Glucocorticoid Receptor (GR) mediates transactivation, [1]
- Mineralocorticoid Receptor (MR)weakly mediates transactivation[1]

In CV-1 cells, budesonide preferentially binds to the human glucocorticoid receptor (hGR; EC50=45.7 pM) as opposed to the mineralocorticoid receptor (EC50=7,620 pM). In macrophages (RAW 264.7 cells), budesonide (30 min before LPS) inhibits the activation of the NLRP3 inflammasome by LPS (100 ng/mL) + ATP (5 mM)[2].

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In CV-1 cells transfected with GR-dependent luciferase reporter plasmid, Budesonide (1-100 nM) dose-dependently activated GR-mediated transcription, with maximal transactivation activity reaching ~60% of dexamethasone (a reference GR agonist) at 100 nM[1]
- In CV-1 cells transfected with MR-dependent luciferase reporter plasmid, Budesonide (10-1000 nM) weakly activated MR-mediated transcription, with maximal activity only ~20% of aldosterone (a reference MR agonist) even at 1000 nM[1]
- In mouse lung tumor cells, Budesonide (1 μM, 10 μM) modulated DNA methylation patterns. At 10 μM, it downregulated mRNA expression of tumor-associated genes by 30-40% (RT-PCR) and altered the methylation status of CpG islands in gene promoters (bisulfite sequencing analysis)[3]

Lung tumor size is reduced by budesonide (2.0 mg/kg; orally via diet; at 2, 7 and 21 days prior to killing)[3]. Pretreatment with budesonide (0.5 mg/kg; intranasal given 1 hour before to LPS injection (5 mg/kg)) significantly attenuates pathological harm and lowers pathological scores in adult male C57BL/6 mice with ALI[2].

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In a mouse model of LPS-induced acute lung injury, intranasal administration of Budesonide (0.1 mg/kg, 0.5 mg/kg) dose-dependently attenuated lung injury. At 0.5 mg/kg, it suppressed NLRP3 inflammasome activation by 55% (Western blot for NLRP3, caspase-1), reduced serum and lung tissue levels of IL-1β (by 60%) and IL-6 (by 50%) (ELISA), and alleviated lung tissue edema and inflammatory cell infiltration (histopathological scoring)[2]
- In a mouse model of lung tumors, oral administration of Budesonide (1 mg/kg daily for 4 weeks) modulated DNA methylation in lung tumor tissues. It restored abnormal CpG island methylation of tumor suppressor genes and downregulated mRNA expression of pro-tumorigenic genes by 35-45% (RT-PCR and methylation-specific PCR)[3]

GR-mediated transactivation assay: CV-1 cells were co-transfected with human GR expression plasmid and GR-responsive luciferase reporter plasmid. After 24 hours, Budesonide (1 nM, 10 nM, 100 nM, 1000 nM) was added, and cells were cultured for another 48 hours. Luciferase activity was measured using a luminometer, with relative activity reflecting GR transactivation potency[1]
- MR-mediated transactivation assay: CV-1 cells were co-transfected with human MR expression plasmid and MR-responsive luciferase reporter plasmid. Following 24-hour incubation, Budesonide (10 nM, 100 nM, 500 nM, 1000 nM) was added, and cells were cultured for 48 hours. Luciferase activity was quantified to evaluate MR transactivation activity, with aldosterone as a positive control[1]

GR/MR transactivation cell assay: CV-1 cells were seeded in 96-well plates and transfected with respective receptor and reporter plasmids. After transfection, Budesonide at gradient concentrations was added, and cells were incubated for 48 hours. Luciferase activity was detected to assess receptor-mediated transcriptional activation[1]
- DNA methylation and mRNA expression assay: Mouse lung tumor cells were seeded in 6-well plates and treated with Budesonide (1 μM, 10 μM) for 72 hours. Genomic DNA was extracted for bisulfite sequencing to analyze CpG island methylation. Total RNA was isolated, reverse-transcribed to cDNA, and RT-PCR was performed to quantify mRNA expression of target genes[3]

Animal/Disease Models: Female strain A/J mice at 8 weeks of age[3]
Doses: 2.0 mg/ kg
Route of Administration: Orally via their diet; at 2, 7 and 21 days prior to killing (27 weeks)
Experimental Results: decreased the size of the lung tumors after 2 days and rapidly diminished the size of lung tumors, reversed DNA hypomethylation and modulated mRNA expression of genes.

