Inspra contains eplerenone, a blocker of aldosterone binding at the mineralocorticoid receptor. INSPRA is indicated to improve survival of stable patients with left ventricular systolic dysfunction (ejection fraction 40%) and clinical evidence of congestive heart failure after an acute myocardial infarction.
INSPRA tablets contain 25 mg or 50 mg of eplerenone. The principal risk of INSPRA is hyperkalemia. Hyperkalemia can cause serious, sometimes fatal, arrhythmias. This risk can be minimized by patient selection, avoidance of certain concomitant treatments, and monitoring. For patient selection and avoidance of certain
INDICATIONS AND USAGE
Congestive Heart Failure Post-Myocardial Infarction
INSPRA is indicated to improve survival of stable patients with left ventricular systolic
dysfunction (ejection fraction £40%) and clinical evidence of congestive heart failure after an
acute myocardial infarction.
INSPRA is indicated for the treatment of hypertension. INSPRA may be used alone or in
combination with other antihypertensive agents.
Inspra side effect profile coming soon:
Drug-drug interaction studies were conducted with a 100 mg dose of eplerenone.
Eplerenone is metabolized primarily by CYP3A4. A potent inhibitor of CYP3A4 (ketoconazole)
caused increased exposure of about 5-fold while less potent CYP3A4 inhibitors (erythromycin,
saquinavir, verapamil, and fluconazole) gave approximately 2- fold increases. Grapefruit juice
caused only a small increase (about 25%) in exposure.
The recommended dose of INSPRA is 50 mg once daily. Treatment should be initiated at 25 mg
once daily and titrated to the target dose of 50 mg once daily preferably within 4 weeks as
tolerated by the patient. INSPRA may be administered with or without food.
Serum potassium should be measured before initiating INSPRA therapy, within the first week
and at one month after the start of treatment or dose adjustment. Serum potassium should be
assessed periodically thereafter. Factors such as patient characteristics and serum potassium
levels may indicate that additional monitoring is appropriate.
INSPRA (Eplerenone) binds to the mineralocorticoid receptor and blocks the binding of aldosterone, a
component of the renin-angiotensin-aldosterone-system (RAAS). Aldosterone synthesis, which
occurs primarily in the adrenal gland, is modulated by multiple factors, including angiotensin II
and non-RAAS mediators such as adrenocorticotropic hormone (ACTH) and potassium.
Aldosterone binds to mineralocorticoid receptors in both epithelial (e.g., kidney) and
nonepithelial (e.g., heart, blood vessels, and brain) tissues and increases blood pressure through
induction of sodium reabsorption and possibly other mechanisms.
INSPRA (Eplerenone) has been shown to produce sustained increases in plasma renin and serum
aldosterone, consistent with inhibition of the negative regulatory feedback of aldosterone on
renin secretion. The resulting increased plasma renin activity and aldosterone circulating levels
do not overcome the effects of INSPRA (Eplerenone).