Human Endogenous Metabolite
Vitamin D2 (Ergocalciferol) is a nutritional vitamin D precursor. It is metabolized in the liver to 25-hydroxyvitamin D (25(OH)D), which is subsequently converted to the active form, 1,25-dihydroxyvitamin D (1,25(OH)2D), by 1α-hydroxylase, primarily in the kidney but also in extrarenal tissues. The active form binds to the vitamin D receptor (VDR) to regulate gene expression, particularly in calcium and phosphate homeostasis, bone metabolism, and immune function.[1]

After receiving omeprazole alone or in combination with either restricted food intake or Ergocalciferol for five weeks, the chickens weighed 15–25% less (P < 0.01) at sacrifice compared to the chickens given a vehicle or fed less[2].
In comparison to either ergocalciferol alone or fasting alone, the combination of the two treatments causes more growth impairments and facial abnormalities[3].

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Observational cohort studies in CKD patients (stages 3-5) and maintenance dialysis patients show that oral supplementation with Ergocalciferol (typically 50,000 IU weekly) significantly increases serum 25-hydroxyvitamin D (25(OH)D) levels.[1]
In CKD patients, Ergocalciferol supplementation is associated with a reduction in plasma intact parathyroid hormone (iPTH) levels, indicating a beneficial effect on secondary hyperparathyroidism.[1]
Some observational studies in dialysis patients reported that Ergocalciferol supplementation was associated with improvements in other parameters, such as a decrease in glycosylated hemoglobin (HbA1c), an increase in hemoglobin (Hb) levels, and a reduction in left ventricular mass index (LVMI).[1]
A randomized controlled trial (RCT) comparing Ergocalciferol (titrated to achieve serum 25(OH)D ≥30 ng/mL) with paricalcitol (1 or 2 µg/day) in CKD stages 3-4 patients showed a significant increase in serum 25(OH)D in the ergocalciferol group, but no significant decrease in iPTH in this group over 4 months.[1]

