2. GPCR/G Protein Neuronal Signaling Apoptosis
  3. Opioid Receptor Apoptosis
  4. (-)-P7C3-S243

(-)-P7C3-S243 是一种具有口服活性的、能穿过血脑屏障的神经保护剂。(-)-P7C3-S243 可结合 μ-阿片受体 (Opioid Receptor) 和 TSPO。(-)-P7C3-S243 可抑制新生海马神经元的过早凋亡 (apoptosis) 性死亡，保护成熟黑质多巴胺能神经元，促进神经元存活并预防认知障碍。(-)-P7C3-S243 可在大鼠模型中改善抑郁样行为。(-)-P7C3-S243 可用于帕金森病和阿尔茨海默病的相关研究。

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(-)-P7C3-S243

(-)-P7C3-S243 Chemical Structure

CAS No. : 1597443-57-6

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(-)-P7C3-S243 相关抗体

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μ Opioid Receptor/MOR κ Opioid Receptor/KOR δ Opioid Receptor/DOR NOP Receptor/ORL1

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

(-)-P7C3-S243 is an orally active, blood-brain barrier permeable neuroprotective agent. (-)-P7C3-S243 binds to μ-opioid Receptor and TSPO. (-)-P7C3-S243 inhibits the premature apoptosis death of newborn hippocampal neurons, protects mature nigral dopaminergic neurons, promotes neuronal survival and prevents cognitive impairment. (-)-P7C3-S243 ameliorates depression-like behaviors in rat models. (-)-P7C3-S243 is applicable to research related to Parkinson's disease and Alzheimer's disease[1][2].

体外研究
(In Vitro)

(−)-P7C3-S243 (Compound 15) 可在体外轻度抑制 CYP1A2 (IC50 = 20 μM) 和 CYP2C19 (IC50 = 1.9 μM)，但对其他多种受试 CYP 亚型无抑制作用[1]。
(−)-P7C3-S243 可在体外结合 μ-阿片受体 (IC50 = 8.2 μM) 和 TSPO (IC50 = 0.35 μM)，但不与大多数其他受试神经元受体及通道结合[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

(-)-P7C3-S243 相关抗体:
体内研究
(In Vivo)

(−)-P7C3-S243 ( 10 μM (12
μL/day)/0.1-10 mg/kg/天；i.c.v./i.p.；每日 2 次；7 天) 可使环境匮乏小鼠体内存活的新生海马神经元数量增加一倍，提高海马神经元的存活率[1]
(−)-P7C3-S243 (1-10 mg/kg；腹腔注射；每日 2 次；连续 21 天) 可剂量依赖性地保护经 MPTP (HY-15608) 处理小鼠黑质中的成熟多巴胺能神经元[1]。
(−)-P7C3-S243 (10 mg/kg；腹腔注射；10 天) 可使 TgF344-AD 大鼠的出生后海马神经发生水平提升 1 倍，保护大鼠免受早期类抑郁行为和晚期认知损伤的影响，减少神经退行性变和神经元丢失，同时还可改善野生型大鼠的年龄相关性类抑郁行为[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/J6 (12-week-old)[1]
Dosage: 10 μM; 0.1-10 mg/kg/day
Administration: i.c.v.; 0.5 μL/h; 7 days; i.p.; BID; 7 days
Result: Approximately doubled the number of surviving BrdU+ newborn hippocampal neurons compared to vehicle-treated mice.
Showed a smooth dose-response curve, with activity detectable at 1 mg/kg/day and maximum efficacy achieved at 10 mg/kg/day; efficacy reflected increased survival of newborn hippocampal neurons via neuroprotection (not increased proliferation).
Animal Model: C57Bl/6 (adult male; MPTP-induced Parkinson's disease)[1]
Dosage: 1, 3, 5, 10 mg/kg/day
Administration: i.p.; BID; 21 days
Result: Showed significant neuroprotective activity at 1 mg/kg/day, and at the highest tested dose of 10 mg/kg/day, rescued over 85% of TH+ dopaminergic neurons in the substantia nigra (compared to MPTP-treated vehicle controls).; Demonstrated higher efficacy than that of P7C3-A20, with strict enantiomeric specificity (only the (−)-S enantiomer was active).
Animal Model: Fischer 344 rats (male and female, 6 months old at treatment initiation; TgF344-AD transgenic overexpressing human mutant APP_SW and PS1ΔE9 genes; wild-type)[2]
Dosage: 10 mg/kg/d
Administration: daily; 9 months (15-month assessments); 18 months (24-month assessments)
Result: Reduced time spent immobile in the Porsolt forced swim test in TgF344-AD rats to levels comparable to WT animals at 15 months.
Did not affect locomotor activity or cause cognitive deficits in any group at 15 months.
Improved performance in the Morris water maze reversal memory probe in TgF344-AD rats, reducing time to locate the target position to levels similar to WT animals at 24 months.
Ameliorated depression-like behavior in 24-month-old WT rats, reducing time spent immobile in the Porsolt forced swim test from mean 45 seconds to mean 20 seconds (p=0.0176), but did not correct depression-like behavior in 24-month-old TgF344-AD rats.
Significantly reduced vacuole formation in the hippocampus and cerebral cortex of TgF344-AD rats at 24 months.
Prevented neuronal cell loss in the hippocampus and cerebral cortex, and increased neuronal cell counts in the dentate gyrus granule cell layer of TgF344-AD rats at 24 months.
Did not alter amyloid plaque deposition, levels of soluble or insoluble Aβ1-40/Aβ1-42 peptides, tau hyperphosphorylation (Tau PS199/202), or glial activation (GFAP+ astrocytes or Iba1+ microglia) in TgF344-AD rats at 24 months.
分子量

507.19

Formula

C21H18Br2FN3O
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

(-)-P7C3-S243 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

(-)-P7C3-S2431597443-57-6Opioid ReceptorApoptosisneuroprotective agentParkinson's diseaseAlzheimer's diseaseC57BL/J6 miceFischer 344 ratsInhibitorinhibitorinhibit

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