- Vitamin D receptor (VDR) – Binds to VDR after conversion to active metabolite calcitriol (1,25-dihydroxyvitamin D3), leading to transcription of vitamin D-dependent genes [1][2]
- CYP27A1 and CYP2R1 – These 25-hydroxylases convert cholecalciferol to 25-hydroxyvitamin D3 (25(OH)D3) [2]
- CYP27B1 – 1-alpha-hydroxylase that converts 25(OH)D3 to active calcitriol [2]
- CYP24A1 – Enzyme that degrades both 1,25D and 25(OH)D [2]

- In endometrial carcinoma cell lines (IK, RL-95/2, HEC-1A) that express VDR, CYP27A1, and CYP2R1, cholecalciferol (VD3) treatment at 2-10 μM for 24, 48, or 72 hours reduced cell viability in a dose- and time-dependent manner; maximal reduction of viability at 72 hours with 10 μM VD3 was 62% in IK cells, 52% in RL-95/2 cells, and 55% in HEC-1A cells [2]
- Cholecalciferol (0-10 μM for 48 hours) caused a dose-dependent decrease in colony formation capacity of all three endometrial carcinoma cell lines [2]
- In IK cells, treatment with 10 μM VD3 for 48 hours resulted in detectable intracellular 25(OH)D synthesis (average 1.24 ng from 7 million cells); no detectable 25(OH)D was produced at 12 or 24 hours [2]
- In IK cells, VD3 treatment for 24 or 48 hours caused marked increases in nuclear VDR staining (immunofluorescence) and nuclear VDR translocation (western blot), with maximal translocation occurring at 48 hours [2]
- In IK cells treated with 10 μM VD3, nuclear VDR expression increased at 48 hours while cytosolic VDR decreased, confirming VDR translocation to the nucleus [2]

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Vitamin D3 is an in vivo inactive molecule of vitamin D. To activate vitamin D3, it goes through two hydroxylation processes. The enzyme 25-hydroxylase (CYP27A1) and possibly other enzymes (such as CYP2R1) hydroxylate vitamin D3 in the liver to create the circulating prohormone 25-hydroxy vitamin D3 [25(OH)D3][1]. The kidneys use the enzyme 1-alpha-hydroxylase to carry out the second hydroxylation, resulting in 1,25-dihydroxycholecalciferol, or calcitriol, the biologically active form of vitamin D[1]. Vitamin D3 (2-10 μM; 24-48 hours) shows effects against proliferation that are dependent on both time and dose. After treating with 10 μM vitamin D3, the viability of 62% (IK), 52% (RL-95-2), and 55% (Hec-1A) is at its lowest point after 72 hours. However, there is no discernible decrease in viable cells after a 24-hour exposure[2]. Cholecalciferol (10 μM; 24-48 hours) exhibits notable increases in nuclear VDR staining and causes IK cells to become activated locally for VDR[1].

- In cycling normal human endometrium, cholecalciferol activation to 25(OH)D via CYP27A1 and CYP2R1 plays a role in VDR antiproliferative actions; nuclear VDR levels correlated inversely with Ki67 proliferation marker, and CYP27A1 and CYP2R1 expression correlated directly with nuclear VDR and inversely with Ki67 [2]
- In endometrial carcinoma tissue samples, CYP27A1 expression was 11-fold higher than in normal endometrium (P < 0.00001); CYP2R1 expression was 1.3-fold higher (P = 0.005) [2]
- In a mouse model, pre-treatment with cholecalciferol (5 mg/kg, oral gavage, once daily for 4 days) significantly increased plasma calcium levels from 7.77 ± 0.70 mg/dL to 13.0 ± 0.97 mg/dL (P < 0.01) [3]
- In mice pre-treated with cholecalciferol followed by CCl4 injection (2 g/kg i.p.), plasma ALT and AST levels were significantly higher than in mice receiving CCl4 alone, indicating potentiation of hepatotoxicity; mortality was also significantly elevated (55.6% vs 0%) [3]
- Cholecalciferol pre-treatment alone had no effect on plasma markers of liver or kidney damage, total antioxidant power, or lipid peroxidation [3]
- Cholecalciferol pre-treatment followed by CCl4 resulted in continued body weight loss (approximately 30% by day 7) compared to transient weight loss in CCl4-only group (approximately 10% on day 1 with recovery) [3]
- Hepatic calcium levels in cholecalciferol + CCl4 group were >3-fold higher than in CCl4 alone group (P < 0.01) [3]
- Cholecalciferol + CCl4 treatment significantly increased hepatic MDA levels and decreased total antioxidant power, GSH levels, ATP, and NADPH compared to CCl4 alone (P < 0.05 or P < 0.01) [3]
- Von Kossa staining confirmed maximum calcium deposition in the cholecalciferol + CCl4 group [3]

