Clevidipine (INN, trade name Cleviprex) is a dihydropyridine calcium channel blocker indicated for the reduction of  blood pressure when oral therapy is not feasible or not desirable. Clevidipine is used IV only and practitioners titrate this drug to lower blood pressure. It has a half-life of approximately one minute. It is rapidly inactivated by esterases. It was approved by the United States Food and Drug Administration on August 1, 2008. Basic chemical and pharmacological properties
Clevidipine is a dihydropyridine L-type calcium channel blocker, highly selective for vascular, as opposed to myocardial, smooth muscle and, therefore, has little or no effect on myocardial contractility or cardiac conduction. It reduces mean arterial blood pressure by decreasing systemic vascular resistance. Clevidipine does not reduce cardiac filling pressure (pre-load), confirming lack of effects on the venous capacitance vessels. No increase in myocardial lactate production in coronary sinus blood has been seen, confirming the absence of myocardial ischemia due to coronary steal. Clevidipine is rapidly metabolized by esterases in the blood and extravascular tissues. Therefore, its elimination is unlikely to be affected by hepatic (liver) or renal (kidney) dysfunction. Clevidipine does not accumulate in the body, and its clearance is independent of body weight. The initial phase half-life is approximately 1 minute and the terminal half-life is approximately 15 minutes. Clevidipine will still be rapidly metabolized in pseudocholinesterase-deficient patients. Clevidipine is formulated as a lipid emulsion in 20% soybean oil (Intralipid) and contains approximately 0.2 g of fat per mL (2.0 kcal/ml).
Urinary calcium excretion balances intestinal calcium absorption and does not increase with calcifediol levels up to ~400 nmol/L (160 ng/mL). Supplementation
Calcifediol supplements have been used in some studies to improve vitamin D status. Indications for their use include vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia, hypoparathyroidism, hypocalcemia and renal osteodystrophy and, with calcium, in primary or corticosteroid-induced osteoporosis.Calcifediol may have advantages over cholecalciferol for the correction of vitamin D deficiency states. A review of the results of nine randomized control trials which compared oral doses of both, found that calcifediol was 3.2-fold more potent than cholecalciferol. Calcifediol is better absorbed from the intestine and has greater affinity for the vitamin-D-binding protein, both of which increase its bioavailability. Orally administered calcifediol has a much shorter half-life with faster elimination. These properties may be beneficial in people with intestinal malabsorption, obesity, or treated with certain other medications.In 2016, the FDA approved a formulation of calcifediol (Rayaldee) 60 microgram daily as a prescription medication to treat secondary hyperparathyroidism in patients with chronic kidney disease. Interactive pathway map
History
Research in the laboratory of Hector DeLuca identified 25(OH)D in 1968 and showed that the liver was necessary for its formation. The enzyme responsible for this synthesis, cholecalciferol 25-hydroxylase, was isolated in the same laboratory by Michael F. Holick in 1972. Research
Studies are ongoing comparing the effects of calcifediol with other forms of vitamin D including cholecalciferol in prevention and treatment of osteoporosis. See also
Hypervitaminosis D
Hypovitaminosis D
Vitamin D

References
External links
"Calcifediol". Drug Information Portal. U.S. National Library of Medicine.