| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Targets |
Dibutyryl-cGMP sodium targets cGMP-dependent protein kinase (PKG), activating it to phosphorylate downstream substrates (e.g., VASP, ion channels). It also inhibits cGMP-specific phosphodiesterases (PDE5, PDE6) and affects cyclic nucleotide-gated (CNG) ion channels. By mimicking cGMP, it mediates smooth muscle relaxation, vasodilation, inhibition of platelet aggregation, and regulation of synaptic plasticity. The butyryl groups confer membrane permeability and resistance to PDE hydrolysis.
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| ln Vitro |
Actin filaments and glial fibrillary acidic protein (GFAP) are redistributed quickly, reversibly, and concentration-dependently in astrocytes in response to dibutyryl-cGMP, which causes process elongation and branching. The amounts of proteins have not changed significantly [1]. In cerebellar astrocytes, the incubation of dibutyryl-cGMP (100 μM) inhibits the formation of stress fibers and causes the cells to take on the appearance of stars [1]. The granule fraction of cells treated with dibutyryl-cGMP (100 μM, 2 h) showed nearly no RhoA protein. Dibutyryl-cGMP inhibits the binding of RhoA membranes [1]. In cells treated with dibutyryl-cGMP post-wounding, the size of the wound was significantly smaller using a scratch wound model, indicating that dbcGMP speeds up wound closure [1].
In vitro studies have demonstrated that Dibutyryl-cGMP sodium induces concentration-dependent relaxation of precontracted vascular smooth muscle strips (EC₅₀ ~ 1-10 μM). It inhibits ADP-induced platelet aggregation with an IC₅₀ ~ 50 μM. In neuronal cultures, it enhances glutamate release and long-term potentiation (LTP) in hippocampal slices. It also activates PKG and increases phosphorylation of VASP in various cell lines. The compound modulates apoptosis in cardiac myocytes and endothelial cells, and protects against oxidative stress. It is also used to study retinal phototransduction via CNG channels. |
| ln Vivo |
Treatment with dibutyryl-cGMP (50-200 μg/paw; subcutaneous injection; male Wistar rats) antagonized the hyperalgesic effects of PGE2 in a dose-dependent manner. The maximum analgesic effect of DbcGMP occurs 1 hour after administration and lasts for more than 2 hours [3].
In vivo studies have shown that Dibutyryl-cGMP sodium, administered intravenously or intracerebroventricularly, reduces blood pressure in hypertensive rats (1-10 mg/kg). It also inhibits platelet aggregation and thrombus formation in mouse models. In models of cardiac ischemia-reperfusion, it reduces infarct size and improves ventricular function. In the central nervous system, it enhances memory consolidation and synaptic plasticity in rodent behavioral tasks. It also attenuates pain responses in models of neuropathic pain via spinal PKG activation. |
| Enzyme Assay |
In vitro enzyme/receptor binding (non-cell) assays for Dibutyryl-cGMP sodium typically involve PKG activation assays using recombinant PKG and a peptide substrate (e.g., Kemptide) with ³³P-ATP, or by measuring phosphorylation by radioactivity or fluorescence polarization. Alternatively, cGMP-dependent protein kinase activity is measured using ELISA-based kits. PDE inhibition assays: PDE5 is incubated with ³H-cGMP and increasing concentrations of the compound, then hydrolyzed product is measured. IC₅₀ values are determined. Binding to CNG channels can be assessed using patch-clamp electrophysiology in excised membrane patches, with the compound applied to the intracellular side.
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| Cell Assay |
For in vitro cell-based assays, various cell lines (e.g., vascular smooth muscle cells, platelets, neurons, HEK293) are cultured. Cells are treated with Dibutyryl-cGMP sodium at concentrations of 0.1-100 μM for 1-48 hours. PKG activation is monitored by Western blot for phosphorylated VASP (p-VASP) at Ser239. Cell relaxation: vascular smooth muscle cells are treated with the compound and cell area or contraction measured. Platelet aggregation is assessed by light transmission aggregometry. Calcium imaging (Fluo-4) is used to measure changes in intracellular Ca²⁺. Apoptosis measured by Annexin V. Neuronal activity: hippocampal slices are treated and field EPSPs recorded.