Absorption, Distribution and Excretion
Ergocalciferol is absorbed in the intestine and transported to the liver in the form of chylomicrons. Intestinal absorption is unrestricted unless a disease associated with fat malabsorption is present. However, the presence of bile is required for absorption. The active form of ergocalciferol—calcitriol—cannot be maintained long-term in storage tissues, especially in the presence of diet or UVB deficiency. Therefore, ergocalciferol and its metabolites are primarily excreted via bile, with less renal excretion. This primary fecal excretion is due to renal reabsorption of vitamin D metabolites bound to vitamin D-binding protein mediated by the cuboprotein-macroprotein receptor system. Circulating ergocalciferol levels are very limited because this compound is rapidly stored in adipose tissue (such as adipose tissue, liver, and muscle). This is clearly reflected in reports showing significantly reduced circulating ergocalciferol levels in obese patients. There are currently no formal reports on ergocalciferol clearance. Due to its structural similarity, the clearance rate of cholecalciferol is recommended for reference. On the other hand, calcitriol's renal clearance rate has been reported to be 31 ml/min. Both vitamin D2 and vitamin D3 can be absorbed in the small intestine, but vitamin D3 absorption may be more efficient. The most efficient intestinal site for vitamin D absorption depends on the vitamin D dissolving carrier. Most vitamins first appear in chylomicrons in the lymph. The presence of bile is necessary for ergocalcitriol absorption, and 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 aimed to monitor breastfed infants exposed to UVB radiation with and without vitamin D2 supplementation, and to longitudinally measure 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 patients with CF, which may lead to decreased bone mineral density.
Metabolism/Metabolites
Ergocalciferol is inactive; therefore, its first step in the body is its conversion to 25-hydroxyvitamin D via the action of CYP2R1, subsequently generating the major circulating metabolite 1,25-dihydroxyvitamin D, or calcitriol. The generation of this major metabolite is regulated by the activity of the key 1-hydroxylase CYP27B1 and CYP24A1, which is responsible for 25-hydroxylation. As part of a secondary metabolic pathway, ergocalciferol is converted to 25-hydroxyvitamin D in the liver via the action of D-25-hydroxylase and CYP2R1. Furthermore, the generation of 24(R),25-dihydroxyvitamin D is primarily accomplished in the kidneys by the action of 25-(OH)D-1-hydroxylase and 25-(OH)D-24-hydroxylase. Other reports indicate that 3-epomerases possess significant activity in the metabolism of ergocalciferol, modifying the C3 hydroxyl group from the α-position to the β-position. The resulting epimer appears to have reduced affinity for vitamin D plasma proteins and vitamin D receptors. An alternative metabolic pathway has also been reported, characterized by the activity of CYP11A1 and its hydroxylation at the C-20 position. This 20-hydroxylated vitamin D appears to have similar biological activity to calcitriol. Vitamin D… is hydroxylated at position 25 in the liver to 25-hydroxyvitamin D3, which is the major circulating metabolite in plasma. This metabolite is further hydroxylated in the kidneys to 1,25-dihydroxyvitamin D3, the most active metabolite initiating intestinal calcium-phosphorus transport and bone mineral mobilization. A polar bioactive metabolite of vitamin D2, 25-hydroxyergocalciferol, has been isolated from porcine plasma, exhibiting approximately 1.5 times the activity of vitamin D2 in treating rickets in rats.
Dihydrotachysterol is a vitamin D analog and can be considered a reduction product of vitamin D2…Dihydrotachysterol's activity in anti-rickets studies is approximately 1/450th that of vitamin D, but at high doses, its ability to mobilize bone minerals is far greater than that of vitamin D.
Known metabolites of vitamin D2 include vitamin D2 3-glucuronide.
In the liver, ergocalciferol is hydroxylated to ergodiol. 25-hydroxyergocalciferol is converted to ergocalciferol by 25-hydroxylase. In the kidneys, ergocalciferol acts as a substrate for 1-α-hydroxylase to generate ergocalcitriol (1,25-dihydroxyergocalciferol), the biologically active form of vitamin D2.
Half-life: 19 to 48 hours (but it can be stored for a long time in adipose tissue).
Biobiological half-life

Ergocalciferol can remain in the bloodstream for 1-2 days. This rapid turnover is due to its conversion in the liver and absorption by fat and muscle cells, where it is converted into its active form. Half-life: 19 to 48 hours (but it can be stored for a long time in adipose tissue in the body). Ergocalciferol is a fat-soluble vitamin. After oral administration, vitamin D is incorporated into chylomicrons and transported to the venous circulation via the lymphatic system. [1] It is transported to the liver, where cytochrome P450 enzymes (mainly CYP2R1) hydroxylate at position 25 to form 25-hydroxyvitamin D2 (25(OH)D2), also known as calcidiol. [1] 25(OH)D2 is the dominant circulating form and is the best indicator of vitamin D status due to its long half-life (2-3 weeks). [1]
In the kidneys (and extrarenal tissues expressing 1α-hydroxylase), 25(OH)D2 can be further hydroxylated to form the active hormone 1,25-dihydroxyvitamin D2 (1,25(OH)2D2, calcitriol). [1]
The conversion of 25(OH)D to 1,25(OH)2D in the kidneys is inhibited by elevated serum phosphorus, elevated fibroblast growth factor 23 (FGF-23), and uremic toxins, and is impaired in chronic kidney disease (CKD). [1]
Extrarenal tissues (e.g., prostate, breast, colon, immune cells) also express 1α-hydroxylase and can utilize circulating 25(OH)D to locally generate 1,25(OH)2D for autocrine/paracrine functions. [1]