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Cholecalciferol (oral gavage; 5 mg/kg; 7 days) increases the toxicity of CCl4 exclusively in the liver, as shown by elevated plasma levels of ALT and AST, two biochemical indicators of hepatic injury. Although renal calcium content does not significantly differ between mice, it significantly raises renal calcium levels in mice[3].

No direct enzyme activity assays (e.g., purified enzyme, SPR, ITC) were described for cholecalciferol in these papers. However, the conversion of cholecalciferol to 25(OH)D is mediated by CYP27A1 and CYP2R1 (25-hydroxylases) in the liver, and further to 1,25(OH)2D by CYP27B1 (1-alpha-hydroxylase) in the kidneys [1][2]

- Cell viability assay (MTT): Endometrial carcinoma cells (IK, RL-95/2, HEC-1A) were seeded in 96-well plates, treated with cholecalciferol (0-10 μM) for 24, 48, or 72 hours. MTT reagent was added, and absorbance was measured at 595 and 620 nm using a spectrophotometer [2]
- Clonogenic assay: Cells were seeded in 6-well plates (IK: 1×10⁴ cells; RL-95/2 and HEC-1A: 2×10⁴ cells per 1.5 mL media), treated with vehicle or cholecalciferol (2-10 μM) for 48 hours, then cultured for 14 days to assess colony formation [2]
- Western blot analysis: Nuclear and cytoplasmic extracts were obtained using a nuclear and cytoplasmic extraction kit. Protein concentrations were determined, and equal amounts of protein were resolved by 10% SDS-PAGE, electroblotted onto PVDF membranes, and probed with primary antibodies against VDR, LDH, Histone 1, or Tubulin overnight at 4°C, followed by secondary antibodies for 1 hour, and visualized using ECL detection system [2]
- Immunofluorescent quantification of nuclear VDR translocation: Cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.2% Triton for 6 minutes, blocked with 0.2% BSA for 1 hour, incubated with VDR antibody (1:50) overnight at 4°C, then with labeled secondary antibody (1:300) for 1 hour. Nuclei were stained with Hoechst. A minimum of 300 cells were analyzed per time point [2]
- Quantitative real-time PCR: Total RNA was extracted using RNeasy kit. Primers for CYP27A1, CYP2R1, and GUSB were used. qRT-PCR was performed in triplicate with the ABI Prism 7900 Sequence Detector System. Relative mRNA expression levels were calculated by the comparative cycle threshold (Ct) method using GUSB as internal reference [2]

