产品
编 号：F374017
分子式：C18H23N5NaO9P
分子量：507.37
分子式：C18H23N5NaO9P
分子量：507.37
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规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
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5mg
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10mg
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询价
结构图
CAS No: 51116-00-8
产品详情
生物活性：
Dibutyryl-cGMP sodium (Bt2cGMP sodium) is a cell-permeable cGMP analogue. Dibutyryl-cGMP sodium preferentially activates cGMP-dependent protein kinase (PKG). Dibutyryl-cGMP sodium inhibits the release of [3H]-arachidonic acid from γ thrombin-stimulated human platelets. Dibutyryl-cGMP sodium induces peripheral antinociception via activation of ATP-sensitive K+ channels.
体内研究：
Dibutyryl-cGMP (50-200?μg/paw; subcutaneous injection; male Wistar rats) treatment antagonizes the hyperalgesic effect of PGE2 in a dose-dependent manner. Maximal antinociceptive effect of DbcGMP is at 1?h after administration and last for plus 2?h.Animal Model:Male Wistar rats (180-?250?g) injection with Prostaglandin E2 (PGE2)
Dosage:50 μg/paw, 75 μg/paw, 100 μg/paw and 200?μg/paw
Administration:Subcutaneous injection
Result:Antagonized the hyperalgesic effect of PGE2 (2?μg/paw), in a dose-dependent manner.
体外研究：
Dibutyryl-cGMP is able to induce process elongation and branching in astrocytes resulting from a rapid, reversible and concentration-dependent redistribution of glial fibrillary acidic protein (GFAP) and actin filaments without significant change in protein levels. When cells are co-incubated with Dibutyryl-cGMP (100 μM) stress fibre formation is prevented and cells acquired a stellate morphology in cerebellar astrocytes. In cells treated with Dibutyryl-cGMP (100 μM, 2 h) the particulate fraction is nearly devoid of RhoA protein. Dibutyryl-cGMP prevents RhoA-membrane association.Using the scratchwound model, the size of the wound is significantly smaller in cells treated with Dibutyryl-cGMP after the wound indicating that dbcGMP accelerates wound closure.
Dibutyryl-cGMP sodium (Bt2cGMP sodium) is a cell-permeable cGMP analogue. Dibutyryl-cGMP sodium preferentially activates cGMP-dependent protein kinase (PKG). Dibutyryl-cGMP sodium inhibits the release of [3H]-arachidonic acid from γ thrombin-stimulated human platelets. Dibutyryl-cGMP sodium induces peripheral antinociception via activation of ATP-sensitive K+ channels.
体内研究：
Dibutyryl-cGMP (50-200?μg/paw; subcutaneous injection; male Wistar rats) treatment antagonizes the hyperalgesic effect of PGE2 in a dose-dependent manner. Maximal antinociceptive effect of DbcGMP is at 1?h after administration and last for plus 2?h.Animal Model:Male Wistar rats (180-?250?g) injection with Prostaglandin E2 (PGE2)
Dosage:50 μg/paw, 75 μg/paw, 100 μg/paw and 200?μg/paw
Administration:Subcutaneous injection
Result:Antagonized the hyperalgesic effect of PGE2 (2?μg/paw), in a dose-dependent manner.
体外研究：
Dibutyryl-cGMP is able to induce process elongation and branching in astrocytes resulting from a rapid, reversible and concentration-dependent redistribution of glial fibrillary acidic protein (GFAP) and actin filaments without significant change in protein levels. When cells are co-incubated with Dibutyryl-cGMP (100 μM) stress fibre formation is prevented and cells acquired a stellate morphology in cerebellar astrocytes. In cells treated with Dibutyryl-cGMP (100 μM, 2 h) the particulate fraction is nearly devoid of RhoA protein. Dibutyryl-cGMP prevents RhoA-membrane association.Using the scratchwound model, the size of the wound is significantly smaller in cells treated with Dibutyryl-cGMP after the wound indicating that dbcGMP accelerates wound closure.
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