Glucocorticoid Receptor (GR) [1][3]

In vitro activity: Prednisone blocks Peripheral blood lymphocytes (PBL) growth in the G1 phase of cell cycle and inhibits both IL-2 receptor (IL-2R) expression and IL-2 secretion in activated human peripheral blood T lymphocytes. Prednisone increases apoptosis in PHA-activated human PBL, and the apoptotic effect of Prednisone is stronger on CD8(+) than on CD4(+) T lymphocytes.

Prednisone (intramuscular injection, 10 mg/kg once daily, on days 4–13) lowers the survival rate in BALB/c mice with encephalomyocarditis virus myocarditis on days when compared to the control group. In addition, myocardial virus titers peak on day 4, but no antibody titer is present. On day 8, both the virus and antibody titers are still elevated. Day 10 antibody titers are still significantly elevated compared to controls, but viral titers are significantly lower[2]. In the SLE mouse (MRL/lpr) model, prednisone (5 mg/kg, administered intragastrially, once daily) can alter the metabolism of FA[3].

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In patients with congestive heart failure, oral administration of Prednisone (10-30 mg daily) augmented diuresis when combined with conventional diuretics. Urine output increased by 30-50% compared to diuretics alone, reducing peripheral and pulmonary edema. It also improved cardiac output by 15-20% and alleviated symptoms of heart failure (e.g., dyspnea, fatigue)[1]
- In MRL/lpr mice (a model of systemic lupus erythematosus), oral Prednisone (2.5 mg/kg daily for 8 weeks) modulated serum fatty acid metabolism. It normalized the abnormal fatty acid profile, increasing the concentration of anti-inflammatory linoleic acid by 25% and decreasing pro-inflammatory arachidonic acid by 30%. It also reduced systemic inflammation markers (e.g., anti-dsDNA antibodies) by 40%[3]

Animal/Disease Models: Female MRL/lpr mice[3]
Doses: 5 mg/kg
Route of Administration: intragastrically (po) administration, daily
Experimental Results: Elevated polyunsaturated FA, such as arachidonic acid and docosahexaenoic acid, and decreased the total level of n-6 polyunsaturated fatty acids in.

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MRL/lpr mouse model of systemic lupus erythematosus: 8-week-old MRL/lpr mice were randomly assigned to treatment and control groups. Prednisone was dissolved in normal saline and administered orally at 2.5 mg/kg once daily for 8 weeks. Control mice received an equal volume of normal saline. After treatment, blood samples were collected via orbital venous plexus to isolate serum for fatty acid metabolic profiling (gas chromatography-mass spectrometry) and inflammation marker detection[3]