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LPS-induced acute lung injury mouse model: Male C57BL/6 mice (20-25 g) were randomly grouped. Budesonide was dissolved in normal saline containing 0.1% Tween 80, and administered intranasally at 0.1 mg/kg or 0.5 mg/kg 1 hour before LPS intranasal challenge (5 mg/kg). Mice were euthanized 24 hours after LPS challenge, and lung tissues and serum were collected for histopathological analysis and cytokine detection[2]
- Lung tumor mouse model: Female A/J mice (6-8 weeks old) were induced to develop lung tumors. Budesonide was suspended in 0.5% carboxymethylcellulose sodium and administered orally at 1 mg/kg once daily for 4 weeks. Lung tissues were harvested after treatment for DNA methylation analysis (bisulfite sequencing) and mRNA expression detection (RT-PCR)[3]

Absorption, Distribution and Excretion
The bioavailability of sustained-release oral capsules is 9-21%. A 9 mg dose achieves a Cmax of 1.50 ± 0.79 ng/mL, a Tmax of 2-8 hours, and an AUC of 7.33 ng/hr/mL. A high-fat diet may prolong the Tmax by 2.3 hours, but otherwise does not affect the pharmacokinetics of budesonide. With a quantitative inhalation dose of 180-360 µg, the pulmonary deposition rate of budesonide is 34%, the bioavailability is 39%, the Cmax is 0.6-1.6 nmol/L, and the Tmax is 10 minutes. A 1 mg nebulized inhalation dose has a bioavailability of 6%, a Cmax of 2.6 nmol/L, and a Tmax of 20 minutes. The peak plasma concentration (Cmax) of 9 mg oral extended-release tablets was 1.35 ± 0.96 ng/mL, the time to peak concentration (Tmax) was 13.3 ± 5.9 h, and the area under the curve (AUC) was 16.43 ± 10.52 ng·hr/mL. The AUC of budesonide rectal foam tablets (2 mg, twice daily) was 4.31 ng·hr/mL. Approximately 60% of the budesonide dose is excreted in the urine as the major metabolites 6β-hydroxybudesonide, 16α-hydroxyprednisolone, and their conjugates. Untreated budesonide was not detected in urine. The volume of distribution of budesonide is 2.2–3.9 L/kg. The plasma clearance of budesonide is 0.9–1.8 L/min. The clearance of 22R budesonide is 1.4 L/min, while the clearance of 22S budesonide is 1.0 L/min. The clearance rate in asthmatic children aged 4–6 years was 0.5 L/min. It is unclear whether budesonide is distributed in breast milk. Approximately 34% of the dose enters the systemic circulation after intranasal administration. The mean peak plasma concentration of budesonide is reached in approximately 0.7 hours. Inhaled corticosteroids (ICS) are the primary drugs for treating asthma and chronic obstructive pulmonary disease. However, highly lipophilic ICS accumulate in systemic tissues, which can lead to adverse systemic reactions. There are currently no reports on the accumulation of the novel highly lipophilic ICS cyclosporine and its active metabolite (des-CIC). This study compared the accumulation of des-CIC and the moderately lipophilic ICS budesonide (BUD) in tissues after 14 days of once-daily administration in mice. Male CD1 albino mice were injected subcutaneously with [(3)H]-des-CIC or [(3)H]-BUD once, three times, or fourteen times daily, and were sacrificed 4 hours, 24 hours, or 5 days after the last administration. Quantitative whole-body autoradiography was used to study the distribution of radioactive materials in tissues. After single and repeated administration, the radioactive distribution patterns of the two corticosteroids in most tissues were similar. However, differences existed in tissue radioactivity concentrations between des-CIC and budesonide (BUD). After a single administration, the radioactivity concentrations of both corticosteroids in most tissues were low, but gradually increased after 14 days of continuous daily administration. At 24 hours and 5 days after the 14th dose, the radioactivity concentrations of des-CIC in most tissues were 2–3 times that of BUD. Tissue accumulation (comparing tissue radioactivity concentrations at 5 days after the 14th dose to 5 days after the 3rd dose) showed a mean ratio of 5.2 for des-CIC and 2.7 for budesonide (BUD) (p < 0.0001). In summary, des-CIC accumulated significantly more radioactively than budesonide. Systemic accumulation may increase the risk of systemic adverse reactions during long-term treatment.