Toxicity Summary
Vitamin D2 is the most commonly added form of vitamin D in foods and nutritional supplements. Vitamin D2 must be converted into one of two active forms (hydroxylation) by the liver or kidneys. After conversion, it binds to vitamin D receptors, thereby exerting a variety of regulatory effects. Vitamin D plays an important role in maintaining calcium homeostasis and regulating parathyroid hormone (PTH). It promotes renal reabsorption of calcium, increases intestinal absorption of calcium and phosphorus, and promotes the mobilization of calcium and phosphorus from bones to plasma. Vitamin D2 and its analogues appear to promote intestinal calcium absorption by binding to specific receptors in the cytoplasm of intestinal mucosal cells. Subsequently, calcium is absorbed by forming calcium-binding proteins. Activated ergocalciferol increases intestinal absorption of calcium and phosphorus primarily by binding to specific receptors in the cytoplasm of intestinal mucosal cells, thereby increasing serum calcium and phosphorus concentrations. Subsequently, calcium is absorbed by forming calcium-binding proteins. 25-Hydroxyergocalciferol is an intermediate metabolite of ergocalciferol. Although this metabolite is 2–5 times more active than the unactivated ergocalciferol in treating rickets and inducing calcium absorption and mobilization (from bone) in animals, this increased activity is still insufficient to affect these functions at physiological concentrations. Activated ergocalciferol stimulates bone resorption and is essential for normal bone mineralization. Physiological doses of ergocalciferol also promote renal calcium reabsorption, but the significance of this effect is unclear. Toxicity Data: LD50 = 23.7 mg/kg (oral in mice) LD50 = 10 mg/kg (oral in rats). Interactions: This article describes the effect of calcitriol (1,25-dihydroxyvitamin D3) on the conversion of ergocalciferol (vitamin D2) to 25-hydroxyvitamin D in 20 healthy subjects. Subjects received two different doses of ergocalciferol, one administered concurrently with calcitriol and the other not concurrently. Concomitant administration of the two drugs had no effect on serum calcitriol concentrations. This article also reports the effect of glutimide (500 mg/day) treatment on vitamin D metabolism in a 77-year-old female patient who had previously taken an overdose of vitamin D2. This patient's hypercalcemia was associated with elevated serum total 25-hydroxyvitamin D and total 1,25-dihydroxyvitamin D concentrations. After 8 days of glutimide administration, plasma gamma-glutamyl transferase activity increased above the upper limit of normal, peaking at 90 IU/L on days 18–22 of treatment. Plasma calcium concentrations returned to normal on day 13. Serum 1,25-dihydroxyvitamin D concentrations began to decline within 4 days, reaching near the lower limit of the reference range (70 pmol/L) after 8 days. Serum total 25-hydroxyvitamin D concentrations showed no significant change before liver enzyme induction; thereafter, they gradually decreased. Although 25-hydroxyvitamin D concentrations remained high, 1,25-dihydroxyvitamin D concentrations did not rise again but remained at the lower limit of normal. This study investigated the effects of a high-cholesterol diet and corticosteroids on vitamin D2 toxicity in rats. Vitamin D2 was orally administered to rats at doses ranging from 5 × 10⁴ to 60 × 10⁴ IU/kg once daily for 4 consecutive days. Animals fed cholesterol showed reduced mortality after vitamin D2 treatment. Dietary cholesterol suppressed the toxic effects induced by sublethal doses of vitamin D2 (20 × 10⁴ IU/kg, once daily for 4 consecutive days), such as slowed growth after anorexia, elevated serum calcium levels, and tissue calcium deposition. Animals fed a high-cholesterol diet two weeks before the first administration of vitamin D2 showed significantly greater symptom relief than those fed a high-cholesterol diet after the first administration of vitamin D2. On the other hand, both dexamethasone and corticosteroids significantly increased mortality from vitamin D2 toxicity. The degree of vitamin D2 toxicity enhanced by dexamethasone was correlated with the degree of hypercalcemia and tissue calcification. Therefore, the inhibitory effect of cholesterol is unlikely to be due to activation of the cholesterol-corticosteroid system in the adrenal glands. This study investigated the effects of short-term pharmacological doses of vitamin D2 or vitamin D3 on serum 1,25(OH)₂D metabolite concentrations in epilepsy patients on long-term antiepileptic medication. Nine patients received 4000 IU of vitamin D2 daily for 24 weeks before and after treatment; another 10 patients received the same dose of vitamin D3 before and after treatment. Before treatment, serum 1,25(OH)₂D and 25(OH)D concentrations in epilepsy patients were significantly lower than in normal subjects (p<0.01). Vitamin D2 treatment increased serum 1,25(OH)₂D₂ concentrations but simultaneously decreased 1,25(OH)₂D₃ concentrations, with the final serum total 1,25(OH)₂D concentration remaining unchanged. Serum 25(OH)D₂ and 25(OH)D concentrations significantly increased, while 25(OH)D₃ concentration slightly decreased. Vitamin D3 treatment did not affect serum 1,25(OH)₂D₃ concentrations, but serum 25(OH)D₃ concentrations were significantly increased. In epileptic patients and healthy subjects receiving vitamin D2 treatment, the correlation between the serum 1,25(OH)₂D₂/1,25(OH)₂D₃ ratio and the 25(OH)D₂/25(OH)D₃ ratio was highly statistically significant (p<0.01). The data indicate that serum 1,25(OH)₂D₂ and 1,25(OH)₂D₃ concentrations are directly proportional to their precursors 25(OH)D₂ and 25(OH)D₃, and that total 1,25(OH)₂D concentrations are tightly regulated. Patients taking cardiac glycosides should use vitamin D analogues with caution, as hypercalcemia in these patients may lead to arrhythmias. Patients allergic to these drugs should also use vitamin D analogs with caution. /Vitamin D analogs/