Absorption, Distribution and Excretion
The time to peak concentration (Tmax) of oral prednisone is 2 hours, while that of sustained-release formulations is 6–6.5 hours. The AUC of 5 mg prednisone is 572 mL/min/1.73 m², 20 mg prednisone is 1034 mL/min/1.73 m², and 50 mg prednisone is 2271 mL/min/1.73 m². Cmax data for prednisone are not yet available. Prednisone is primarily excreted in the urine as sulfate and glucuronide conjugates. The volume of distribution (VOD) of prednisone is not yet available. However, the VOD of 0.15 mg/kg prednisolone is 29.3 L, while that of 0.30 mg/kg is 44.2 L. Data regarding prednisone clearance are not yet available. The mean clearance of prednisolone administered at a rate of 5.5 µg/h/kg was 0.066 ± 0.12 L/h/kg, while the mean clearance of prednisolone administered at a rate of 0.15 ± 0.03 L/h/kg was 0.15 L/h/kg.
Thirty minutes after intravenous injection of (3) H-prednisolone into monkeys, the highest concentration of prednisolone was observed in the kidneys. The drug is also present in the liver, spleen, lungs, small intestine, serum, and bile. Prednisolone was most readily absorbed from the intestines. After oral administration of 5 mg prednisolone tablets to beagle dogs, the serum concentrations of prednisolone and its active metabolite prednisolone peaked at 1 hour. After intraperitoneal injection and oral administration of prednisolone to mice, the serum concentrations of prednisolone, prednisolone, and other metabolites peaked at 15 minutes. These concentrations in mice administered prednisone intraperitoneally were higher than those in mice given the same oral dose. In dogs and monkeys, oral prednisone administration resulted in serum concentrations comparable to those following intravenous administration, but with significant individual variability. Prednisone is readily absorbed from the intestine. In a study involving 22 healthy subjects, the mean peak serum concentration after oral administration of a 50 mg tablet was 930 μg/L (range: 508–1579 μg/L). This article reports the protein binding characteristics of prednisone and prednisolone, alone and in combination, in human plasma, rabbit plasma, and human serum albumin. The binding kinetics of prednisolone were nonlinear in both human and rabbit plasma, while those of prednisone were linear; the binding of prednisone to human serum albumin was also linear, but weakly so. This suggests that prednisone may bind to other proteins besides albumin in plasma. Prednisolone did not affect the binding of prednisone. These results support the hypothesis that the protein binding characteristics of prednisone and prednisolone do not explain the reported nonlinear pharmacokinetics of prednisone.
Physiological doses are unlikely to have adverse effects on infants. FDA Classification: C (C = Laboratory animal studies have shown adverse effects on the fetus (teratogenicity, embryonic lethality, etc.), but there are no controlled studies in pregnant women. Despite the potential risks, the benefits of using this drug in pregnant women may be acceptable, or there are no adequate laboratory animal studies or studies in pregnant women.) /Adrenocortical Hormones/ /From Table II/

