulting in a small but significant reduction in REM sleep latency and an increase in REM sleep duration.
Seltorexant hydrochloride (JNJ-42847922 hydrochloride) is an orally active, high-affinity, and selective OX2R antagonist (pKi values of 8.0 and 8.1 for human and rat OX2R). Seltorexant hydrochloride crosses the blood-brain barrier and quickly occupies OX2R binding sites in the rat brain.
体内研究：
Seltorexant (JNJ-42847922) hydrochloride (3-30 mg/kg；口服) 剂量依赖性地诱导和延长雄性 Sprague-Dawley 大鼠的睡眠。 Seltorexant hydrochloride (30 mg/kg；口服每天，持续 7 天) 的延长睡眠的作用在大鼠中重复给药 7 天后得以维持。Animal Model:Male Sprague-Dawley rats (350-450 g)
Dosage:30 mg/kg
Administration:p.o.; per day for 7 days
Result:The reduced sleep onset (non–rapid eye movement (NREM) latency) and the increased NREM sleep duration were maintained upon 7-day repeated dosing with JNJ-42847922. The prolongation of NREM sleep time was due to a significant increase in NREM bout duration throughout the treatment period assessed on D1 and D7. Rapid eye movement (REM) sleep was only marginally affected on D4 of treatment, resulting in a small but significant reduction in REM sleep latency and an increase in REM sleep duration.
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