- V.D3 pre-treatment for CCl4 toxicity study: Male ddY mice (8 weeks old) were divided into two groups. On days -4 to -1 (4 days prior to CCl4 injection), animals were administered once daily by oral gavage with cholecalciferol (5 mg/kg formulated in olive oil) or an equivalent volume of olive oil vehicle alone. On day 0 (24 hours after final gavage), each mouse was injected intraperitoneally with CCl4 at 2 g/kg (5 mL/kg). Blood samples were collected before CCl4 injection to confirm V.D3 effects on plasma Ca concentrations. At 24 hours after CCl4 injection, three randomly selected mice from each group were euthanized and livers harvested. Remaining mice (9 per group) were maintained through day 7. Body weight and mortality were recorded daily. Blood samples were collected on days 1, 3, and 7 for biochemical marker determination. Surviving mice were sacrificed using pentobarbital [3]
- Calcium chloride direct injection study: Mice were divided into three groups (Ca + olive oil, saline + CCl4, and Ca + CCl4). Animals were injected i.p. with calcium chloride (150 mg/kg in physiological saline) or equivalent volume of saline vehicle. Ten minutes later, animals were injected i.p. with CCl4 at 2 g/kg or equivalent volume of olive oil. Whole blood was collected at 10 and 30 minutes and at 1, 3, 6, 12, and 24 hours after CaCl2 injection. Blood was centrifuged (3000×g, 10 min), and plasma was frozen at -80°C for calcium concentration determination (all time points) or hepatic injury markers (terminal samples). Livers were harvested at 24 hours and flash-frozen for hepatic calcium determination [3]

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Male ddY mice on CCl4 toxicity[3]
5 mg/kg
Oral gavage; 5 mg/kg; 7 days

