2. Apoptosis NF-κB
  3. TNF Receptor NF-κB
  4. Cloricromen

Cloricromen (Cloricromene) is an orally active platelet inhibitor. Cloricromen inhibits thromboxane B2 release, β-thromboglobulin, and thrombus formation. Cloricromen inhibits LPS (HY-D1056)-induced NF-κB activation, oxidative activity, and TNF-α expression. Cloricromen exhibits protective activity in animal models of shock and peripheral ischaemia. Cloricromen can be used for the research of myocardial ischaemia/reperfusion injury, and ischaemic cerebrovascular disease.

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Cloricromen

Cloricromen Chemical Structure

CAS No. : 68206-94-0

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Description

Cloricromen (Cloricromene) is an orally active platelet inhibitor. Cloricromen inhibits thromboxane B2 release, β-thromboglobulin, and thrombus formation. Cloricromen inhibits LPS (HY-D1056)-induced NF-κB activation, oxidative activity, and TNF-α expression. Cloricromen exhibits protective activity in animal models of shock and peripheral ischaemia. Cloricromen can be used for the research of myocardial ischaemia/reperfusion injury, and ischaemic cerebrovascular disease[1][2][3][4].

In Vitro

Cloricromen (1-50 μM; 10 min pre-incubation before 24 h LPS exposure) potently inhibits lipopolysaccharide-induced TNF-α release in rat alveolar macrophages with an IC50 of 5.9 μM, without inducing cytotoxicity[3].
Cloricromen (10 μM; 10 min pre-incubation before 2 h LPS exposure) inhibits LPS-induced TNF-α mRNA expression in rat alveolar macrophages, indicating a pre-transcriptional mechanism of action[3].
Cloricromen (1-50 μM; 10 min pre-incubation before 15 min LPS exposure) LPS-induced NF-κB activation in a dose-dependent manner in rat alveolar macrophages by targeting activation, not direct DNA binding[3].
Cloricromen (10 μM; 10 min pre-incubation before 5 min LPS exposure) has only a slight effect on lipopolysaccharide-induced PKC-βII translocation in rat alveolar macrophages[3].
Cloricromen (10 μM; 10 min pre-incubation before LPS exposure) significantly inhibits lipopolysaccharide-induced cellular oxidative activity in rat alveolar macrophages[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cloricromen Related Antibodies

RT-PCR[3]

Cell Line: rat alveolar macrophages
Concentration: 10 μM
Incubation Time: 10 min pre-incubation before 2 h LPS exposure
Result: Inhibited LPS-induced TNF-α mRNA expression by ~60%.
In Vivo

Cloricromen (30-300 μg/kg/min; i.v.; continuous infusion; from 15 minutes pre-occlusion through 2-hour reperfusion) induces dose-dependent cardioprotection in rabbits with myocardial ischaemia-reperfusion injury[1].
Cloricromene protects against LPS-induced endotoxic shock in male Sprague-Dawley rats by inhibiting TNF-α production, improving survival, and reversing associated hemodynamic and hematological abnormalities[3].
Cloricromene reduces myocardial infarct size in male Sprague-Dawley rats subjected to ischemia-reperfusion injury[3].
Cloricromene (0.25-0.50 mg/kg; i.v.; continuous infusion; up to 70 minutes) reduces myocardial ischemia-reperfusion injury in rabbits[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: New Zealand white rabbits (male, 2-3 kg, myocardial ischaemia-reperfusion model via 1 hour left coronary artery occlusion followed by 2 hours reperfusion)[1]
Dosage: 30; 300 μg/kg/min
Administration: i.v.; continuous infusion; from 15 minutes pre-occlusion through 2-hour reperfusion
Result: Reduced infarct size to 40.8% of the area at risk.
Significantly reduced myeloperoxidase activity in infarcted myocardial tissue.
Showed no attenuation of occlusion-induced ST-segment elevation.
Detected no inhibition of ex vivo platelet aggregation induced by ADP or collagen.
Caused no significant changes in mean arterial blood pressure, pressure-rate index, left ventricular systolic pressure, or heart rate relative to controls.
Significantly reduced myeloperoxidase activity in infarcted myocardial tissue.
Significantly reduced occlusion-induced ST-segment elevation to 0.08 mV at 20 minutes post-occlusion and returned to basal levels by 1 hour post-occlusion.
Inhibited ex vivo platelet aggregation, with collagen-induced aggregation reduced to 57% at end of occlusion and 13% after 2-hour reperfusion, and ADP-induced aggregation reduced to 74% at end of occlusion and 53% after 2-hour reperfusion.
Caused a slight, non-significant decrease in mean arterial blood pressure, a significant decrease in left ventricular systolic pressure at end of occlusion, and a significant increase in heart rate at end of reperfusion, with no change in pressure-rate index.
Animal Model: New Zealand white rabbits (pathogen-free, 2.5-3.5 kg)[4]
Dosage: 3.6 μg/kg/min; 7.1 μg/kg/min (for transient ST elevations); total 0.25-0.50 mg/kg
Administration: i.v.; continuous infusion; up to 70 minutes
Result: Reversed transient ST-segment elevations in 3 out of 4 affected rabbits.
Showed no significant difference in chemiluminescence between anterior and posterior ventricular walls.
Achieved an anterior/posterior wall chemiluminescence ratio of 0.95.
Resulted in an overall myocardial-cell injury score of 1.4.
Preserved myocyte subcellular architecture with only mild or moderate mitochondrial edema.
Maintained well-preserved capillary structure with occasional mild/moderate endothelial luminal protrusions.
Observed focal subendocardial necrosis in 3 out of 10 treated rabbits.
Prevented reperfusion arrhythmias.
Molecular Weight

395.88

Formula

C20H26ClNO5
CAS No.
SMILES

O=C(COC1=CC=C(C(C)=C2CCN(CC)CC)C(OC2=O)=C1Cl)OCC
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Room temperature in continental US; may vary elsewhere.
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Cloricromen68206-94-0Cloricromene AD6AD6AD 6AD-6TNF ReceptorNF-κBTumor Necrosis Factor ReceptorTNFRNuclear factor-κBNuclear factor-kappaBendothelial cellspolymorphonuclear leukocyterat alveolar macrophagesplatelet aggregationthromboxane B2NF-kBmyocardial ischaemia/reperfusion injuryplatelet factor 4TNF-αβ-thromboglobulinInhibitorinhibitorinhibit

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