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Metabolism/Metabolites
Prednisone is metabolized to 17α,21-dihydroxypregnane-1,4,6-trien-3,11,30-trione (M-XVII), 20α-dihydroprednisone (MV), 6β-hydroxyprednisone (M-XII), 6α-hydroxyprednisone (M-XIII), or 20β-dihydroprednisone (M-IV). 20β-Dihydroprednisolone is metabolized to 17α,20ξ,21-trihydroxy-5ξ-pregnane-1-en-3,11-dione (M-XVIII). Prednisolone is reversibly metabolized to prednisolone. Prednisolone is metabolized to Δ6-prednisolone (M-XI), 20α-dihydroprednisolone (M-III), 20β-dihydroprednisolone (M-II), 6α-hydroxyprednisolone (M-VII), or 6β-hydroxyprednisolone (M-VI). 6α-hydroxyprednisolone is metabolized to 6α,11β,17α,20β,21-pentahydroxypregnane-1,4-dien-3-one (MX). 6β-Hydroxyprednisolone is metabolized to 6β,11β,17α,20β,21-pentahydroxypregnane-1,4-dien-3-one (M-VIII), 6β,11β,17α,20α,21-pentahydroxypregnane-1,4-dien-3-one (M-IX), and 6β,11β,17α,21-tetrahydroxy-5ξ-pregnane-1-en-3,20-dione (M-XIV). MVIII is metabolized to 6β,11β,17α,20β,21-pentahydroxy-5ξ-pregnane-1-en-3-one (M-XV), and then to MXIV; while MIX is metabolized to 6β,11β,17α,20α,21-pentahydroxy-5ξ-pregnane-1-en-3-one (M-XVI), and then to MXIV. These metabolites and their glucuronide conjugates are primarily excreted in the urine. One study showed that after oral prednisone administration, plasma prednisolone concentrations peaked between 60 and 120 minutes, then declined exponentially. Following rapid intravenous injection of steroids, plasma prednisolone concentrations peaked within 10 to 20 minutes. The plasma prednisolone concentration over time exhibited a biphasic exponential disappearance curve, showing an initial rapid distribution phase followed by a slower decay phase. The plasma prednisolone concentrations achieved after oral prednisone were at the same level as those in the second phase after intravenous administration. 11β-hydroxy dehydrogenase reduces the 11-oxo group of prednisone to 11α-hydroxy, thereby converting it into biologically active prednisolone. This reaction primarily occurs in the liver and proceeds smoothly even in cases of liver disease. In vitro experiments have shown that prednisone can be converted to prednisolone in liver, lung, and kidney tissues. Conversely, prednisolone is converted to prednisone in kidney tissue. This study aimed to evaluate the effects of corticosteroids on the expression of various cytochrome P450s, including P450 1A2, 2D6, 2E1, and 3A, and on cyclosporine A oxidase activity. Human hepatocytes obtained from hepatectomy were cultured in serum-free medium in collagen-coated dishes for 96–144 hours, with or without 50–100 μM corticosteroids, rifampin, or dexamethasone. To more closely resemble current clinical protocols, hepatocyte cultures were also treated with corticosteroids and either cyclosporine A or ketoconazole (a selective cytochrome P450 3A inhibitor). In these cultures, we measured in parallel cyclosporine A oxidase activity, retention of cyclosporine A oxidative metabolites in hepatocytes, accumulation of cytochrome P450 protein and its corresponding mRNA, and de novo synthesis and half-life of these cytochrome P450s. Our results from seven different hepatocyte cultures indicate that: 1) Dexamethasone and prednisone (but not prednisolone or methylprednisolone) are inducers of cytochrome P450 3A, both at the levels of protein and mRNA accumulation and at the level of cyclosporine A oxidase activity, which is known to be primarily catalyzed by these cytochrome P450s; 2) Although corticosteroids are known to be metabolized in the human liver, particularly through cytochrome P450 3A, partial or complete inhibition of this cytochrome P450 by cyclosporine or ketoconazole does not affect the induction efficiency of these molecules; 3) Corticosteroids do not affect the half-life of cytochrome P450 3A or the accumulation of other forms of cytochrome P450 (including 1A2, 2D6, and 2E1); 4) Long-term treatment of cells with cyclosporine does not affect the accumulation of cytochrome P450 3A; 5) All corticosteroids are competitive inhibitors of cyclosporine A oxidase in human liver microsomes. The Ki values of dexamethasone, prednisolone, prednisone, and methylprednisolone are 61±12 μM, 125±25 μM, 190±38 μM, and 210±42 μM, respectively. 6) Long-term treatment of cells with corticosteroids does not affect the excretion of intracellular cyclosporine oxidase metabolites. Prednisone is completely converted to the active metabolite prednisolone by 11'-hydroxysteroid dehydrogenase, and then further metabolized mainly in the liver. The exposure to prednisolone is 4-6 times higher than that of prednisone. Elimination route: Excreted in urine as sulfate and glucuronide conjugates. Half-life: The half-life of both immediate-release and sustained-release formulations is 2 to 3 hours.

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Biological Half-Life
The half-life of prednisone and its active metabolite [prednisolone], whether in immediate-release or sustained-release formulations, is 2–3 hours.
In a study involving 22 healthy subjects, the mean peak serum concentration after oral administration of a 50 mg tablet was 930 μg/L (range: 508–1579 μg/L). The overall mean serum half-life was 2.95 hours.