Absorption, Distribution and Excretion
Cholecalciferol is readily absorbed from the small intestine if fat absorption is normal. Furthermore, bile is also essential for absorption. In particular, recent studies have identified several aspects of vitamin D absorption, such as: a) the 25-hydroxyvitamin D metabolite of cholecalciferol is absorbed more readily than the non-hydroxy form of cholecalciferol; b) the amount of fat ingested with cholecalciferol appears to have little effect on its bioavailability; and c) age does not appear to affect the absorption of vitamin D by cholecalciferol. Observations have shown that ingested cholecalciferol and its metabolites are primarily excreted via bile and feces. Studies have shown that in 49 kidney transplant patients, the mean central volume of distribution after cholecalciferol supplementation was approximately 237 liters. Studies have also shown that in 49 kidney transplant patients, the mean clearance after cholecalciferol supplementation was approximately 2.5 liters/day. It is readily absorbed from the small intestine (proximal or distal); the rate and completeness of cholecalciferol absorption may be superior to ergocalciferol.
Excretion route: Bile/Kidney. /Vitamin D and its analogues/
Many vitamin D analogues are rapidly absorbed by the gastrointestinal tract after oral administration if fat absorption is normal. Ergocalciferol absorption requires the presence of bile, and patients with liver, biliary tract, or gastrointestinal diseases (e.g., Crohn's disease, Whipple's disease, celiac disease) may experience reduced gastrointestinal absorption. Because vitamin D is fat-soluble, it is incorporated into chylomicrons and absorbed via the lymphatic system; approximately 80% of ingested vitamin D appears to be absorbed systemically through this mechanism, primarily in the small intestine. While some evidence suggests that intestinal absorption of vitamin D may be reduced in older adults, other evidence does not show clinically significant age-related changes in gastrointestinal absorption of vitamin D at therapeutic doses. It is currently unclear whether aging alters the gastrointestinal absorption of physiological doses of vitamin D. /Vitamin D analogues/
After absorption, ergocalciferol and cholecalciferol enter the bloodstream via lymphatic chylomicrons and then bind primarily to a specific α-globulin (vitamin D-binding protein). The hydroxylated metabolites of ergocalciferol and cholecalciferol also cycle with the same α-globulin. 25-hydroxylated ergocalciferol and cholecalciferol can be stored for extended periods in fat and muscle. Vitamin D enters the systemic circulation via the thoracic duct from the lymphatic system or skin and accumulates in the liver within hours. For more complete data on the absorption, distribution, and excretion of cholecalciferol (a total of 7 types), please visit the HSDB record page. Metabolites/Metabolites In the liver, cholecalciferol is hydroxylated to calcidiol (25-hydroxycholecalciferol) by vitamin D-25-hydroxylase. In the kidneys, calcidiol then acts as a substrate for 1-α-hydroxylase to generate calcitriol (1,25-dihydroxycholecalciferol), the biologically active form of vitamin D3. The metabolic activation of cholecalciferol and ergocalciferol occurs in two steps, first in the liver and second in the kidneys. The metabolic activation of calcidiol occurs in the kidneys; dihydrotachysterol, alfacalcidol, and docecalcidol are activated in the liver. The normal plasma total concentration (i.e., 25-hydroxyvitamin D) of the main circulating metabolites of cholecalciferol and ergocalciferol—25-hydroxycholecalciferol (calcidiol) and 25-hydroxyergocalciferol—has been reported to range from 8 to 80 ng/mL, depending on the assay method used and varying with ultraviolet radiation. Depending on geographical location (e.g., values in Southern California are higher than in Massachusetts), the lower limit of normal is typically reported to be 8–15 ng/mL. In the liver, ergocalciferol and cholecalciferol are converted to their 25-hydroxy derivatives in the mitochondria by vitamin D 25-hydroxylase. The activity of vitamin D 25-hydroxylase in the liver is regulated by the concentrations of vitamin D and its metabolites; therefore, the increase in systemic 25-hydroxyl metabolites after sunlight exposure or vitamin D ingestion is relatively small compared to the cumulative production or intake of vitamin D. Due to storage in adipose tissue or metabolism in the liver, the concentration of unhydroxylated vitamin D in serum is short-lived. In the kidneys, these metabolites are further hydroxylated at the 1-position by vitamin D 1-hydroxylase to produce their active forms: 1,25-dihydroxycholecalciferol (calcitriol) and 1,25-dihydroxyergocalciferol. The activity of vitamin D 1-hydroxylase requires molecular oxygen, magnesium ions, and malate, and is primarily regulated by parathyroid hormone (PTH), which is influenced by serum calcium and phosphate concentrations, and possibly also by circulating concentrations of 1,25-dihydroxyergocalciferol and 1,25-dihydroxycholecalciferol. Other hormones (such as cortisol, estrogen, prolactin, and growth hormone) may also affect the metabolism of cholecalciferol and ergocalciferol. The liver enzyme system responsible for the 25-hydroxylation of vitamin D (vitamin D-25-hydroxylase) is associated with the microsomal and mitochondrial components of the homogenate and requires NADPH (reduced nicotinamide adenine dinucleotide phosphate) and molecular oxygen. The kidney enzyme system responsible for the 1-hydroxylation of 25-hydroxyvitamin D (25-OHD) (25-OHD-1-α-hydroxylase) is associated with the mitochondria of the proximal renal tubules. It is a mixed-function oxidase that requires molecular oxygen and NADPH as cofactors. Cytochrome P450, a flavoprotein, and ferroredoxin are components of this enzyme complex. In the liver, cholecalciferol is hydroxylated to calcidiol (25-hydroxycholecalciferol) by 25-hydroxylase. In the kidneys, calcidiol acts as a substrate for 1α-hydroxylase to produce calcitriol (1,25-dihydroxycholecalciferol), the biologically active form of vitamin D3. Half-life: Weeks
Biological half-life
Currently, some data indicate that the half-life of cholecalciferol is approximately 50 days, while others suggest that the half-life of calcitriol (1,25-dihydroxyvitamin D3) is approximately 15 hours, and the half-life of calcidiol (25-hydroxyvitamin D3) is approximately 15 days. Furthermore, due to individual differences in vitamin D-binding protein concentration and genotype, the half-life of any given dose of vitamin D appears to vary.
The half-life of vitamin D in plasma is 19 to 25 hours, but it is stored for a long time in adipose tissue. …The biological half-life of the 25-hydroxy derivative is 19 days… It is estimated that the plasma half-life of calcitriol (1,25-dihydroxyvitamin D) in the human body is 3 to 5 days…

