1. Membrane Transporter/Ion Channel
  2. Potassium Channel
  3. Dibutyryl-cGMP sodium

Dibutyryl-cGMP sodium (Synonyms: Bt2cGMP sodium)

Cat. No.: HY-130354 Purity: >98.0%
Handling Instructions

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.

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Dibutyryl-cGMP sodium Chemical Structure

Dibutyryl-cGMP sodium Chemical Structure

CAS No. : 51116-00-8

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Based on 1 publication(s) in Google Scholar

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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].

IC50 & 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.
Molecular Weight

507.37

Formula

C₁₈H₂₃N₅NaO₉P

CAS No.

51116-00-8

SMILES

CCCC(NC1=NC2=C(C(N1)=O)N=CN2[[email protected]]3[[email protected]@H]([[email protected]]4[[email protected]](O3)COP(O4)(O[Na])=O)OC(CCC)=O)=O

Shipping

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)

References

Purity: >98.0%

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Keywords:

Dibutyryl-cGMPBt2cGMPPotassium ChannelKcsARhoA-membraneLPSastrocytesantinociceptionwoundclosurecell-permeableproteinkinaseInhibitorinhibitorinhibit

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Dibutyryl-cGMP sodium
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