Indication |
Diagnostic agent for radionuclide myocardial perfusion imaging (MPI) |
Mechanism of action |
Regadenoson is an selective low-affinity (Ki= 1.3 uM) A2A receptor agonist that mimics the effects of adenosine in causing coronary vasodilatation and increasing myocardial blood flow. It is a very weak agonist of the A1 adenosine receptor (Ki > 16.5 uM). Furthermore, it has negligible affinity to A2B and A3 adenosine receptors. Regadenoson is undergoing trials for use in pharmacological stress tests. Adenosine slows conduction time through the A-V node, can interrupt the reentry pathways through the A-V node, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White Syndrome. |
Absorption |
The pharmacokinetic profile of regadenoson is best described by a 3-compartment model.
T max, injection = 1 to 3 minutes;
Onset of pharmacodynamic response = 1 to 3 minutes;
E max 12.3 ng/mL
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Protein binding |
Not Available |
Biotransformation |
The metabolism of regadenoson is unknown in humans. The cytochrome P450 enzyme system is not likely to be involved with the metabolism of regadenoson. |
Route of elimination |
58% of total regadenoson eliminate is via renal excretion |
Toxicity |
The most common (incidence >= 5%) adverse reactions to regadenoson are dyspnea, headache, flushing, chest discomfort, dizziness, angina pectoris, chest pain, and nausea.
MTD (male, supine position): 20 ug/kg;
MTD (male, standing position): 10 ug/kg; |
Affected organisms |
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