Chemical formula: C₁₅H₁₈N₈O₅ Molecular mass: 390.354 g/mol PubChem compound: 219024
Regadenoson interacts in the following cases:
Regadenoson may have a modest inhibitory effect on the active renal transporter, OCT2, and has been found to be likely substrate for BCRP, ENT1 or ENT2 mediated transport. However, given the proposed duration of use, the effects of the drug transporters are unlikely to be clinically relevant.
Methylxanthines (e.g., caffeine and theophylline) are non-specific adenosine receptor antagonists and may interfere with the vasodilation activity of regadenoson. Patients should avoid consumption of any medicinal products containing methylxanthines as well as any medicinal products containing theophylline for at least 12 hours before regadenoson administration.
Dipyridamole increases blood adenosine levels and the response to regadenoson may be altered when blood adenosine levels are increased. When possible, dipyridamole should be withheld for at least two days prior to regadenoson administration.
Regadenoson may cause clinically significant increases in blood pressure, which in some patients can lead to hypertensive crisis. The risk of significant increases in blood pressure may be higher in patients with uncontrolled hypertension. Consideration should be given to delaying regadenoson administration until blood pressure is well controlled.
Use of regadenoson involving exercise has been associated with serious adverse reactions including hypotension, hypertension, syncope and cardiac arrest. Patients who have had any symptoms or signs suggestive of acute myocardial ischaemia during exercise or recovery are likely to be at especially high risk of serious adverse reactions.
Regadenoson can cause transient ischaemic attack. In post-marketing experience there have also been reports of cerebrovascular accident (CVA).
Regadenoson should be used with caution in patients with a history of atrial fibrillation or flutter. In post-marketing experience there have been cases of worsening or recurrence of atrial fibrillation after administration of regadenoson.
Regadenoson may cause bronchoconstriction and respiratory arrest, especially in patients with known or suspected bronchoconstrictive disease, chronic obstructive pulmonary disease (COPD) or asthma. Appropriate bronchodilator therapy and resuscitative measures should be available prior to regadenoson administration.
Caution should be used when administering regadenoson to patients with a history of seizures or other risk factors for seizures, including the concomitant administration of medicinal products that lower seizure threshold (e.g. antipsychotics, antidepressants, theophyllines, tramadol, systemic steroids and quinolones).
Aminophylline should be used with caution in patients with a history of seizures or who have other risk factors for seizures as it may prolong a seizure or cause multiple seizures because of its proconvulsant effect. Therefore administration of aminophylline solely for the purpose of terminating a seizure induced by regadenoson is not recommended.
Regadenoson stimulates sympathetic output and may increase the risk of ventricular tachyarrhythmias in patients with a long QT syndrome.
There are no adequate data from the use of regadenoson in pregnant women. Animal studies on pre- and post-natal development have not been conducted. Fetotoxicity, but not teratogenicity, was noted in embryo-fetal development studies. The potential risk for humans is unknown. Regadenoson should not be used during pregnancy unless clearly necessary.
It is unknown whether regadenoson is excreted in human breast milk. The excretion of regadenoson in milk has not been studied in animals. A decision should be made whether to discontinue breast- feeding or to abstain from regadenoson administration taking into account the benefit of breast-feeding for the child and the benefit of therapy for the woman. If regadenoson is administered, the woman should not breast-feed for at least 10 hours (that is, at least 5 times the plasma elimination half-life) following regadenoson administration.
Fertility studies with regadenoson have not been performed.
Regadenoson administration may result in adverse reactions such as dizziness, headache, and dyspnoea soon after administration. However, most adverse reactions are mild and transient, resolving within 30 minutes after receiving regadenoson. Therefore, regadenoson would be expected to have no or negligible influence on the ability to drive or use machines once treatment has been completed and these reactions have resolved.
Adverse reactions in most patients receiving regadenoson in clinical trials were mild, transient (usually resolving within 30 minutes after receiving regadenoson) and required no medical intervention. Adverse reactions occurred in approximately 80% of patients. The most common adverse reactions reported during clinical development in a total of 1,651 patients/subjects were: dyspnoea (29%), headache (27%), flushing (23%), chest pain (19%), electrocardiogram ST segment changes (18%), gastrointestinal discomfort (15%) and dizziness (11%).
Regadenoson may cause myocardial ischaemia (potentially associated with fatal cardiac arrest, life-threatening ventricular arrhythmias, and myocardial infarction), hypotension leading to syncope and transient ischaemic attacks, elevated blood pressure leading to hypertension and hypertensive crises, and SA/AV node block leading to first, second or third degree AV block, or sinus bradycardia requiring intervention. Signs of hypersensitivity (rash, urticaria, angioedema, anaphylaxis and/or throat tightness) may be immediate or delayed onset. Aminophylline may be used to attenuate severe or persistent adverse reactions to regadenoson but should not be used solely for the purpose of terminating a seizure induced by regadenoson.