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- Cholecalciferol is a prohormone that can be obtained from exogenous sources (supplements or foods of animal origin) or synthesized endogenously in the skin upon exposure to UVB radiation from sunlight, which converts 7-dehydrocholesterol to cholecalciferol [1]
- Absorption: Intestinal absorption occurs through passive diffusion and membrane carriers; cholecalciferol shares structural resemblance with cholesterol and utilizes cholesterol carriers for absorption; absorption is enhanced when taken with a high-fat meal or the largest meal of the day (though data on food effect are conflicting) [1]
- Distribution: As a fat-soluble vitamin, highest distribution in adipose tissue, followed by muscles and liver; adipose tissue stores cholecalciferol in its original form; people with high body fat are at higher risk of vitamin D deficiency due to lower plasma levels [1]
- Metabolism: In the liver, enzyme 25-hydroxylase (CYP2R1, CYP27A1) converts cholecalciferol to 25-hydroxyvitamin D3 (25(OH)D3). Vitamin D-binding proteins transport 25(OH)D3 to the kidneys. In the kidneys, enzyme 1-alpha-hydroxylase (CYP27B1) hydroxylates 25(OH)D3 to 1,25-dihydroxyvitamin D3 (calcitriol), the active hormone. Non-renal calcitriol synthesis also occurs but is minimal [1]
- Half-life: Half-life of 25(OH)D is 15 days; half-life of 1,25(OH)2D is 15 hours [1]
- Elimination: Bile acid secretions from the liver transport cholecalciferol to the intestine, which then excretes it in feces [1]

Toxicity Summary
The first step in vitamin D3 activation is 25-hydroxylation, a reaction catalyzed by 25-hydroxylase in the liver, followed by further catalysis by other enzymes. Mitochondrial sterol 27-hydroxylase catalyzes the first step in the oxidation of the side chain of sterol intermediates. The active form of vitamin D3 (calcitriol) binds to intracellular receptors, which subsequently regulate gene expression as transcription factors. Like receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has both a hormone-binding domain and a DNA-binding domain. The vitamin D receptor forms a complex with another intracellular receptor—the retinoid X receptor—which binds to DNA. In most studies, vitamin D acts as an activator of transcription, but there are also cases where vitamin D inhibits transcription. Calcitriol increases serum calcium concentrations through increased gastrointestinal absorption of phosphorus and calcium, increased osteoclast reabsorption of calcium, and increased distal renal tubular reabsorption of calcium. Calcitriol appears to promote intestinal calcium absorption by binding to vitamin D receptors in the cytoplasm of intestinal mucosal cells. Subsequently, calcium is absorbed by forming calcium-binding proteins. Protein Binding The protein binding rate of cholecalciferol has been recorded to be 50% to 80%. Specifically, in plasma, vitamin D3 (from diet or skin) binds to vitamin D-binding protein (DBP) produced by the liver for transport to the liver. Ultimately, the form of vitamin D3 reaching the liver is 25-hydroxylated, and this 25-hydroxycholecalciferol binds to DBP (α2-globulin) during plasma circulation. Toxicity Data
LC50 (rat) = 130-380 ppm/4 hours. Interactions Corticosteroids can counteract the effects of vitamin D analogs. /Vitamin D Analogs/ In patients with hypoparathyroidism, concomitant use of thiazide diuretics and pharmacological doses of vitamin D analogs may lead to hypercalcemia, which may be transient, self-limiting, or may require discontinuation of vitamin D analogs. Hypercalcemia induced by thiazide diuretics in patients with hypoparathyroidism may be due to increased calcium release from bones. /Vitamin D analogs/
Excessive use of mineral oil may interfere with intestinal absorption of vitamin D analogs. Vitamin D analogs:
Orlistat may reduce the gastrointestinal absorption of fat-soluble vitamins (such as vitamin D analogs). At least 2 hours should be allowed between taking any dose of orlistat and taking a vitamin D analog (before or after). Vitamin D analogs:
For more complete data on interactions with cholecalciferol (6 in total), please visit the HSDB records page.