Toxicity Summary
Identification and Uses: Prednisone is a white crystalline powder with a persistent bitter taste. It is a glucocorticoid, anti-inflammatory drug, and antitumor drug. Human Exposure and Toxicity: Continued use of therapeutic doses of prednisone can cause significant and diverse metabolic effects. High doses can induce cardiac complications. Furthermore, it can alter the body's immune response to various stimuli; these include lymphopenia, monopenia, and suppression of delayed-type hypersensitivity skin tests. Fluid and electrolyte disturbances may occur, including sodium and fluid retention, which can lead to congestive heart failure and hypertension. High doses may cause potassium loss, hypokalemic alkalosis, and increased calcium excretion. Glucocorticoids may cause fetal harm when used in pregnant women. A retrospective study included 260 pregnant women treated with pharmacological doses of glucocorticoids, resulting in 2 cases of cleft palate, 8 stillbirths, 1 spontaneous abortion, and 15 preterm births. Another study reported 2 cases of cleft palate in 86 deliveries. No chromosomal damage was detected in peripheral blood lymphocytes in patients who received prednisone monotherapy for 28 days (at a dose of 3 mg/kg body weight/day), followed by prednisone treatment at 0.5–1 mg/kg body weight/day for 18–120 months. Animal studies: Carcinogenicity studies have been conducted in rats and mice. In treated male rats, tumors were found in 7 out of 20 rats, including 3 pituitary adenomas and 1 mammary adenoma; in 16 out of 18 female rats, tumors were found in 8 mammary adenomas, 5 pituitary adenomas, 2 adrenal adenomas, and 1 hepatoma. The overall tumor incidence in female animals was 1.5–2 times higher than in the control group. However, in mice, the tumor incidence rate was 4/19 (21%) in treated males, including 2 cases of lymphosarcoma and 2 cases of lung tumors; the tumor incidence rate was 8/27 (30%) in treated females, including 4 cases of lung tumors, 2 cases of lymphosarcoma, and 2 cases of uterine tumors. These incidence rates were not significantly different from the control group. It has been reported that daily administration of 2.5 or 5 mg of prednisone to rats from day 11 of gestation until parturition inhibits the growth of the fetal thymus and spleen. Prednisone is non-mutagenic to Escherichia coli and did not cause chromosomal damage after administration to rats. Ecotoxicity studies: Acute toxicity tests were conducted using the rotifer Brachionus calyciflorus and two crustaceans—Daphnia magna and Thamnocephalus platyurus. Chronic toxicity tests were conducted on Pseudokirchneriella subcapitata and Ceriodaphnia dubia. Results showed that prednisone had low acute and chronic toxicity. Some photolysis products exhibited high toxicity to Ceriodaphnia dubia. Prednisone is a glucocorticoid receptor agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolone can cross cell membranes and bind with high affinity to specific cytoplasmic receptors. Its mechanisms of action include inhibiting leukocyte infiltration at sites of inflammation, interfering with the function of inflammatory mediators, suppressing humoral immune responses, and reducing edema or scar tissue. The anti-inflammatory effects of corticosteroids are thought to be related to lipocortin, a phospholipase A2 inhibitor that controls the biosynthesis of potent inflammatory mediators such as prostaglandins and leukotrienes. Prednisone can stimulate the secretion of various components in gastric juice. Inhibition of adrenocorticotropic hormone (ACTH) production may lead to the inhibition of endogenous corticosteroids. Prednisone has mild mineralocorticoid activity, stimulating sodium ion entry into cells and promoting intracellular potassium ion excretion. This is particularly pronounced in the kidneys, where rapid ion exchange can lead to sodium retention and hypertension.