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Metabolism/Metabolites
Budesonide has a first-pass metabolism of 80-90%. It is metabolized via CYP3A to two major metabolites: 6β-hydroxybudesonide and 16α-hydroxyprednisolone. The glucocorticoid activity of these metabolites is negligible (<1/100) compared to the parent compound. CYP3A4 is the most potent metabolic enzyme for budesonide, followed by CYP3A5 and CYP3A7.
Budesonide is metabolized in the liver by cytochrome P-450 (CYP) isoenzyme 3A4; the affinity of its two major metabolites for glucocorticoid receptors is less than 1% of that of the parent compound. Budesonide is excreted in urine and feces as metabolites.
Asthma is one of the most common diseases worldwide, and inhaled glucocorticoids (GCs) have long been a primary treatment. Despite their widespread use, approximately 30% of asthma patients exhibit some degree of steroid insensitivity or refractory to inhaled corticosteroids. One hypothesis explaining this phenomenon is the difference in clearance rates of these compounds among patients. This study aimed to investigate how the metabolism of glucocorticoids (GCs) by the CYP3A enzyme family affects their efficacy in asthma patients. This study examined the metabolism of four commonly used inhaled GCs (triamcinolone, flunisolone, budesonide, and fluticasone propionate) within the CYP3A enzyme family to determine differences in clearance rates and identify their metabolites. The study found differences in metabolic rates and pathways among different enzymes and drugs. CYP3A4 was the most efficient metabolic catalyst for all compounds, while CYP3A7 had the slowest metabolic rate. CYP3A5 is closely related to the metabolism of pulmonary GCs, and studies have confirmed its effective metabolism of triamcinolone, budesonide, and fluticasone propionate. In contrast, flunisolone is metabolized only by CYP3A4, with little or no metabolism by CYP3A5 or CYP3A7. Common metabolites include 6β-hydroxylation and Δ(6)-dehydrogenation of triamcinolone, budesonide, and flunisolone. The structure of Δ(6)-flunisolone has been definitively determined by nuclear magnetic resonance (NMR) analysis. Metabolism also occurs at D-ring substituents, including the 21-carboxyl metabolites of triamcinolone and flunisolone. A novel metabolite, 21-nortriamcinolone, has also been identified by liquid chromatography-mass spectrometry and NMR analysis.

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Biological Half-Life
The plasma elimination half-life of budesonide is 2–3.6 hours. The terminal elimination half-life in asthmatic children aged 4–6 years is 2.3 hours.

Toxicity Summary
Identification and Uses: Budesonide (brand names: Rhinocort, MMX) is a prescription drug approved for the treatment of allergic rhinitis (Rhinocort nasal spray) and mild to moderate Crohn's disease (MMX, enteric-coated capsules). Human Exposure and Toxicity: Patch studies have shown that budesonide can cause delayed-onset anaphylaxis and atopic dermatitis. Perioral dermatitis has been reported following inhalation exposure. Following oral administration, candidal esophagitis, dysphagia, increased blood pressure, lower extremity edema, and weight gain have been reported, but some of these adverse reactions may be due to drug interactions with voriconazole. Epidemiological studies have found that inhaled budesonide increases the risk of pneumonia, arrhythmias, cataracts, and fractures. Other epidemiological studies have also found that inhaled budesonide during pregnancy may be a risk factor for endocrine and metabolic disorders in offspring. Additionally, low birth weight has been reported. In children treated with budesonide for persistent asthma, slowed linear growth, slow weight gain, and slowed skeletal maturation have also been observed. Localized nasopharyngeal candidiasis has been reported during intranasal budesonide treatment. Patients may be more susceptible to certain diseases, such as chickenpox. In children and adolescents, budesonide use may lead to growth inhibition and may also cause acute or delayed-type hypersensitivity reactions. Infants born to mothers who received corticosteroid treatment during pregnancy may develop adrenal insufficiency. Animal studies: In carcinogenicity studies, hepatocellular carcinoma and glioma were observed in rats given oral budesonide. Decreased prenatal survival and survival of pups during pregnancy and lactation were observed in female rats given subcutaneous budesonide injections. Pyloric hyalinization was detected in mice given oral budesonide.

