Calcitriol CAS 32222-06-3

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Model: MOS 32222-06-3
Place of Origin: Zhejiang,China (Mainland)
Name: Calcitriol
CAS: 32222-06-3
Molecular Formula: C27H44O3
Brand: MOSINTER
Content: 98%min
Molecular Weight: 416.64
Synonyms 1: VITAMIN D3
Synonyms 2: 1ALPHA,25-DIHYDROXY
Synonyms 3: 1ALPHA,25-DIHYDROXY-VITAMIN D8
Melting point: 119-121℃
Category:

Calcitriol CAS: 32222-06-3

Calcitriol (INN), also called 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin D3,

is the hormonally active metabolite of vitamin D with three hydroxyl groups(abbreviated 

1,25-(OH)2D3 or simply 1,25(OH)2D).[6] It was first identified by Michael F. Holick in

work published in 1971. Calcitriol increases the level of calcium(Ca2+) in the blood by

increasing the uptake of calcium from the gut into the blood, increasing reabsorption of

calcium by the kidneys, and possibly increasing the release of calcium into the blood from bone.

Calcitriol increases blood calcium levels ([Ca2+]) by:

Promoting absorption of dietary calcium from the gastrointestinal tract.

Increasing renal tubular reabsorption of calcium, thus reducing the loss of calcium in the urine.

Stimulating release of calcium from bone. For this it acts on the specific type of bone cells

referred to as osteoblasts, causing them to release RANKL, which in turn activates osteoclasts.

For instance, PTH also indirectly stimulates osteoclasts. However, the main effect of PTH is to increase the

rate at which the kidneys excrete inorganic phosphate (Pi), thecounterion of Ca2+. The resulting

decrease in serum phosphate causes hydroxyapatite (Ca5(PO4)3OH) to dissolve out of bone thus

increasing serum calcium. PTH also stimulates the production of calcitriol (see below).

Many of the effects of calcitriol are mediated by its interaction with the calcitriol receptor, also

called the vitamin D receptor or VDR. For instance, the unbound inactive form of the calcitriol

receptor in intestinal epithelial cells resides in the cytoplasm. When calcitriol binds to the receptor,

the ligand-receptor complex translocates to the cell nucleus, where it acts as a transcription factor 

promoting the expression of a gene encoding a calcium binding protein. The levels of the calcium

binding protein increase enabling the cells to actively transport more calcium (Ca2+) from the

intestine across the intestinal mucosa into the blood.

The maintenance of electroneutrality requires that the transport of Ca2+ ions catalyzed by the

intestinal epithelial cells be accompanied by counterions, primarily inorganic phosphate.

This calcitriol also stimulates the intestinal absorption of phosphate.

The observation that calcitriol stimulates the release of calcium from bone seems contradictory,

given that sufficient levels of serum calcitriol generally prevent overall loss of calcium from bone.

It is believed that the increased levels of serum calcium resulting from calcitriol-stimulated intestinal

uptake causes bone to take up more calcium than it loses by hormonal stimulation of osteoclasts.

Only when there are conditions, such as dietary calcium deficiency or defects in intestinal transport,

which result in a reduction of serum calcium does an overall loss of calcium from bone occur.

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