Dibutyryl-cGMP sodium

• CAT Number: R065172
• CAS Number: 51116-00-8
• Molecular Formula: C18H23N5NaO9P
• Molecular Weight: 507.37
• Purity: ≥95%
• Synonyms: sodium;[(4aR,6R,7R,7aR)-6-[2-(butanoylamino)-6-oxo-1H-purin-9-yl]-2-oxido-2-oxo-4a,6,7,7a-tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-7-yl] butanoate
• InChI: InChI=1S/C18H24N5O9P.Na/c1-3-5-10(24)20-18-21-15-12(16(26)22-18)19-8-23(15)17-14(31-11(25)6-4-2)13-9(30-17)7-29-33(27,28)32-13;/h8-9,13-14,17H,3-7H2,1-2H3,(H,27,28)(H2,20,21,22,24,26);/q;+1/p-1/t9-,13-,14-,17-;/m1./s1
• InChIKey: MGBPJXVWDGGLKI-GBIKJYCISA-M
• SMILES: CCCC(=O)NC1=NC2=C(C(=O)N1)N=CN2C3C(C4C(O3)COP(=O)(O4)[O-])OC(=O)CCC.[Na+]

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].
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].
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].

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.
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[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.
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[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.
 [Content Brief]