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The main toxic effects of excessive vitamin D supplementation (including ergocalciferol) are hypercalcemia and hyperphosphatemia. In reviewed studies, the incidence of hypercalcemia caused by nutritional vitamin D supplementation is up to 3% and hyperphosphatemia up to 7% [1]. These adverse reactions (hypercalcemia/hyperphosphatemia) can be relieved after discontinuation of vitamin D treatment and/or phosphate binders [1]. Serum 25(OH)D levels >80-100 ng/mL are generally considered to be potentially toxic and increase the risk of hypercalcemia [1]. This article cites earlier studies (1950s-1970s) that showed that very high doses of cholecalciferol (100,000-300,000 IU/day) used to treat renal osteodystrophy were associated with a significant risk of hypercalcemia [1].

[1]. Ergocalciferol and cholecalciferol in CKD. Am J Kidney Dis. 2012 Jul;60(1):139-56.

[2]. Chicken parathyroid hormone gene expression in response to gastrin, omeprazole, ergocalciferol, and restricted food intake. Calcif Tissue Int. 1997 Sep;61(3):210-5.

[3]. Growth retardation induced in rat fetuses by maternal fasting and massive doses of ergocalciferol. J Nutr. 1987 Feb;117(2):342-8.

Therapeutic Uses
Veterinary Drug: ...Recommended for the prevention of postpartum hypocalcemia in dairy cows. ...Prevention of atrophic rhinitis in pigs. ...Aids in the healing of fractures in cats and dogs. Veterinary Drug: For effective ...supplementation of calcium and phosphate. ...Fish meal and irradiated yeast can be used as supplements...sources. ...Routine supplementation in the daily diet...1400-1600 IU/kg. Rickets Treatment...The daily dose is 10-20 times the daily requirement, taken every other day for 1 week. /Vitamin D/ For adults and children with nutritional rickets or osteomalacia and normal gastrointestinal absorption, daily oral administration of...ergocalciferol will restore serum calcium and phosphate concentrations to normal after approximately 10 days. X-rays will show bone healing within 2-4 weeks, and complete healing will occur after approximately 6 months. Dietary adjustments should be made. After bone healing, ergocalciferol supplementation can be discontinued for patients with normal gastrointestinal absorption. For adults with severe malabsorption and vitamin D deficiency, daily doses of ergocalciferol have been given to correct osteomalacia. For children with malabsorption, oral ergocalciferol has been recommended. For vitamin D-deficient infants with tetany and rickets, oral or intravenous calcium should be administered to control tetany. Then, daily oral ergocalciferol should be given to treat vitamin D deficiency until bone healing. For adults with Fanconi syndrome, oral ergocalciferol has been given concurrently with treatment for acidosis. Oral ergocalciferol has been used in children with Fanconi syndrome. For more complete data on the therapeutic uses of vitamin D2 (11 in total), please visit the HSDB records page. Drug Warnings: …Ergocalciferol should be used with extreme caution, or even contraindicated, in patients with impaired renal function; it should also be used with extreme caution in patients with heart disease, kidney stones, or arteriosclerosis. Initial signs and symptoms include weakness, fatigue, weakness, headache, nausea, vomiting, and diarrhea. Confusion and coma may occur. Early renal impairment due to hypercalcemia manifests as polyuria, polydipsia, nocturia, decreased urine concentrating ability, and proteinuria. Pharmacodynamics: Following vitamin D