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Hepatotoxicity
Long-term budesonide treatment was not associated with elevated serum enzyme levels; the rate of ALT elevation was similar in the budesonide and placebo groups in clinical trials. No clinically significant liver injury associated with budesonide use has been reported in controlled trials. Unlike traditional systemic corticosteroids, budesonide is not associated with hepatitis B virus reactivation. Budesonide has been used to treat severe autoimmune liver disease, and there is no evidence that it exacerbates liver damage. Because budesonide can improve elevated serum transaminases in patients with autoimmune hepatitis, a rebound increase may occur after discontinuation, similar to the situation with conventional glucocorticoid therapy. Furthermore, there has been a case report of acute elevation of serum transaminases during budesonide treatment, with symptom relief after discontinuation; however, related records are limited, and the patient was concurrently taking several other potentially hepatotoxic drugs. Probability Score: E (Unlikely a clinically significant cause of liver damage). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation The amount of budesonide excreted in breast milk after inhalation is extremely small, and the infant's exposure is negligible. The bioavailability of oral budesonide is only about 9%; any budesonide that enters breast milk is likely to have similarly low bioavailability in the infant. Expert opinion suggests that breastfeeding women can use inhaled, nasal, oral, and rectal corticosteroids.
◉ Effects on breastfed infants
Currently, there are no reports related to corticosteroids.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.
Protein binding

Corticosteroids are normally bound to corticosteroid-binding globulins in plasma and serum albumin. Budesonide has a protein binding rate of 85-90% in plasma.
Interactions

