Absorption, Distribution and Excretion
Both vitamin D2 and vitamin D3 can be absorbed from the small intestine, but vitamin D3 may be absorbed more efficiently. The most efficient intestinal site for vitamin D absorption depends on the solubility medium. Most vitamins first appear in chylomicrons in the lymph. The presence of bile is necessary for ergocalciferol absorption, but patients with liver, biliary tract, or gastrointestinal diseases (e.g., Crohn's disease, Whipple's disease, celiac disease) may experience reduced gastrointestinal absorption. A 6-month longitudinal, randomized, double-blind, placebo-controlled study monitored the exposure of breastfed infants to UVB radiation with and without vitamin D2 supplementation, and longitudinally measured bone mineral content, growth, and serum concentrations of calcium, phosphorus, 25-hydroxyvitamin D3, 25-hydroxyvitamin D2, 1,25-dihydroxyvitamin D, and parathyroid hormone. The study involved serial sampling of 46 breastfed Caucasian infants; 24 infants received 400 IU of vitamin D2 daily, and 22 infants received a placebo. An additional 12 patients fed standard infant formula were followed up. 83% of the patients completed the full 6-month study. There were no differences in UVB exposure or growth parameters between the groups. At 6 months, there were no significant differences in bone mineral content, serum parathyroid hormone, or 1,25-dihydroxyvitamin D concentration between the breastfed and supplemented groups, but the total 25-hydroxyvitamin D level was significantly lower in the non-supplemented breastfed group than in the supplemented group (23.53 ± 9.94 vs 36.96 ± 11.86 ng/ml; p < 0.01). However, at 6 months, the serum 25-hydroxyvitamin D3 concentration was significantly higher in the non-supplemented breastfed group than in the supplemented group (21.77 ± 9.73 vs 11.74 ± 10.27 ng/ml; p < 0.01). The study concluded that breastfed infants not supplemented with vitamin D showed no signs of vitamin D deficiency in the first 6 months of life. Researchers compared the ability of ergocalciferol and cholecalciferol to increase plasma vitamin D and 25-hydroxyvitamin D concentrations in cats. After oral administration of cholecalciferol in oil form, plasma cholecalciferol concentrations rapidly increased and then rapidly decreased. In contrast, plasma 25-hydroxyvitamin D concentrations peaked on day 3 after administration and remained elevated for 5 days. When 337 μg of cholecalciferol and ergocalciferol were administered orally in oil form, peak plasma concentrations of cholecalciferol and ergocalciferol in 10 cats occurred at 8 hours and 12 hours after administration, respectively. The peak concentration of cholecalciferol was more than twice that of ergocalciferol (570 ± 80 nmol/L vs. 264 ± 42 nmol/L). The area under the curve (AUC) for cholecalciferol from 0 to 169 hours was also more than twice that of ergocalciferol. When ergocalciferol and cholecalciferol are administered parenterally in oil-based emulsion form, plasma concentrations of 25-hydroxyvitamin D3 are higher than those of 25-hydroxyvitamin D2. When both vitamins are present in the diet and intake is within the nutritional range, plasma concentrations of 25-hydroxyvitamin D2 are 0.68 times higher than those of 25-hydroxyvitamin D3. Discrimination against ergocalciferol in cats appears to be due to the different affinities of binding proteins to the two vitamin D metabolites. These results suggest that cats exhibit discrimination against ergocalciferol, utilizing it at only 0.7 times the efficiency of cholecalciferol to maintain plasma 25-hydroxyvitamin D concentrations. Osteoporosis reduces the quality of life in adult patients with cystic fibrosis (CF). Vitamin D deficiency due to malabsorption may be one of the causes of decreased bone mineral density (BMD) in CF patients. Objective: To compare the absorption of oral ergocalciferol (vitamin D2) and its effect on 25-hydroxyvitamin D levels in 10 adult patients with CF and exocrine pancreatic insufficiency with 10 healthy controls. Design: In this pharmacokinetic study, patients with cystic fibrosis (CF) and healthy controls were matched by age, sex, and ethnicity. Each subject received 2500 μg of vitamin D2 orally with a meal. The CF group also received a pancreatic enzyme preparation providing ≥80,000 units of lipase. Blood samples were collected at baseline and at 5, 10, 24, 30, and 36 hours after vitamin D2 administration to determine serum vitamin D2 and 25-hydroxyvitamin D concentrations. Results: Baseline vitamin D2 concentrations were close to zero in all subjects. CF patients absorbed less than half the amount of orally administered vitamin D2 as healthy controls (P < 0.001). Absorption varied considerably among CF patients; two patients absorbed almost no vitamin D2. In the cystic fibrosis (CF) group, the increase in 25-hydroxyvitamin D over time after vitamin D2 absorption was significantly lower than in the control group (P = 0.0012). Conclusion: Vitamin D2 absorption is significantly lower in CF patients than in the control group. These results may help explain the etiology of vitamin D deficiency in CF patients, which may lead to decreased bone mineral density.

