Glucocorticoid receptor

Dexamethasone, also known as hexadecadrol, acts as a regulator of several transcription factors, including as nuclear factor-AT, nuclear factor-kB, and activator protein-1, which in turn activates and inhibits important genes related to the inflammatory response [1]. With an EC50 of 2.2 nM, dexamethasone efficiently prevents A549 cells from releasing granulocyte-macrophage colony-stimulating factor (GM-CSF). At dosages greater than those that suppress GM-CSF production, dexamethasone (EC50=36 nM) is shown to be related with glucocorticoid receptor (GR) DNA binding, happening 10-100-fold higher. It also promotes β2 receptor transcription. The inhibition of GM-CSF release is linked to the inhibition of 3×κB (NF-κB, IκBα, and I-κBβ) by dexamethasone (IC50=0.5 nM) [2].

Dexamethasone can be used to create models of nerve injury, muscular atrophy, and mitochondrial diseases in animals. It has been previously documented that lipopolysaccharide (LPS)-induced inflammation can be effectively inhibited by treatment with dexamethasone (Hexadecadrol) at a dose of 2 × 5 mg/kg. When compared to mice exposed to lipopolysaccharide (LPS) and injected with vehicle (saline) alone, treatment with a single dosage of dexamethasone 10 mg/kg (ip) dramatically decreased the recruitment of granulocytes and the spontaneous generation of oxygen radicals in our experimental system. The impact was statistically significant when given one hour prior to and one hour following LPS inhalation. By administering water aerosol, the quantity of granulocytes in BALF is lowered to levels similar to those in healthy animals [3]. Dexamethasone-treated rats ate less food and weighed less than rats in the control group. Despite eating the same amount of food, the treated rats weighed less than the animals fed in pairs. Dexamethasone injections for five days caused a notable rise in liver mass (+42%) and the liver-to-body weight ratio (+65%). After five days of treatment, the wet weight of the gastrocnemius muscle dropped by 20%, but it did not change in relation to body weight (g/100 g body weight), suggesting that weight reduction and muscle weight loss were synchronized [4].

1. Glucocorticoids are highly effective in controlling chronic inflammatory diseases, such as asthma and rheumatoid arthritis, but the exact molecular mechanism of their anti-inflammatory action remains uncertain. They act by binding to a cytosolic receptor (GR) resulting in activation or repression of gene expression. This may occur via direct binding of the GR to DNA (transactivation) or by inhibition of the activity of transcription factors such as AP-1 and NF-kappaB (transrepression). 2. The topically active steroids fluticasone propionate (EC50= 1.8 x 10(-11) M) and budesonide (EC50=5.0 x 10(-11) M) were more potent in inhibiting GM-CSF release from A549 cells than tipredane (EC50 = 8.3 x 10(-10)) M), butixicort (EC50 = 3.7 x 10(-8) M) and dexamethasone (EC50 = 2.2 x 10(-9) M). The anti-glucocorticoid RU486 also inhibited GM-CSF release in these cells (IC50= 1.8 x 10(-10) M). 3. The concentration-dependent ability of fluticasone propionate (EC50 = 9.8 x 10(-10) M), budesonide (EC50= 1.1 x 10(-9) M) and dexamethasone (EC50 = 3.6 x 10(-8) M) to induce transcription of the beta2-receptor was found to correlate with GR DNA binding and occurred at 10-100 fold higher concentrations than the inhibition of GM-CSF release. No induction of the endogenous inhibitors of NF-kappaB, IkappaBalpha or I-kappaBbeta, was seen at 24 h and the ability of IL-1beta to degrade and subsequently induce IkappaBalpha was not altered by glucocorticoids. 4. The ability of fluticasone propionate (IC50=0.5 x 10(-11) M), budesonide (IC50=2.7 x 10(-11) M), dexamethasone (IC50=0.5 x 10(-9) M) and RU486 (IC50=2.7 x 10(-11) M) to inhibit a 3 x kappaB was associated with inhibition of GM-CSF release. 5. These data suggest that the anti-inflammatory properties of a range of glucocorticoids relate to their ability to transrepress rather than transactivate genes[2].