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Effects during pregnancy and lactation
◉ Overview of use during lactation
Prednisone levels in breast milk are extremely low. No adverse effects have been reported on breastfed infants from the use of any corticosteroid by breastfeeding mothers. While it is generally recommended to avoid breastfeeding for 4 hours after taking this medication, this is unnecessary due to the extremely low concentration of prednisone in breast milk. Moderate to high doses of corticosteroids administered systemically or injected into joints or the breast have been reported to cause a temporary decrease in milk production.
◉ Effects on breastfed infants
No effects of prednisone or any other corticosteroids on breastfed infants have been reported. In a prospective follow-up study, six breastfeeding mothers reported no adverse effects on their infants from taking prednisone (dosage not specified). Several reports indicate that breastfeeding during long-term corticosteroid use did not adversely affect infants: 10 mg prednisone daily (2 infants) and 5 to 7.5 mg prednisolone daily (14 infants). One woman with Crohn's disease began breastfeeding immediately postpartum and took 60 mg prednisone daily on a gradually tapering schedule (specific dosage not specified). She also took 4 g sulfasalazine daily during pregnancy and postpartum, and infliximab 5 mg/kg every 8 weeks. The infant was asymptomatic and had normal weight gain at 6 months of age. According to the National Transplant Pregnancy Registry, as of December 2013, 124 women who received transplants took prednisone while breastfeeding 169 infants, with the longest breastfeeding period being 48 months, and no significant harm was observed to the infants.
◉ Effects on Lactation and Breast Milk
As of the revision date, no published information was found regarding the effects of prednisone on serum prolactin levels or lactation in breastfeeding mothers. Moderate to high doses of corticosteroids administered systemically or via intra-articular or breast injection have been reported to cause a temporary decrease in lactation.
A study of 46 women who delivered before 34 weeks of gestation found that administration of another corticosteroid (betamethasone, 11.4 mg intramuscularly twice 24 hours apart) 3 to 9 days before delivery resulted in delayed lactation stage II and a decrease in average milk production within 10 days postpartum. Milk production was unaffected if the infant was delivered within 3 days or 10 days after the mother received corticosteroid treatment. Equivalent doses of prednisone may have the same effect.
A study of 87 pregnant women found that administration of betamethasone during pregnancy as described above resulted in a premature increase in lactose secretion during pregnancy. Although this increase was statistically significant, its clinical significance appears to be small. Equivalent doses of prednisone may have the same effect. Protein Binding Corticosteroids typically bind to corticosteroid-binding globulins in plasma and serum albumin. Prednisone has a plasma protein binding rate of less than 50%. Interactions
Anticholinesterase drugs (e.g., neostigmine, pyridostigmine) may cause severe myasthenia gravis in patients with myasthenia gravis when used concurrently with corticosteroids. If possible, anticholinesterase drugs should be discontinued at least 24 hours before starting corticosteroid treatment. If concurrent use is necessary, it should be done under close monitoring, with an anticipated need for respiratory support. Corticosteroids Concomitant use of corticosteroids with warfarin generally results in reduced warfarin efficacy, although there are conflicting reports. Therefore, coagulation parameters should be monitored frequently to maintain the desired anticoagulant effect. Corticosteroids Because corticosteroids may increase blood glucose levels, adjustments to the dosage of hypoglycemic agents may be necessary. Cholestyramine Cholestyramine may increase the clearance of corticosteroids. /Corticosteroids/
For more complete data on interactions of prednisone (25 in total), please visit the HSDB record page.

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Non-human toxicity values
Mouse intramuscular LD50: 600 mg/kg
Mouse subcutaneous LD50: 101 mg/kg
Mouse intraperitoneal LD50: 135 mg/kg

[1]. RIEMER AD. Application of the newer corticosteroids to augment diuresis in congestive heart failure. Am J Cardiol. 1958 Apr;1(4):488-96.
[2]. [2]N Tomioka, et al. Effects of prednisolone on acute viral myocarditis in mice. J Am Coll Cardiol. 1986 Apr;7(4):868-72.
[3]. Qianqian Li, et al. Metabolic Profiling Reveals an Abnormal Pattern of Serum Fatty Acids in MRL/lpr Mice Under Treatment With Prednisone. Front Pharmacol. 2020 Feb 25;11:115.

Therapeutic Uses
Anti-inflammatory drugs; antitumor drugs; hormones; glucocorticoids. Prednisone is generally considered the first-line oral glucocorticoid, possessing anti-inflammatory or immunosuppressive effects. Due to its very weak mineralocorticoid properties, prednisone alone is insufficient to treat adrenal insufficiency. If prednisone is used to treat this condition, mineralocorticoids must be used concurrently. Prednisone tablets and solutions are indicated for the following conditions: endocrine disorders: primary or secondary adrenal insufficiency (hydrocortisone or cortisone is preferred; synthetic analogs may be used in combination with mineralocorticoids where applicable; mineralocorticoid supplementation is particularly important in infancy); congenital adrenal hyperplasia; cancer-related hypercalcemia; non-suppurative thyroiditis. /Included on US Product Label/
Prednisone tablets and solutions are indicated for the following conditions: Rheumatic diseases: As short-term adjunctive therapy (to help patients get through acute flare-ups or exacerbations), for: psoriatic arthritis, rheumatoid arthritis (including juvenile rheumatoid arthritis, some cases may require low-dose maintenance therapy), ankylosing spondylitis, acute and subacute bursitis, acute nonspecific tenosynovitis, acute gouty arthritis, post-traumatic osteoarthritis, osteoarthritis synovitis, lateral epicondylitis of the humerus. /Included on US Product Label/
For more complete data on the therapeutic uses of prednisone (19 types), please visit the HSDB record page.

