Bioactivity | 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[1][2][3]. |
Target | cGMP-dependent protein kinase (PKG);ATP-sensitive K+ channels |
Invitro | 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[1]. When cells are co-incubated with Dibutyryl-cGMP (100 μM) stress fibre formation is prevented and cells acquired a stellate morphology in cerebellar astrocytes[1]. 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[1].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[1]. |
In Vivo | 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[3]. Animal Model: |
Name | Dibutyryl-cGMP sodium |
CAS | 51116-00-8 |
Formula | C18H23N5NaO9P |
Molar Mass | 507.37 |
Appearance | Solid |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | -20°C, stored under nitrogen, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen, away from moisture) |
Reference | [1]. Borán MS, et al. The cyclic GMP-protein kinase G pathway regulates cytoskeleton dynamics and motility in astrocytes. J Neurochem. 2007 Jul;102(1):216-30. [2]. Sane DC, et al. Cyclic GMP analogs inhibit gamma thrombin-induced arachidonic acid release in human platelets. Biochem Biophys Res Commun. 1989 Dec 15;165(2):708-14. [3]. Soares AC, et al. Dibutyryl-cyclic GMP induces peripheral antinociception via activation of ATP-sensitive K(+) channels in the rat PGE2-induced hyperalgesic paw. Br J Pharmacol. 2001 Sep;134(1):127-31. |