cGMP-dependent protein kinase (PKG);
ATP-sensitive K ⁺ channels

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 (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.