Dibutyryl-cGMP sodium (Bt2cGMP sodium) is a cell-permeable cGMP analog. Dibutyryl-cGMP sodium preferentially activates cGMP-dependent protein kinase (PKG). Dibutyryl-cGMP sodium inhibits [3H]-arachidonic acid release in human platelets stimulated by gamma thrombin. Dibutyryl-cGMP sodium can induce peripheral analgesia by activating ATP-sensitive K + channels.

Dibutyryl-cGMP can induce the process of prolongation and branching of astrocytes, which is caused by the rapid, reversible and concentration-dependent redistribution of glial fibrillary acidic protein (GFAP) and actin filaments, while the protein level No significant changes. When the cells were incubated with succinyl-cGMP (100 μM), the formation of stress fibers was prevented, and the cells obtained a star-like morphology in cerebellar astrocytes. In cells treated with dibutyryl-cGMP (100 μM, 2 h), the particle fraction contained almost no RhoA protein. Dibutyryl-cGMP prevents RhoA-membrane binding. Using the scratch model, the size of the wound in cells treated with succinyl-cGMP after the wound was significantly reduced, indicating that dbcGMP accelerated the 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. The maximum analgesic effect of DbcGMP was 1 h after the administration and continued for more than 2 h.