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- Cholecalciferol is generally considered safe, but adverse effects can occur due to high vitamin D levels; high loading doses (300,000-600,000 IU) have been associated with falls and fractures [1]
- Vitamin D toxicity is rare and occurs when serum 25(OH)D levels exceed 220 nmol/L; symptoms are nonspecific and may include confusion, vomiting, abdominal pain, polydipsia, polyuria, and dehydration [1]
- Cholecalciferol toxicity may result in hypercalcemia and hypercalciuria, potentially leading to complications such as nephrolithiasis, nephrotoxicity, and hyperphosphatemia [1]
- Management of overdose includes discontinuing cholecalciferol, supportive therapy, loop diuretics or bisphosphonates for hypercalcemia, and intermittent hemodialysis for life-threatening hypercalcemia [1]
- In mice, pre-treatment with cholecalciferol (5 mg/kg for 4 days) alone had no effect on plasma markers of liver or kidney damage, total antioxidant power, or lipid peroxidation; however, it significantly potentiated CCl4-induced hepatotoxicity and increased mortality when combined with CCl4 [3]
- Likelihood of vitamin D toxicity from excessive sunlight exposure is low, as the skin naturally degrades excess vitamin D [1]

[1]. https://www.ncbi.nlm.nih.gov/books/NBK549768/

[2]. Role of local bioactivation of vitamin D by CYP27A1 and CYP2R1 in the control of cell growth in normal endometrium and endometrial carcinoma. Lab Invest. 2014 Jun;94(6):608-22.

[3]. Vitamin D3-induced hypercalcemia increases carbon tetrachloride-induced hepatotoxicity through elevated oxidative stress in mice. PLoS One. 2017 Apr 27;12(4):e0176524.

- Vitamin D deficiency is defined as serum 25(OH)D < 20 ng/mL; insufficiency as 21-29 ng/mL; target level >30 ng/mL [1]
- FDA-approved indication: Cholecalciferol is indicated for use as a dietary supplement [1]
- Off-label uses with proven benefits include preventing bone loss or treating osteoporosis in postmenopausal women, preventing falls in older adults, and preventing fractures [1]
- The National Osteoporosis Foundation recommends daily oral intake of cholecalciferol 800-1000 IU for adults aged 50 or older [1]
- The highest prevalence of vitamin D deficiency is observed among African Americans (82.1%), Hispanics (62.9%), adults with obesity, pregnant women, and children aged 1-11 years [1]
- In endometrial carcinoma, CYP27A1 expression is 11-fold higher than in normal endometrium, and CYP2R1 expression is 1.3-fold higher, suggesting that enhanced 25-hydroxylating capacity may partially compensate for reduced nuclear VDR in EC progression [2]
- In cycling normal endometrium, CYP27A1 and CYP2R1 expression increased in secretory phase compared to proliferative phase, correlating with lower proliferation rates and higher nuclear VDR levels [2]

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Therapeutic Uses
Bone mineralization protectants; Vitamins
Veterinary drugs: Nutritional factors (anti-rickets drugs)
Therapeutic doses of specific vitamin D analogs are used to treat chronic hypocalcemia, hypophosphatemia, rickets, and osteodystrophy associated with a variety of diseases, including chronic renal failure, familial hypophosphatemia, and hypoparathyroidism (postoperative, idiopathic, or pseudohypoparathyroidism). Some analogs have been found to reduce elevated parathyroid hormone levels in patients with renal osteodystrophy accompanied by hyperparathyroidism. Theoretically, any vitamin D analog can be used to treat the above-mentioned diseases, but due to differences in their pharmacological properties, some analogs may be more effective than others in specific situations. For patients with renal failure, alfacalcidol, calcitriol, and dihydrotachysterol are usually preferred because these patients have impaired ability to synthesize calcitriol, thus making the efficacy more predictable. Furthermore, these drugs have shorter half-lives, making toxicity easier to control (hypercalcemia reverses more quickly). Ergocalciferol may not be the first-line treatment for familial hypophosphatemia or hypoparathyroidism because the required high doses carry the risk of overdose and hypercalcemia; dihydrotachysterol and calcitriol may be more suitable in these cases. /US product label contains/

