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PDE9-IN-1

CAS No. 2305087-92-5

PDE9-IN-1 ( —— )

产品货号. M26362 CAS No. 2305087-92-5

PDE9-IN-1 是一种有效的、选择性的、口服生物可利用的磷酸二酯酶-9A (PDE9A) 抑制剂(IC50 为 8.7 nM)。

纯度: >98% (HPLC)

COA Datasheet HNMR HPLC MSDS Handing Instructions
规格 价格/人民币 库存 数量
5MG ¥818 有现货
10MG ¥1311 有现货
25MG ¥2213 有现货
50MG ¥3097 有现货
100MG ¥4257 有现货
200MG ¥5787 有现货
500MG 获取报价 有现货
1G 获取报价 有现货
1 mL x 10 mM in DMSO ¥658 有现货

生物学信息

  • 产品名称
    PDE9-IN-1
  • 注意事项
    本公司产品仅用于科研实验,不得用于人体或动物的临床与诊断
  • 产品简述
    PDE9-IN-1 是一种有效的、选择性的、口服生物可利用的磷酸二酯酶-9A (PDE9A) 抑制剂(IC50 为 8.7 nM)。
  • 产品描述
    PDE9-IN-1 is a potent, selective, and orally bioavailable Inhibitor of phosphodiesterase-9A (PDE9A)(IC50 of 8.7 nM).(In Vivo):In the Unilateral common carotid artery occlusion (UCCAO) mouse model, PDE9-IN-1 (2.5-5.0 mg/kg; orally) significantly reduces the day 6 escape latency time, increases the frequency of platform area crossings, and recoveres learning and memory function. High dose group possibly improved the escape latency time of mice.
  • 体外实验
    PDE9-IN-1 is excellent selectivity across PDE families.
  • 体内实验
    PDE9-IN-1 (2.5 and 5.0 mg/kg; Oral administration; daily for 21 days) effectively recovers learning and memory function. Animal Model:Unilateral common carotid artery occlusion (UCCAO) mouse model Dosage:2.5 and 5.0 mg/kg Administration:Oral administration; daily for 21 days Result:Significantly reduced the day 6 escape latency time and increased the frequency of platform area crossings, and recovered learning and memory function. High dose group possibly improved the escape latency time of mice.
  • 同义词
    ——
  • 通路
    Others
  • 靶点
    Other Targets
  • 受体
    NMDA receptor
  • 研究领域
    ——
  • 适应症
    ——

化学信息

  • CAS Number
    2305087-92-5
  • 分子量
    362.409
  • 分子式
    C17H23FN6O2
  • 纯度
    >98% (HPLC)
  • 溶解度
    In Vitro:?DMSO : 100 mg/mL (275.94 mM)
  • SMILES
    C[C@@H](Nc1nc2n(ncc2c(=O)[nH]1)C1CCCC1)C(=O)N1CC[C@H](F)C1
  • 化学全称
    ——

运输与储存

  • 储存条件
    (-20℃)
  • 运输条件
    With Ice Pack
  • 稳定性
    ≥ 2 years

参考文献

1.Lozovaya N, Gataullina S, et al. Selective suppression of excessive GluN2C expression rescues early epilepsy in a tuberous sclerosis murine model. Nat Commun. 2014 Aug 1;5:4563.
产品手册
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