---

Metabolism/Metabolites
Vitamin D…is hydroxylated at position 25 in the liver to produce 25-hydroxyvitamin D3, the main circulating metabolite in plasma. This metabolite is further hydroxylated in the kidneys to 1,25-dihydroxyvitamin D3, the most active metabolite initiating intestinal calcium and phosphate transport and mobilizing bone minerals.
25-hydroxyergocalciferol, a polar bioactive metabolite of vitamin D2, has been isolated from porcine plasma and exhibits approximately 1.5 times the activity of vitamin D2 in treating rickets in rats.
Dihydrotachysterol is a vitamin D analogue and can be considered a reduction product of vitamin D2…Dihydrotachysterol showed approximately 1/450th the activity of vitamin D in anti-rickets studies, but at high doses, it is much more effective than vitamin D in mobilizing bone minerals.

---

Biological half-life
19 to 48 hours (however, it can be stored for a long time in fat deposits in the body).

Effects During Pregnancy and Lactation
◉ Overview of Lactation Medication Use
Vitamin D is a normal component of breast milk. If the mother supplements with 10 to 50 micrograms (400 to 2000 IU) of vitamin D2 or D3 daily, the concentration in her breast milk will not be sufficient to meet the daily needs of an exclusively breastfed infant, nor can it correct an existing vitamin D deficiency in the infant solely through breastfeeding. Breastfeeding mothers taking vitamin D supplements within this dosage range should supplement their infants with at least 10 micrograms (400 IU) of vitamin D daily, in accordance with pediatric nutrition guidelines. When the mother's daily vitamin D dose reaches or exceeds 100 micrograms (4000 IU), the vitamin D concentration in her breast milk may meet the infant's daily vitamin D intake target of 10 micrograms, depending on the mother's own vitamin D level and the infant's daily breast milk intake. Obese mothers may require higher vitamin D intake.
◉ Effects on Breastfed Infants
Maternal daily intake of 400 to 6400 IU (10 to 160 mcg) of vitamin D was not associated with any short-term biochemical abnormalities in breastfed infants.
An 11-day-old, exclusively breastfed, full-term female infant presented with asymptomatic, mild hypercalcemia (serum total calcium 11.4 mg/dL). The mother had undergone thyroid-parathyroidectomy before pregnancy and was taking 100,000 IU of vitamin D2 daily to maintain normal calcium and phosphorus levels, and was also taking prenatal vitamins containing 400 IU of vitamin D (unspecified form) daily during pregnancy and lactation. At 14 days of age, the infant's umbilical cord blood and breast milk levels of vitamin D2 and 25-hydroxyvitamin D2 were significantly elevated. Serum vitamin D levels in the infant were not measured. The high daily intake of vitamin D2 in breast milk, combined with the infant's high serum vitamin D2 levels at birth, may have contributed to the abnormal calcium levels. In a study in northern India, infants exclusively breastfed who received 60,000 IU of vitamin D3 orally daily for 10 days postpartum showed no difference in serum calcium or phosphorus levels, or urinary calcium/creatinine ratios, at 14 weeks and 6 months of age compared to infants born to mothers receiving a placebo. Infants born to mothers receiving vitamin D had a lower incidence of biochemical rickets (0% vs 17%) compared to the placebo group, but no difference in the incidence of radiographic rickets (3.6% vs 3.4%). 152 mothers in northern India (most of whom were vitamin D deficient) were randomized to two groups: one group received a single dose of 120,000 IU (3000 mcg) of vitamin D within 7 days postpartum, followed by repeat doses at 6, 10, and 14 weeks postpartum (coinciding with the infant's scheduled immunization schedule); the other group received a placebo. Infants born to mothers in the placebo group received 400 IU (10 mcg) of vitamin D daily, while infants born to mothers in the treatment group received a placebo. At 14 weeks, growth parameters and serum biochemical markers of bone mineralization and liver homeostasis were similar between the two groups. At 9 months, there were also no differences in tooth development and the frequency of diarrhea or respiratory illness.
114 vitamin D-deficient mothers in northern India were randomly assigned to receive a single dose of 60,000 IU (1,500 mcg) of vitamin D3 or a placebo, administered between 24 and 48 hours postpartum, and then repeated at 6, 10, and 14 weeks postpartum. Over 90% of participants were exclusively breastfed. At 6 months of age, 6 infants in the control group developed biochemical rickets, while none in the treatment group developed biochemical rickets; 2 infants in the control group developed radiographic rickets, and 1 infant in the treatment group developed radiographic rickets. Reports indicate that infants born to mothers in the treatment group had normal serum calcium and phosphorus levels at 6 months of age, but specific results were not provided, and the control group also did not report such results. In Qatar, 190 mothers were randomly assigned to receive either 600 IU or 6000 IU of vitamin D within 4 weeks postpartum. Infants born to mothers in the low-dose group received 400 IU daily, while infants born to mothers in the high-dose group received a placebo daily. At the planned 4- and 7-month postpartum follow-ups, there were no differences between the two groups in growth parameters, serum calcium and parathyroid hormone levels, or parent-reported infant health status. In Rajasthan, India, 220 healthy, non-obese breastfeeding mothers were randomly assigned to receive either 120,000 IU or 12,000 IU of vitamin D3 monthly for 12 months, starting from the first month postpartum. Infants in both groups had normal serum calcium, phosphate, and alkaline phosphatase levels at baseline and 12 months. At 12 months, there were no significant differences in growth parameters, bone mineral content, or bone density between the two groups of infants. In Dhaka, Bangladesh, 1300 pregnant women were randomly assigned to receive weekly oral vitamin D3 tablets (4200 IU, 16800 IU, 28000 IU) or a placebo, starting from week 17 to 24 of gestation. The placebo group and a subset of the 28000 IU group continued their assigned treatment for 26 weeks postpartum, while the others discontinued treatment after delivery. All participants had similar baseline maternal vitamin D levels, with 65% of pregnant women exhibiting biochemical vitamin D deficiency. The median duration of exclusive breastfeeding was 12 to 14 weeks, similar across groups. Vitamin D supplementation in infants was uncommon (<10%). A total of 1164 infants were available for analysis. There were no differences in growth and development between the groups at 1 year postpartum. Infant mortality, hospitalization rates, respiratory infection rates, serum calcium levels, early childhood bone mineral density, and grip strength were also similar. The incidence of hypercalcemia and hypercalciuria in infants was very low (≤1%), and there were no differences between groups. Radiographically confirmed rickets occurred in 4 infants (0.3%), including 3 in the placebo group and 1 in the lowest dose group. However, due to the extremely low incidence, differences between groups could not be determined. The incidence of biochemical rickets in 6-month-old infants was significantly higher in the placebo group (7.9%) than in the high-dose group (1.3%), but not significantly different from other groups. 148 exclusively breastfed postpartum patients started daily vitamin D3 at 4 to 6 weeks postpartum. The baseline serum 25-hydroxyvitamin D level in infants was <50 nmol/L (range: undetectable to 113.8 nmol/L). Infants born to mothers who received 400 IU of vitamin D daily were supplemented with 400 IU of vitamin D daily, while infants born to mothers who received 6400 IU of vitamin D daily received a placebo. There were no differences in biochemical indicators of calcium status, bone mineral content, or bone density between the two groups at 1, 4, and 7 months of age. Emerging evidence suggests that vitamin D supplementation during pregnancy and lactation, and adequate vitamin D provision to infants through breast milk, is crucial for regulating the developing immune system in infants. ◉ Effects on Lactation and Breast Milk As of the revision date, no relevant published information was found.