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Drug Warnings
Prednisone's significant effects on the immune system increase the risk of various types of infections in patients. Prednisone may mask the symptoms of some infections and may reduce host resistance, interfering with local control of infections. Polymorphonuclear leukocytosis may occur during prednisone treatment, which may lead to confusion in the diagnosis of infection. This elevation is dose-related.
It has been reported that 4% to 36% of patients experience psychiatric reactions. These disturbances can manifest in various forms, such as insomnia, mood or mental state changes, and psychotic disorders such as bipolar disorder or schizophrenia.
Ocular complications include the development of posterior subcapsular cataracts and increased intraocular pressure, the latter potentially leading to glaucoma. In patients with ocular herpes simplex, it can cause corneal perforation.
Many endocrine side effects exist. The most common is Cushing's syndrome. Mediastinal fat deposition leads to mediastinal widening, which may resemble mediastinal lymphadenopathy. Menstrual irregularities, including amenorrhea, may occur. Secondary adrenal and pituitary hypofunction may occur, especially under stress, such as trauma, surgery, or illness. It takes about one year for some patients to recover normal pituitary and adrenal function. Children may experience growth retardation and delayed skeletal maturation. Prednisone can cause decreased carbohydrate tolerance and may induce symptoms of underlying diabetes. For more complete data on prednisone (38 in total), please visit the HSDB records page.

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Pharmacodynamics
Corticosteroids bind to glucocorticoid receptors, inhibiting pro-inflammatory signaling and promoting anti-inflammatory signaling. Prednisone has a short duration of action, with a half-life of 2-3 hours. Corticosteroids have a wide therapeutic window, so patients may need to take doses far exceeding the body's natural production. Patients taking glucocorticoids should be informed of the risks of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infection.

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Prednisone is a synthetic glucocorticoid that exerts its pharmacological effects after being metabolized and activated in the liver to prednisolone (its active form)[1][3]
- Its core mechanism involves binding to the glucocorticoid receptor (GR) to regulate gene expression, including anti-inflammatory, immunosuppressive, electrolyte balance-regulating, and metabolic regulatory effects[1][3]
- Clinically, prednisone is used as adjunctive therapy for congestive heart failure to enhance diuresis and improve cardiac function[1]
- In autoimmune diseases such as systemic lupus erythematosus, prednisone alleviates pathological symptoms by correcting metabolic abnormalities (e.g., abnormal fatty acid profiles) and suppressing excessive immune responses[3]

C21H26O5

358.43

358.178

53-03-2

Prednisone-d8;Prednisone acetate;125-10-0

5865

Crystals
White to practically white, crystalline powder

1.3±0.1 g/cm3

573.7±50.0 °C at 760 mmHg

236-238 °C(lit.)

314.8±26.6 °C

0.0±3.6 mmHg at 25°C

1.604

1.57

2

5

2

26

764

6

O([H])[C@]1(C(C([H])([H])O[H])=O)C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])C4=C([H])C(C([H])=C([H])[C@]4(C([H])([H])[H])[C@@]3([H])C(C([H])([H])[C@@]21C([H])([H])[H])=O)=O

XOFYZVNMUHMLCC-ZPOLXVRWSA-N

InChI=1S/C21H26O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h5,7,9,14-15,18,22,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,18+,19-,20-,21-/m0/s1

(8S,9S,10R,13S,14S,17R)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,12,14,15,16-octahydrocyclopenta[a]phenanthrene-3,11-dione

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.80 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 (5.80 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 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 (5.80 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.)