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| Animal Protocol |
Animal/Disease Models: Male Wistar rats (180-250 g) injected with prostaglandin E2 (PGE2) [3]
Doses: 50 μg/paw, 75 μg/paw, 100 μg/paw and 200 μg/paw Route of Administration: subcutaneous injection Experimental Results: Antagonized the hyperalgesic effect of PGE2 (2 μg/paw) in a dose-dependent manner. In vivo animal studies with Dibutyryl-cGMP sodium: For cardiovascular, rats are anesthetized, blood pressure is measured via carotid catheter, and compound is given i.v. (1-10 mg/kg) or i.p., and hemodynamic parameters monitored. For thrombosis, mice are injected with the compound i.p. (10 mg/kg) and then challenged with collagen/epinephrine to induce pulmonary embolism; survival and platelet counts measured. For memory, mice are injected i.c.v. (1-5 μg) and tested in Morris water maze or fear conditioning. For pain, rats with spinal nerve ligation are given intrathecal injections (10-50 nmol) and paw withdrawal thresholds measured. Blood/tissue samples collected for PK and pharmacodynamics. |
| ADME/Pharmacokinetics |
Tissue distribution and elimination half-life are not extensively reported for this analog. The compound has a molecular weight of ~492 g/mol (sodium salt) and is soluble in water and DMSO. It is hydrolyzed to cGMP intracellularly by esterases. The butyryl groups improve cell permeability. In vivo, the compound is rapidly cleared from plasma (t₁/₂ < 30 min) due to esterase hydrolysis and renal excretion. For experiments, it is often given acutely. Storage at -20°C as a powder.
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| Toxicity/Toxicokinetics |
In preclinical studies, Dibutyryl-cGMP sodium is well-tolerated at pharmacological doses. In rodents, i.p. doses up to 50 mg/kg produce no significant toxicity; higher doses may cause hypotension and tachycardia. No genotoxicity reported. Chronic administration may cause mild GI effects. It is not intended for human use; safety for therapeutic use has not been established.
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| References |
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| Additional Infomation |
The compound is a cell-permeable cGMP analog widely used in research to dissect NO-cGMP signaling pathways. It activates PKG, PDEs, and CNG channels. It is supplied as a sodium salt for solubility. Used in cardiovascular, neuroscience, and platelet research. Not FDA-approved; for research purposes only.
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| Molecular Formula |
C₁₈H₂₃N₅NAO₉P
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| Molecular Weight |
507.37
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| Exact Mass |
507.113
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| CAS # |
51116-00-8
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| PubChem CID |
136069596
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| Appearance |
White to light yellow solid powder
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| LogP |
1.494
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
11
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| Rotatable Bond Count |
8
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| Heavy Atom Count |
34
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| Complexity |
892
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| Defined Atom Stereocenter Count |
4
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| SMILES |
CCCC(=O)NC1=NC2=C(C(=O)N1)N=CN2[C@H]3[C@@H]([C@H]4[C@H](O3)COP(=O)(O4)[O-])OC(=O)CCC.[Na+]
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| InChi Key |
MGBPJXVWDGGLKI-GBIKJYCISA-M
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| InChi Code |
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
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| Chemical Name |
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
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| Synonyms |
DibutyrylcGMP sodium Dibutyryl cGMP sodium
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~100 mg/mL (~197.09 mM)
DMSO : ~100 mg/mL (~197.09 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.93 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (4.93 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (4.93 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9709 mL | 9.8547 mL | 19.7095 mL | |
| 5 mM | 0.3942 mL | 1.9709 mL | 3.9419 mL | |
| 10 mM | 0.1971 mL | 0.9855 mL | 1.9709 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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