Calcifediol has an elimination half-life of around 15 to 30 days.Calcifediol is further hydroxylated at the 1-alpha-position in the kidneys to form 1,25-(OH)2D3, calcitriol. This enzymatic 25(OH)D-1α-hydroxylase reaction is performed exclusively by CYP27B1, which is highly expressed in the kidneys where it is principally regulated by parathyroid hormone, but also by FGF23 and calcitriol itself. CYP27B1 is also expressed in a number of other tissues, including macrophages, monocytes, keratinocytes, placenta and parathyroid gland and extra-renal synthesis of calcitriol from calcifediol has been shown to have biological effects in these tissues.Calcifediol is also converted into 24,25-dihydroxycholecalciferol by 24-hydroxylation. This enzymatic reaction is performed by CYP24A1 which is expressed in many vitamin D target tissues including kidney, and is induced by calcitriol. This will inactivate calcitriol to calcitroic acid, but 24,25-(OH)2D3 may have some biological actions itself. Blood test for vitamin D deficiency
In medical practice, a  blood test for 25-hydroxy-vitamin D, 25(OH)D, is used to determine an individuals vitamin D status. The name 25(OH)D refers to any combination of calcifediol (25-hydroxy-cholecalciferol), derived from vitamin D3, and ercalcidiol (25-hydroxy-ergocalciferol), derived from vitamin D2. The first of these (also known as 25-hydroxy vitamin D3) is made by the body, or is sourced from certain animal foods or cholecalciferol supplements. The second (25-hydroxy vitamin D2) is from certain vegetable foods or ergocalciferol supplements. Clinical tests for 25(OH)D often measure the total level of both of these two compounds together, generally without differentiating.This measurement is considered the best indicator of overall vitamin D status.
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.