Meglumine cyclic adenylate
Meglumine cyclic adenylate is a cAMP analog. Meglumine cyclic adenylate promotes STAT3 phosphorylation at Ser727 and mitochondrial translocation. Meglumine cyclic adenylate inhibits cell apoptosis by reducing cytochrome c release and caspase-3 activation. Meglumine cyclic adenylate suppresses the expression of NF-κBp65, activates adenylate cyclase 3, and inhibits phosphodiesterase 4D. Meglumine cyclic adenylate enhances myocardial contractility, increases myocardial Ca2+ influx, dilates peripheral blood vessels, improves hypotension and bradycardia, promotes spinal cord function recovery, and regulates fear extinction and anxiety-like behaviors. Meglumine cyclic adenylate can be used in research related to cerebral ischemia/reperfusion injury, systemic inflammatory response syndrome, acute T4 thoracic spinal cord injury, and post-traumatic stress disorder (PTSD).
For research use only. We do not sell to patients.
- CAS No.: 113960-50-2
- Formula: C17H29N6O11P
- Molecular Weight:524.42
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
STAT3 |
Caspase 3 |
In Vitro
Meglumine cyclic adenylate (200 μM; present during and after OGD, with cell collection at 3 h post-reoxygenation) protects HT22 cells against OGD/R injury via STAT3-Ser727 phosphorylation-dependent mitochondrial translocation of STAT3 and inhibition of the mitochondrial-associated apoptosis pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Meglumine cyclic adenylate (2 mg/kg; intravenous injection; single administration 20 minutes prior to LPS injection) alleviates LPS (HY-D1056)-induced systemic inflammatory response syndrome in rats by reducing pro-inflammatory cytokine levels, increasing anti-inflammatory cytokine levels, downregulating NF-κBp65 expression, and elevating plasma cAMP levels[2].
Meglumine cyclic adenylate (2 mg/kg/d; intravenous injection; once daily; for 3 consecutive weeks) improves cardiovascular hemodynamics in rats with acute T4 spinal cord injury, increases cAMP levels in cardiomyocytes and injured spinal cord tissues, and promotes the recovery of motor function[3].
Meglumine cyclic adenylate (10 mg/kg; i.p.; single injection administered 30 minutes prior to re-exposure during fear extinction training (FET)) promotes fear extinction and reduces anxiety-like behaviors in mice with post-traumatic stress disorder (PTSD), as evidenced by decreased post-fear freezing duration and increased extinction coefficient[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (adult male, 250-280 g, four-vessel occlusion global cerebral ischemia/reperfusion model)[1]
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Dosage:5 mg/kg
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Administration:i.v.; single dose; 30 min before ischemia
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Result:Increased the number of surviving pyramidal neurons in the hippocampal CA1 region to 126 per millimeter.
Enhanced STAT3-Ser727 phosphorylation in the hippocampal CA1 region.
Reversed the ischemia/reperfusion-induced decrease of mitochondrial p-Ser727-STAT3 and total STAT3.
Ameliorated the loss of mitochondrial cytochrome c.
Reduced cytosolic cytochrome c levels and active caspase-3 levels.
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Animal Model:Sprague-Dawley (male, 2-3 months old, 200-250 g, LPS-induced endotoxemia)[2]
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Dosage:2 mg/kg
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Administration:i.v.; single dose 20 min prior to LPS injection
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Result:Reduced plasma levels of proinflammatory cytokines IL-1, IL-6, and TNF-α compared to LPS-only rats.
Increased plasma levels of anti-inflammatory cytokine IL-10 compared to LPS-only rats.
Reduced plasma NF-κBp65 expression compared to LPS-only rats.
Increased plasma cAMP levels compared to LPS-only rats.
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Animal Model:Sprague-Dawley (adult, male and female, 250-310 g, acute T4 thoracic spinal cord contusion injury induced via weight-drop method)[3]
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Dosage:2 mg/kg/d
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Administration:i.v.; once daily; 3 weeks
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Result:Reduced heart rate decline to 25.4 beats/min and mean arterial pressure decline to 20.4 mmHg at 6 weeks post-injury.
Reduced spinal cord blood flow decline to 15.9 mL/100g/min at 7 days post-injury.
Achieved Basso, Beattie, and Bresnahan locomotor scale score of 13.1 and inclined plane maintaining ratio of 0.4 at 6 weeks post-injury.
Increased mean density of Nissl bodies in spinal cord neurons to 327.2 at 7 days post-injury.
Increased cAMP concentration to 112.5 pM/mL in injured spinal cord tissue and 42.1 pmol/mL in myocardial cells at 7 days post-injury.
Produced larger areas of spared gray matter, fewer vacuolations and hemorrhage, more neurons with normal subcellular ultrastructure, less mitochondrial swelling, and more abundant rough endoplasmic reticulum and ribosomes in spinal cord tissue compared to control groups.
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Animal Model:mice (male) [4]
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Dosage:10 mg/kg
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Administration:i.p.; single injection 30 min before re-exposure during FET
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Result:Reduced freezing time during the 24-h post-fear test compared to untreated SPS mice.
Increased extinction coefficient compared to untreated SPS mice, matching levels seen in control mice.
Improved anxiety-like behaviors.
Chemical Information
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CAS No. 113960-50-2
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Molecular Weight 524.42
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Formula C17H29N6O11P
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SMILES
OC[C@@H](O)[C@@H](O)[C@H](O)[C@@H](O)CNC.NC1=NC=NC2=C1N=CN2[C@H]3[C@H](O)[C@H](OP4(O)=O)[C@@H](CO4)O3
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)