8-Bromo-cGMP sodium

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

8-Bromo-cGMP sodium 是 cGMP 的膜渗透性类似物，是一种 PKG 激活剂。8-Bromo-cGMP sodium 可显着抑制 Ca2+ 宏观电流并损害高 K+ 刺激的胰岛素释放。8-Bromo-cGMP sodium 具有缓解疼痛和血管舒张作用。

8-Bromo-cGMP sodium, a membrane-permeable analogue of cGMP, is a PKG (protein kinase G) activator.8-Bromo-cGMP sodium significantly inhibits Ca2+ macroscopic currents and impairs insulin release stimulated with high K+. 8-Bromo-cGMP sodium has antinociceptive effects and results in vasodilator responses.

8-Bromo-cGMP sodium (1-100 μM; 8 h) increases resistance of LLC-PK1 cells to CsA toxicity concentration-dependently. 8-Bromo-cGMP sodium (1-100 μM; 16 h) induces the synthesis of HO-1 protein in a concentration-dependent fashion. Cell Viability Assay Cell Line:LLC-PK1 cells (ATCC CL 101) Concentration:1-100 μM Incubation Time:8 hours Result:Increased resistance of LLC-PK1 cells to Cyclosporin A (CsA) toxicity concentration-dependently and augmented cell viability by up to 65%.Western Blot Analysis Cell Line:LLC-PK1 cells (ATCC CL 101) Concentration:1-100 μM Incubation Time:16 hours Result:Induced the synthesis of HO-1 protein in a concentration-dependent fashion.

8-Bromo-cGMP sodium (0.3, 1, 3.0 nmol; intrathecal administration; 10 min before test) dose-dependently and significantly increases the tail-flick latency in Vincristine-treated mice to the level observed in vehicle-treated naive mice (male ICR mice, 4weeks of age and weighing 20 g). Vincristine (0.05 mg/kg 1 day after the pre-drug tail-flick latency, and then 0.125 mg/kg twice a week for 6 weeks) can induce painful neuropathy in mice. 8-Bromo-cGMP sodium (10 mg/kg; iv; single dose) results in vasodilator responses in eNOS-Tg mice and WT littermates in C57BL/6 background (19-35 g).

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Apoptosis

PKA

PKA | Calcium Channel

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51116-01-9

446.09

C10H10BrN5NaO7P

>98% (HPLC)

In Vitro:?H2O 中的溶解度 : 100 mg/mL (224.18 mM; 超声助溶)

[Na+].Nc1nc(=O)c2nc(Br)n(C3OC4COP([O-])(=O)OC4C3O)c2[nH]1

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(-20℃)

With Ice Pack

≥ 2 years