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Drug Warnings
Studies have shown that older adults may have increased vitamin D requirements due to decreased skin production of vitamin D3 precursors, reduced sun exposure, impaired kidney function, or impaired vitamin D absorption.
Vitamin D analogs at doses not exceeding physiological requirements are generally non-toxic. However, some infants and patients with sarcoidosis or hypoparathyroidism may be more sensitive to vitamin D analogs. /Vitamin D Analogs/
Acute or chronic overdose of vitamin D analogs, or an enhanced response to physiological doses of ergocalciferol or cholecalciferol, can lead to vitamin D overdose, manifested as hypercalcemia. /Vitamin D Analogs/
It has been reported that patients with hypoparathyroidism who have been treated with vitamin D analogs for a long time have also experienced a decline in renal function, but without hypercalcemia. Serum phosphate concentrations must be controlled before starting vitamin D analog treatment. To avoid ectopic calcification, the ratio of serum calcium (mg/dL) to phosphorus (mg/dL) should not exceed 70. Because taking vitamin D analogs may increase phosphate absorption, patients with renal failure may need to adjust the dosage of aluminum-containing antacids used to reduce phosphate absorption. /Vitamin D Analogs/
For more complete data on drug warnings for cholecalciferol (10 in total), please visit the HSDB record page.

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Pharmacodynamics
The synthesis of the two main bioactive metabolites of vitamin D in vivo occurs in two steps. The first hydroxylation of vitamin D3 (cholecalciferol) (or vitamin D2) occurs in the liver, producing 25-hydroxyvitamin D; the second hydroxylation occurs in the kidneys, producing 1,25-dihydroxyvitamin D. These vitamin D metabolites then promote the absorption of calcium and phosphorus in the small intestine, thereby increasing serum calcium and phosphorus levels to promote bone mineralization. Conversely, these vitamin D metabolites also help mobilize calcium and phosphorus from bones and may increase the reabsorption of calcium (and perhaps phosphorus) through the renal tubules. Because the liver and kidneys need to synthesize active vitamin D metabolites, it takes 10 to 24 hours from the time cholecalciferol is taken to its effect in the body. Parathyroid hormone is responsible for regulating this metabolism at renal levels.

C27H44O

384.6377

384.339

C, 84.31; H, 11.53; O, 4.16

67-97-0

Vitamin D3-d7;1627523-19-6;3-epi-Vitamin D3;57651-82-8;Vitamin D3-13C3;Vitamin D3-d3;80666-48-4;Vitamin D3-13C5

5280795

White to off-white solid powder

1.0±0.1 g/cm3

496.4±24.0 °C at 760 mmHg

83-86 °C(lit.)

214.2±15.1 °C

0.0±2.9 mmHg at 25°C

1.523

9.72

1

1

6

28

610

5

O([H])[C@@]1([H])C([H])([H])C([H])([H])C(=C([H])[H])/C(/C1([H])[H])=C(/[H])\C(\[H])=C1/C([H])([H])C([H])([H])C([H])([H])[C@@]2(C([H])([H])[H])[C@@]/1([H])C([H])([H])C([H])([H])[C@]2([H])[C@]([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])C([H])(C([H])([H])[H])C([H])([H])[H]

QYSXJUFSXHHAJI-YRZJJWOYSA-N

InChI=1S/C27H44O/c1-19(2)8-6-9-21(4)25-15-16-26-22(10-7-17-27(25,26)5)12-13-23-18-24(28)14-11-20(23)3/h12-13,19,21,24-26,28H,3,6-11,14-18H2,1-2,4-5H3/b22-12+,23-13-/t21-,24+,25-,26+,27-/m1/s1

(1S,3Z)-3-[(2E)-2-[(1R,3aS,7aR)-7a-methyl-1-[(2R)-6-methylheptan-2-yl]-2,3,3a,5,6,7-hexahydro-1H-inden-4-ylidene]ethylidene]-4-methylidenecyclohexan-1-ol

Activated 7-dehydrocholesterol; Cholecalciferol; Calciol; Vitamin D3; Colecalciferol; Arachitol; Ricketon; Trivitan; Vigorsan; Deparal; Vigantol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.  (3). This product is not stable in solution, please use freshly prepared working solution for optimal results.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~259.98 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.08 mg/mL (5.41 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)