Glucocorticoids are anti-inflammatory agents that are widely used in clinical practice. Increasing evidence has identified exosomes as important mediators in inflammation, but it is unknown whether glucocorticoids regulate exosome secretion and function. In the present study, we observed a reduction of exosome secretion in lipopolysaccharide (LPS)-induced RAW264.7 macrophages following treatment with dexamethasone. Importantly, exosomes isolated from LPS-induced RAW264.7 macrophages increased TNF-α and IL-6 production in RAW264.7 cells. However, this increase was less pronounced following treatment with exosomes isolated from dexamethasone-treated cells. Moreover, dexamethasone decreased expression of pro-inflammatory microRNA-155 in exosomes from LPS-induced RAW264.7 macrophages. We postulate that exosomes are novel targets in the anti-inflammatory effect of glucocorticoids in LPS-induced macrophage inflammatory responses. These findings will benefit the development of new approaches for anti-inflammatory therapeutics[7].

Synthetic glucocorticoids are pharmaceutical compounds prescribed in human and veterinary medicine as anti-inflammatory agents and have the potential to contaminate natural watersheds via inputs from wastewater treatment facilities and confined animal-feeding operations. Despite this, few studies have examined the effects of this class of chemicals on aquatic vertebrates. To generate data to assess potential risk to the aquatic environment, we used fathead minnow 21-d reproduction and 29-d embryo-larvae assays to determine reproductive toxicity and early-life-stage effects of Dexamethasone. Exposure to 500 µg Dexamethasone/L in the 21-d test caused reductions in fathead minnow fecundity and female plasma estradiol concentrations and increased the occurrence of abnormally hatched fry. Female fish exposed to 500 µg dexamethasone/L also displayed a significant increase in plasma vitellogenin protein levels, possibly because of decreased spawning. A decrease in vitellogenin messenger ribonucleic acid (mRNA) expression in liver tissue from females exposed to the high dexamethasone concentration lends support to this hypothesis. Histological results indicate that a 29-d embryo-larval exposure to 500 µg dexamethasone/L caused a significant increase in deformed gill opercula. Fry exposed to 500 µg dexamethasone/L for 29 d also exhibited a significant reduction in weight and length compared with control fry. Taken together, these results indicate that nonlethal concentrations of a model glucocorticoid receptor agonist can impair fish reproduction, growth, and development.[1]

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For vaccination, RNA was formulated with liposomes consisting of DOTMA and DOPE at a charge ratio (+):(-) of 1.3:2 yielding negatively charged RNA-Lipoplexes (RNA-LPX) as described previously.23 RNA-LPX comprising 20 µg gp70 RNA, 15 µg Reps1 and Adpgk RNA each or 30 µg eGFP RNA was injected i.v. in C57BL/6 or BALB/c mice as described in Figures 1 and 6(a). If not otherwise stated, Dexamethasone was injected i.p. at a dose of 4 mg/kg in 200 µL PBS. For lung metastasis experiments, 5 × 105 CT26 cells were injected i.v. in 100 µL PBS and treatment with 40 µg gp70 RNA-LPX and Dexa was performed as depicted in Figure 5(a). CT26 lung tumor burden was quantified after tracheal ink (1:10 diluted in PBS) injection and fixation with Fekete’s solution (5 ml 70% ethanol, 0.5 ml formalin, and 0.25 ml glacial acetic acid). A total of 1 × 105 MC38 tumor cells was implanted subcutaneously in the right hind flank in 100 µL of HBSS + matrigel. MC38 tumor-bearing mice were vaccinated with 50 µg RNA-LPX and treated with 4 mg/kg Dexamethasone as depicted in Figure 5(e), 5 mg/kg Methylprednisolone (Pfizer) or with 0.25 mg/kg Dexamethasone 5 minutes post-vaccination. Tumors were monitored at least twice per week and mice were euthanized if tumors became ulcerated or exceeded the acceptable size limit of 2000 mm3 according to IACUC.[8]