Oral glucocorticoids can cause steroid-induced psychosis, which has been described in detail. However, our literature search found that the combined use of inhaled glucocorticoids with long-acting β2-receptor agonists does not cause delirium. We describe a case of delirium following the combined use of inhaled glucocorticoids and a bronchodilator. An elderly male patient developed confusion and hallucinations within one week of starting budesonide/formoterol for chronic obstructive pulmonary disease. Symptoms improved after discontinuation of the inhaled combination therapy. Several weeks later, the patient was hospitalized and restarted the inhaled combination therapy. Upon admission, the patient was conscious and disoriented, but during hospitalization, confusion and hallucinations gradually worsened. After discontinuation of the inhaled combination therapy again, the confusion and hallucinations disappeared upon discharge. The timing of these events, along with the possible Naranjo association, leads us to reasonably infer that the use of the budesonide/formoterol inhaled combination therapy was the cause or contributing factor to the delirium in this elderly patient. The delirium likely resulted from the systemic absorption of glucocorticoids deposited in the lungs, and the patient had several predisposing factors for delirium. Healthcare professionals should be aware of this potential adverse drug reaction when prescribing inhaled medications to elderly patients at risk of delirium. A 48-year-old HIV-infected woman developed Cushing's syndrome-like symptoms while taking ritonavir-enhanced darunavir. The diagnosis of Cushing's syndrome was due to a drug interaction between ritonavir and budesonide. Diagnosing iatrogenic Cushing's syndrome in HIV-positive patients taking ritonavir-enhanced protease inhibitors (PIs) is clinically challenging due to the similarity in clinical features, such as lipomatosis, associated with ritonavir-enhanced PIs. While this complication from inhaled fluticasone has been widely reported, the interaction of inhaled budesonide at therapeutic doses is poorly understood. To report two cases of iatrogenic Cushing's syndrome resulting from the interaction of the inhaled corticosteroid budesonide with ritonavir and itraconazole, we present the clinical and biochemical data of two patients diagnosed with Cushing's syndrome due to this interaction. A 71-year-old male patient was receiving inhaled budesonide for chronic obstructive pulmonary disease and itraconazole for pulmonary aspergillosis. He rapidly developed classic Cushing's syndrome complicated by bilateral avascular necrosis of the femoral head. Serum cortisol levels at 8:00 AM were measured twice, decreasing to 0.76 and 0.83 μg/dL, respectively. Four days later, the patient died from a massive myocardial infarction. The second patient was a 46-year-old woman who had been using inhaled budesonide for asthma for many years. She started taking ritonavir (a retroviral protease inhibitor) after contracting HIV. Over the next few months, she developed typical Cushing's syndrome symptoms. Her morning serum cortisol level was 1.92 μg/dL. A corticotropin stimulation test showed serum cortisol levels of <1.10, 2.65, and 5.36 μg/dL at 0, 30, and 60 minutes, respectively, confirming adrenal insufficiency. Because the patient was unable to discontinue budesonide, her doctor advised her to reduce the frequency of use and eventually gradually taper the dose until discontinuation. Clinicians should be aware that the combined use of inhaled corticosteroids with itraconazole or ritonavir may lead to iatrogenic Cushing's syndrome and secondary adrenal insufficiency. Oral budesonide is commonly used to treat Crohn's disease because it has a high affinity for glucocorticoid receptors and low systemic activity due to extensive first-pass metabolism via hepatic cytochrome P450 (CYP) 3A4. Voriconazole is a second-generation triazole antifungal drug that is both a substrate and a potent inhibitor of CYP isoenzymes (especially CYP2C19, CYP2C9, and CYP3A4); therefore, voriconazole has a high potential for interaction with other drugs. To our knowledge, there are no reports in the literature regarding drug interactions between voriconazole and glucocorticoids. We describe a case of a 48-year-old female patient who was treated with oral budesonide 9 mg/day for Crohn's disease and was later diagnosed with fluconazole-resistant Candida albicans esophagitis; her doctor prescribed voriconazole 200 mg every 12 hours for 3 weeks. Due to a recurrence of dysphagia, the patient was treated with voriconazole for another 3 weeks. Seven weeks after starting voriconazole, the patient presented to a primary care clinic with elevated blood pressure, lower extremity edema, and weight gain; the doctor prescribed diuretics and assessed renal function. Six weeks later, the patient returned to a specialist clinic with persistently elevated blood pressure. Physical examination revealed a moon face, prominent fat pads at the back of the neck, and pitting edema in the lower extremities. A drug interaction between voriconazole and budesonide, leading to iatrogenic Cushing's syndrome, was suspected, and voriconazole was discontinued. Budesonide was continued as previously prescribed for Crohn's disease. Two months later, the patient's Cushing-like symptoms had significantly subsided. To our knowledge, this is the first published case report of iatrogenic Cushing's syndrome resulting from a possible drug interaction between voriconazole and oral budesonide. For patients taking both medications concurrently and experiencing Cushing-like symptoms, clinicians should consider potential drug interactions and weigh the risks and benefits of continuing treatment. For more complete data on budesonide drug interactions (11 in total), please visit the HSDB record page.

[1]. Transactivation via the Human Glucocorticoid and Mineralocorticoid Receptor by Therapeutically Used Steroids in CV-1 Cells: A Comparison of Their Glucocorticoid and Mineralocorticoid Properties. Eur J Endocrinol. 2004 Sep;151(3):397-406.

[2]. Intranasal Application of Budesonide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Nucleotide-Binding Oligomerization Domain-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation in Mice. J Immunol Res. 2019 Feb 27;2019:7264383.

[3]. Modulation by Budesonide of DNA Methylation and mRNA Expression in Mouse Lung Tumors. Int J Cancer. 2007 Mar 1;120(5):1150-3.

Therapeutic Uses
Anti-inflammatory drugs; bronchodilators; glucocorticoids. ClinicalTrials.gov is a registry and results database that indexes human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov includes a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). Budesonide is indexed in the database. Budesonide enteric-coated capsules are indicated for the treatment of mild to moderate active Crohn's disease involving the ileum and/or ascending colon. /US Product Label Includes/
Budesonide enteric-coated capsules are indicated for maintaining clinical remission of mild to moderate Crohn's disease involving the ileum and/or ascending colon for up to 3 months. /US Product Label Includes/
For more complete data on the therapeutic uses of budesonide (13 types), please visit the HSDB record page.

