IMPORTANT SAFETY INFORMATION
Cleviprex is intended for intravenous use. Titrate drug depending on the response of the individual patient to achieve the desired blood pressure reduction. Monitor blood pressure and heart rate continually during infusion, and then until vital signs are stable. Patients who receive prolonged Cleviprex infusions and are not transitioned to other antihypertensive therapies should be monitored for the possibility of rebound hypertension for at least 8 hours after the infusion is stopped.
Cleviprex is contraindicated in patients with allergies to soybeans, soy products, eggs, or egg products; defective lipid metabolism such as pathologic hyperlipemia, lipoid nephrosis, or acute pancreatitis if it is accompanied by hyperlipidemia; and in patients with severe aortic stenosis.
Hypotension and reflex tachycardia are potential consequences of rapid upward titration of Cleviprex. Dihydropyridine calcium channel blockers can produce negative inotropic effects and exacerbate heart failure. Monitor heart failure patients carefully. Cleviprex gives no protection against the effects of abrupt beta-blocker withdrawal.
Most common adverse reactions (> 2%) are headache, nausea, and vomiting.
Cleviprex should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Maintain aseptic technique while handling Cleviprex. Cleviprex contains phospholipids and can support microbial growth. Do not use if contamination is suspected. Once the stopper is punctured, use and discard within 4 hours.
DESCRIPTION
The Clevipidine Molecule
Clevidipine ButyrateCleviprex is supplied as a sterile, milky white, ready-to-use lipid emulsion that contains clevidipine butyrate, soybean oil, glycerin, purified egg yolk phospholipids, and sodium hydroxide to adjust pH.1 Cleviprex is formulated and administered in a lipid emulsion because clevidipine butyrate is practically insoluble in water.1
Rapidly Metabolized by Tissue and Blood Esterases
Cleviprex is rapidly metabolized by hydrolysis of the ester linkage, primarily by esterases in the blood and extravascular tissues, making its elimination unlikely to be affected by hepatic or renal dysfunction1 In vitro studies show that Cleviprex and its metabolite, at the concentrations achieved in clinical practice, will not inhibit or induce any cytochrome P (CYP) enzyme1 The potential of Cleviprex to interact with other drugs is low1
Metabolism in Blood and Extravascular Tissues2
Figure adapted from Ericsson H et al. Anesthesiology. 2000;92:993-1001.
Hemodynamics
A New Dynamic for Targeted BP Control
Cleviprex is a vascular and arterial selective dihydropyridine L-type calcium antagonist that mediates the influx of calcium during depolarization in vascular smooth muscle.1 It reduces mean arterial BP by decreasing systemic vascular resistance (SVR) while increasing cardiac output (CO) and stroke volume (SV).2 As a pure afterload reducer, Cleviprex has no effect on venous return or cardiac filling pressure (preload).1
Cleviprex Lowers BP With Targeted Hemodynamics*
*Studied in 9 postoperative cardiac bypass graft patients. This graph shows the effects at the highest Cleviprex dose (3 micrograms/kg/min); +P<.001; ++P<.05. BP=blood pressure; CO=cardiac output; MAP=mean arterial pressure; SBP=systolic blood pressure; SV=stroke volume; SVR=systemic vascular resistance |