Ergocalciferol is a tasteless, white crystalline powder used as a dietary supplement and food additive. (EPA, 1998)
5,6-trans-vitamin D2 is a type of vitamin D.
5,6-trans-vitamin D2 has been reported in hops and in the human body, and relevant data exist.
See also: Ergocalciferol (note moved here).
Mechanism of Action
The mechanism of action of active vitamin D—calcitriol—is similar to that of steroids and thyroid hormones. Calcitriol binds to cytoplasmic receptors within target cells, and the receptor-hormone complex interacts with the DNA of certain genes, thereby enhancing or inhibiting the transcription of these genes. Structural analysis of the calcitriol receptor indicates that it belongs to the same supergene family as steroid receptors. Calcitriol also appears to have some effects that occur too rapidly to be explained by genomic action. /Calcitriol/
The mechanism of bone salt mobilization is not fully elucidated and appears to involve the interaction of multiple factors. Paradoxically, the cells responsible for bone resorption (osteoclasts) are not directly affected by calcitriol, nor do they appear to contain calcitriol receptors. Instead, calcitriol increases the number of osteoclasts available for bone resorption; this is likely due to its action on myeloid hematopoietic progenitor cells, inducing their differentiation into functional osteoclasts. The cells responsible for bone formation (osteoblasts) do contain receptors, and calcitriol prompts them to produce various proteins, including osteocalcin, a vitamin K-dependent protein containing γ-carboxyglutamate residues. The exact role of this protein is unclear, but it also produces other unknown substances that appear to stimulate osteoclast function. Furthermore, calcitriol synergistically increases the production of interleukin-1 (a lymphokine that promotes bone resorption) in conjunction with interferon-gamma.

C28H44O

396.64836

396.339

51744-66-2

Vitamin D2;50-14-6

6536972

Prisms from acetone
White crystals
Colorless crystals

239 to 244 °F (EPA, 1998)
116.5 °C

7.641

1

1

5

29

678

6

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

MECHNRXZTMCUDQ-VLOQVYPSSA-N

InChI=1S/C28H44O/c1-19(2)20(3)9-10-22(5)26-15-16-27-23(8-7-17-28(26,27)6)12-13-24-18-25(29)14-11-21(24)4/h9-10,12-13,19-20,22,25-27,29H,4,7-8,11,14-18H2,1-3,5-6H3/b10-9+,23-12+,24-13+/t20-,22+,25-,26+,27-,28+/m0/s1

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

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.

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

DMSO : ~25 mg/mL (~63.03 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.30 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 25.0 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.

---

Solubility in Formulation 2: 2.5 mg/mL (6.30 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 25.0 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.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (6.30 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

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