Absorption, Distribution and Excretion
Absorption via the intramuscular route is slower than via the intravenous route. A 3mg intramuscular dose reaches a Cmax of 34.6±6.0ng/mL with a Tmax of 2.0±1.2h and an AUC of 113±38ng\*h/mL. A 1.5mg oral dose reaches a Cmax of 13.9±6.8ng/mL with a Tmax of 2.0±0.5h and an AUC of 331±50ng\*h/mL. Oral dexamethasone is approximately 70-78% bioavailable in healthy subjects.
Corticosteroids are generally eliminated predominantly in the urine. However, dexamethasone is <10% elminated in urine.
A 1.5mg oral dose of dexamethasone has a volume of distribution of 51.0L, while a 3mg intramuscular dose has a volume of distribution of 96.0L.
A 20mg oral tablet has a clearance of 15.7L/h. A 1.5mg oral dose of dexamethasone has a clearance of 15.6±4.9L/h while a 3.0mg intramuscular dose has a clearance of 9.9±1.4L/h.
Absorbed into aqueous humor, cornea, iris, choroid ciliary body, and retina. Systemic absorption occurs, but may be significant only at higher dosages or in extended pediatric therapy. /Corticosteroids (Ophthalmic)/
Dogs (mixed-breed) were administered dexamethasone alcohol or dexamethasone 21-isonicotinate as a solution iv or im (1 mg/kg bw), or dexamethasone 21-isonicotinate as a suspension im (0.1 or 1 mg/kg bw). Plasma concentrations were determined with HPLC up to 120 hours after treatment. The elimination half-life after iv administration was 120-140 minutes for both formulations. Following im administration, absorption was rapid with peak plasma concentrations at 30-40 minutes for both solutions. Bioavailability after im administration was 100% for dexamethasone alcohol but 40% for dexamethasone 21-isonicotinate. After im administration of dexamethasone 21-isonicotinate as a suspension, dexamethasone was not detected in plasma, suggesting a long absorption phase
Crl:SD(CD)BR rats were administered a single im dose of 9 ug, (1,2,4-3H)-dexamethasone/kg bw. Radioactivity was measured up to 96 hours after administration in plasma (pre- and post-freeze dried), urine, feces and expired air. Tritium exchange was measured in stored urine. Highest plasma levels were observed 6 hours after dosing (3.7 ug equivalents/g), declining rapidly thereafter to 0.15 ug equivalents/g. Within 24 hours 41% of the radioactivity was excreted in the urine. After 96 hours a mean of 44% of the radio-activity was excreted. Tritium exchange was observed both in plasma and urine. Following freeze-drying, the mean loss of radioactivity 96 hours after dosing was 87% and 37% in plasma and urine, respectively
Male Wistar albino rats were administered 0.23 umol (1,2-3H) dexamethasone/kg bw, ip. Urine and feces were collected up to 4 days after treatment. Within 96 hours 74% of the dose was excreted, 30% in the urine and 44% in the feces
For more Absorption, Distribution and Excretion (Complete) data for DEXAMETHASONE (11 total), please visit the HSDB record page.

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Metabolism / Metabolites
Dexamethasone is 6-hydroxylated by CYP3A4 to 6α- and 6β-hydroxydexamethasone. Dexamethasone is reversibly metabolized to 11-dehydrodexamethasone by corticosteroid 11-beta-dehydrogenase isozyme 2 and can also be converted back to dexamethasone by Corticosteroid 11-beta-dehydrogenase isozyme 1.
Male Wistar albino rats were administered (3)H-dexamethasone orally at a dose of 1.14 nmol/kg bw. Thirty-one percent of the administered radioactivity was excreted in the urine within 4 days (most of it within the first 24 hours) as unconjugated metabolites. Unchanged dexamethasone accounted for 14%, 6-hydroxydexamethasone for 7.4%, and 20-dihydrodexamethasone for 1.1% of the urine radioactivity.
In the urine of rats administered 0.23 umol/kg bw (1,2-3H)- dexamethasone ip, 10% of the administered radioactivity was associated with one polar metabolite of dexamethasone, likely to be 6-hydroxy-dexamethasone
No parent compound could be detected in urine of patients after oral administration of a small dose of dexamethasone (<4 mg/day) for a few weeks. However, 60% was recovered as 6-beta-hydroxy-dexamethasone and 5-10% as 6-beta-hydroxy-20-dihydrodexamethasone. After the administration of about 15 mg dexamethasone/day metabolism occurred by an additional route involving epoxidation and subsequent hydrolysis, resulting in glycol formation in ring A
Dexamethasone has known human metabolites that include 6-beta-OH DEXAMETHASONE and 6-alpha-OH DEXAMETHASONE.
Hepatic.