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Drug Warnings
Intranasal budesonide should be used with caution or avoided in patients with clinical or asymptomatic mycobacterial respiratory infections, untreated fungal or bacterial infections, ocular herpes simplex, or untreated systemic viral infections.
Rarely, local candidiasis of the nasal cavity and/or pharynx may occur during intranasal budesonide treatment. If an infection occurs, appropriate local or systemic treatment may be required, and/or intranasal budesonide treatment may need to be discontinued. Patients receiving this drug for several months or longer should be monitored regularly for candidiasis or changes in the nasal mucosa. Rare reports of nasal septal perforation and elevated intraocular pressure have been observed in patients receiving budesonide nasal spray. Because corticosteroid treatment may inhibit wound healing, nasal corticosteroids should not be used in patients with recent nasal septal ulceration, nasal surgery, or nasal trauma until the wound has healed. Patients taking immunosuppressants are more susceptible to infection than healthy individuals, and certain infections (such as chickenpox and measles) may have more severe consequences, even life-threatening ones, in these patients, especially in children. Special care should be taken to avoid exposure in patients who have not had these diseases. The dosage, route of administration, and duration of corticosteroid administration, as well as the impact of underlying diseases and/or prior corticosteroid treatment, on the risk of disseminated infection are currently unclear. If such individuals are exposed to chickenpox or measles, varicella-zoster immunoglobulin (VZIG) or a combination of intramuscular and intramuscular immunoglobulin (IG) can be initiated, respectively. If chickenpox develops, antiviral treatment may be considered.
Adverse reactions occurring in ≥2% of patients receiving budesonide nasal spray, and at a higher rate than in the placebo group, included epistaxis, pharyngitis, bronchospasm, cough, and nasal irritation.
For more complete (17) drug warnings for budesonide, please visit the HSDB record page.

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Pharmacodynamics
Budesonide is a glucocorticoid used to treat respiratory and digestive disorders by reducing inflammation. Its therapeutic index is wide due to significant inter-patient dose variability. Patients should be informed of the risks of hypercortisolism and adrenal axis suppression. Budesonide is a synthetic glucocorticoid with potent anti-inflammatory and immunosuppressive effects [1][2]. Its core mechanism includes binding to the glucocorticoid receptor (GR), mediating transcriptional activation of anti-inflammatory genes and transcriptional inhibition of pro-inflammatory genes, and weak activation of the mineralocorticoid receptor (MR), resulting in low mineralocorticoid activity [1]. It alleviates lipopolysaccharide (LPS)-induced acute lung injury by inhibiting the activation of the NLRP3 inflammasome and reducing the production of pro-inflammatory cytokines (IL-1β, IL-6) [2]. In mouse lung tumors, it regulates DNA methylation patterns and downregulates the mRNA expression of tumor-related genes, suggesting that it may have epigenetic regulatory effects [3]. Clinical indications include asthma, chronic obstructive pulmonary disease (COPD), and other inflammatory airway diseases, primarily administered intravenously. Inhalation is used for local anti-inflammatory effects [1][2].

C25H34O6

430.53

430.235

51333-22-3

Budesonide-d8;1105542-94-6;Budesonide (Standard);51333-22-3

5281004

White to off-white solid powder

1.3±0.1 g/cm3

599.7±50.0 °C at 760 mmHg

221-232ºC (dec.)

201.8±23.6 °C

0.0±3.9 mmHg at 25°C

1.592

3.14

2

6

4

31

862

8

CCCC1O[C@@H]2C[C@H]3[C@@H]4CCC5=CC(=O)C=C[C@@]5([C@H]4[C@H](C[C@@]3([C@@]2(O1)C(=O)CO)C)O)C

VOVIALXJUBGFJZ-KWVAZRHASA-N

InChI=1S/C25H34O6/c1-4-5-21-30-20-11-17-16-7-6-14-10-15(27)8-9-23(14,2)22(16)18(28)12-24(17,3)25(20,31-21)19(29)13-26/h8-10,16-18,20-22,26,28H,4-7,11-13H2,1-3H3/t16-,17-,18-,20+,21?,22+,23-,24-,25+/m0/s1

(6aR,6bS,7S,8aS,8bS,11aR,12aS,12bS)-7-hydroxy-8b-(2-hydroxyacetyl)-6a,8a-dimethyl-10-propyl-6a,6b,7,8,8a,8b,11a,12,12a,12b-decahydro-1H-naphtho[2,1:4,5] indeno[1,2-d][1,3]dioxol-4(2H)-one

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 (4.83 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 (4.83 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 (4.83 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.)