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Dibutyryl-cGMP sodium

Names

[ CAS No. ]:
51116-00-8

[ Name ]:
Dibutyryl-cGMP sodium

[Synonym ]:
sodium,[6-[2-(butanoylamino)-6-oxo-3H-purin-9-yl]-2-oxido-2-oxo-4a,6,7,7a-tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-7-yl] butanoate
Butanoic acid, (4aR,6R,7R,7aR)-6-[1,6-dihydro-6-oxo-2-[(1-oxobutyl)amino]-9H-purin-9-yl]tetrahydro-2-hydroxy-2-oxido-4H-furo[3,2-d]-1,3,2-dioxaphosphorin-7-yl ester, sodium salt (1:1)
Sodium (4aR,6R,7R,7aR)-6-[2-(butyrylamino)-6-oxo-1,6-dihydro-9H-purin-9-yl]-7-(butyryloxy)tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-2-olate 2-oxide

Biological Activity

[Description]:

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].

[Related Catalog]:

Research Areas >> Cardiovascular Disease
Signaling Pathways >> Membrane Transporter/Ion Channel >> Potassium Channel

[Target]

cGMP-dependent protein kinase (PKG)[1]; ATP-sensitive K+ channels[3]


[In Vitro]

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: Male Wistar rats (180- 250 g) injection with Prostaglandin E2 (PGE2)[3] 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.

[References]

[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.

Chemical & Physical Properties

[ Molecular Formula ]:
C18H23N5NaO9P

[ Molecular Weight ]:
507.367

[ Exact Mass ]:
507.113098

[ PSA ]:
196.60000

[ LogP ]:
1.49450

MSDS


Related Compounds