Assessment of adverse reactions for regadenoson is based on safety data from clinical studies and post-marketing experience. All adverse reactions are presented in the list below and are listed by system organ class and frequency. Frequencies are defined as very common (≥1/10), common (≥1/100 to <1/10) uncommon (≥1/1,000 to <1/100) and rare (≥1/10,000 to <1/1,000). Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
Uncommon: Hypersensitivity reactions including: Rash, urticaria, angioedema, anaphylaxis
Uncommon: Anxiety, insomnia
Very common: Headache, dizziness
Common: Paraesthesia, hypoaesthesia, dysgeusia
Uncommon: Convulsions, syncope, transient ischaemic attack, unresponsiveness to stimuli, depressed level of consciousness, tremor, somnolence
Rare: Cerebrovascular accident
Uncommon: Vision blurred, eye pain
Uncommon: Tinnitus
Very common: Electrocardiogram ST segment changes
Common: Angina pectoris, atrioventricular block, tachycardia, palpitations, other ECG abnormalities including electrocardiogram QT corrected interval prolonged
Uncommon: Cardiac arrest, myocardial infarction, complete AV block, bradycardia, atrial flutter, new-onset, worsening or recurrence of atrial fibrillation
Very common: Flushing
Common: Hypotension
Uncommon: Hypertension, pallor, peripheral coldness
Very common: Dyspnoea
Common: Throat tightness, throat irritation, cough
Uncommon: Tachypnoea, wheezing
Not known: Bronchospasm, Respiratory arrest
Very common: Gastrointestinal discomfort
Common: Vomiting, nausea, oral discomfort
Uncommon: Abdominal distension, diarrhoea, faecal incontinence
Common: Hyperhidrosis
Uncommon: Erythema
Common: Back, neck or jaw pain, pain in extremity, musculoskeletal discomfort
Uncommon: Arthralgia
Very common: Chest pain
Common: Malaise, asthenia
Uncommon: Pain at injection site, general body pain
Fatal cardiac arrest, life-threatening ventricular arrhythmias and myocardial infarction may result from the ischaemia induced by pharmacologic stress agents. Cardiac resuscitation equipment and trained staff should be available before administering regadenoson.
Regadenoson, can depress the SA and AV nodes and may cause first, second or third degree AV block, or sinus bradycardia requiring intervention. In clinical trials first degree AV block (PR prolongation >220 msec) developed in 3% of patients within 2 hours of regadenoson administration; transient second degree AV block with one dropped beat was observed in one patient receiving regadenoson. In postmarketing experience, third degree heart block and asystole have been reported within minutes of regadenoson administration.
Adenosine receptor agonists, including regadenoson induce arterial vasodilation and hypotension. In clinical trials, decreased systolic blood pressure (>35 mmHg) was observed in 7% of patients and decreased diastolic blood pressure (>25 mmHg) was observed in 4% of patients within 45 minutes of regadenoson administration. The risk of serious hypotension may be higher in patients with autonomic dysfunction, hypovolemia, left main coronary artery stenosis, stenotic valvular heart disease, pericarditis or pericardial effusions, or stenotic carotid artery disease with cerebrovascular insufficiency. In postmarketing experience, syncope and transient ischaemic attacks have been reported.
In clinical trials, increased systolic blood pressure (≥50 mmHg) was observed in 0.7% of patients and increased diastolic blood pressure (≥30 mmHg) in 0.5% of patients. Most increases resolved within 10 to 15 minutes, but in some cases, increases were observed at 45 minutes following administration.
Regadenoson increases sympathetic tone, which causes an increase in heart rate and a shortening of the QT interval. In a patient with a long QT syndrome, sympathetic stimulation can result in less shortening of the QT interval than is normal and may even cause a paradoxical increase in the QT interval. In these patients, the phenomenon of R-on-T syndrome can occur, wherein an extra beat interrupts the T wave of the previous beat, and this increases the risk of a ventricular tachyarrhythmia.
Headache was reported by 27% of subjects who received regadenoson in clinical trials. The headache was considered severe in 3% of subjects.
Older patients (≥75 years of age; n=321) had a similar adverse reaction profile compared to younger patients (<65 years of age; n=1,016), but had a higher incidence of hypotension (2% versus <1%).
© All content on this website, including data entry, data processing, decision support tools, "RxReasoner" logo and graphics, is the intellectual property of RxReasoner and is protected by copyright laws. Unauthorized reproduction or distribution of any part of this content without explicit written permission from RxReasoner is strictly prohibited. Any third-party content used on this site is acknowledged and utilized under fair use principles.