receptor activation, ergocalciferol induces several biological changes, including the mobilization and deposition of calcium and phosphorus in bones, intestinal absorption of calcium and phosphorus, and renal reabsorption of calcium and phosphorus. Other known effects of vitamin D include osteoblast formation, fetal development, induction of pancreatic function, induction of nerve function, improvement of immune function, cell growth, and cell differentiation. Compared to the vitamin D analog cholecalciferol, ergocalciferol has a weaker induction effect on calcidiol, and therefore lower potency. Studies have shown that ergocalciferol supplementation in patients with end-stage renal disease significantly improves laboratory indicators of bone and mineral metabolism, improves glycemic control, serum albumin levels, and reduces inflammatory marker levels.

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Ergocalciferol (vitamin D2) is derived from plants (e.g., irradiated fungi) and dietary supplements. [1]
It is classified as “nutritional vitamin D” along with cholecalciferol (vitamin D3), rather than as “active vitamin D” compounds like calcitriol, paricalciferol, and docecalciferol. [1]
Vitamin D deficiency (usually defined as serum 25(OH)D <20 ng/mL) and insufficiency (20–30 ng/mL) are very common in people with chronic kidney disease (CKD) and end-stage renal disease (ESRD). [1]
The National Kidney Foundation KDOQI and KDIGO Clinical Practice Guidelines recommend that for patients with stage 3–4 chronic kidney disease and secondary hyperparathyroidism, if their 25(OH)D level is <30 ng/mL, nutritional vitamin D (e.g., ergocalciferol) should be used first, and then active vitamin D analogues should be considered. [1]
According to the guidelines (author's interpretation), for patients with 25(OH)D <30 ng/mL, the recommended treatment regimen is: 50,000 IU of ergocalciferol orally once a week for 8 weeks, followed by reassessment. If the level is still <30 ng/mL, repeat the 8-week course. Maintenance therapy after correction: 50,000 IU of ergocalciferol orally once a month. [1]
Compared to cholecalciferol (vitamin D3), ergocalciferol (vitamin D2) has been reported to be less effective in raising and maintaining serum 25(OH)D levels in humans. [1]
This article emphasizes the current lack of large-scale, well-designed randomized controlled trials (RCTs) to assess the effects of ergocalciferol supplementation on hard clinical outcomes (e.g., mortality, cardiovascular events, infections) in patients with chronic kidney disease (CKD) and dialysis. Most evidence comes from observational studies and small-scale RCTs focusing on biochemical indicators. [1]

C28H44O

396.65

396.339

C, 84.79; H, 11.18; O, 4.03

50-14-6

5,6-trans-Vitamin D2;51744-66-2;(R)-Vitamin D2;116559-84-3;Vitamin D2-d6;1311259-89-8

5280793

White to off-white solid powder

1.0±0.1 g/cm3

504.2±29.0 °C at 760 mmHg

114-118 °C(lit.)

218.2±16.5 °C

0.0±2.9 mmHg at 25°C

1.530

9.56

1

1

5

29

678

6

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

MECHNRXZTMCUDQ-RKHKHRCZSA-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,3Z)-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

Viosterol; Vitamin D2; Ergocalciferol; Ercalciol; calciferol

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: ~31.3 mg/mL (78.8 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.24 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 (5.24 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 (5.24 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.)