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Biological Half-Life
The mean terminal half life of a 20mg oral tablet is 4 hours. A 1.5mg oral dose of dexamethasone has a half life of 6.6±4.3h, while a 3mg intramuscular dose has a half life of 4.2±1.2h.
190 minutes (plasma) /Dexamethasone sodium phosphate/
Dogs (mixed-breed) were administered dexamethasone alcohol or dexamethasone 21-isonicotinate as a solution iv or im (1 mg/kg bw), or dexamethasone 21-isonicotinate as a suspension im (0.1 or 1 mg/kg bw). Plasma concentrations were determined with HPLC up to 120 hours after treatment. The elimination half-life after iv administration was 120-140 minutes for both formulations.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Topical dexamethasone has not been studied during breastfeeding. Since only extensive application of the most potent corticosteroids cause systemic effects in the mother, it is unlikely that short-term application of topical corticosteroids would pose a risk to the breastfed infant by passage into breastmilk. However, it would be prudent to use the least potent drug on the smallest area of skin possible. It is particularly important to ensure that the infant's skin does not come into direct contact with the areas of skin that have been treated. Current guidelines allow topical corticosteroids to be applied to the nipples just after nursing for eczema, with the nipples cleaned gently before nursing. Only water-miscible cream or gel products should be applied to the breast because ointments may expose the infant to high levels of mineral paraffins via licking.
Because absorption from the eye is limited, ophthalmic dexamethasone, including ocular inserts, would not be expected to cause any adverse effects in breastfed infants. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.
◉ Effects in Breastfed Infants
Topical application of a corticosteroid with relatively high mineralocorticoid activity (isofluprednone acetate) to the mother's nipples resulted in prolonged QT interval, cushingoid appearance, severe hypertension, decreased growth and electrolyte abnormalities in her 2-month-old breastfed infant. The mother had used the cream since birth for painful nipples.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
◉ Summary of Use during Lactation
Because little information is available on the use of systemic dexamethasone during breastfeeding, an alternate corticosteroid may be preferred, especially while nursing a newborn or preterm infant. Local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants. Medium to large doses of corticosteroids, including dexamethasone, given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation. See also Dexamethasone, Topical.
◉ Effects in Breastfed Infants
None reported with any corticosteroid.
◉ Effects on Lactation and Breastmilk
Dexamethasone can cause a decrease in basal serum prolactin and thyrotropin-releasing hormone stimulated serum prolactin increase in nonnursing women. Medium to large doses of corticosteroids given systemically or injected into joints or the breast have been reported to cause temporary reduction of lactation.
A study of 46 women who delivered an infant before 34 weeks of gestation found that a course of another corticosteroid (betamethasone, 2 intramuscular injections of 11.4 mg of betamethasone 24 hours apart) given between 3 and 9 days before delivery resulted in delayed lactogenesis II and lower average milk volumes during the 10 days after delivery. Milk volume was not affected if the infant was delivered less than 3 days or more than 10 days after the mother received the corticosteroid. An equivalent dosage regimen of dexamethasone might have the same effect.
A study of 87 pregnant women found that betamethasone given as above during pregnancy caused a premature stimulation of lactose secretion during pregnancy. Although the increase was statistically significant, the clinical importance appears to be minimal. An equivalent dosage regimen of dexamethasone might have the same effect.
A woman with postpartum depression who was breastfeeding her 8-week-old infant was treated with endovascular embolization for a spinal-dural arteriovenous fistula. Following the procedure, she was treated with intravenous dexamethasone 4 mg every 8 hours for 5 days, followed by oral dexamethasone 12 mg daily in a tapering regimen. After stopping breastfeeding for 3 days after the procedure, she noted a decreased milk supply on restarting breastfeeding, and a complete cessation of milk production 11 days after the procedure. Several measures to increase milk including domperidone supply failed. Breastmilk production resumed 36 hours after discontinuing dexamethasone and reached normal production after 8 days. At hospital discharge, she was exclusively nursing her infant.

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Protein Binding
Dexamethasone is approximately 77% protein bound in plasma. The majority of protein binding is with serum albumin. Dexamethasone does not significantly bind to corticosteroid binding protein.

[1]. LaLone CA, et al. Effects of a glucocorticoid receptor agonist, Dexamethasone, on fathead minnow reproduction, growth, and development. Environ Toxicol Chem. 2012 Mar;31(3):611-22.
[2]. Adcock IM, et al. Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement. Br J Pharmacol. 1999 Jun;127(4):1003-11
[3]. Rocksén D, et al. Differential anti-inflammatory and anti-oxidative effects of Dexamethasone and N-acetylcysteine in endotoxin-induced lung inflammation. Clin Exp Immunol. 2000 Nov;122(2):249-56
[4]. Roussel D, et al. Dexamethasone treatment specifically increases the basal proton conductance of rat liver mitochondria. FEBS Lett. 2003 Apr 24;541(1-3):75-9.
[5]. Ballabh P, et al. Neutrophil and monocyte adhesion molecules in bronchopulmonary dysplasia, and effects of corticosteroids. Arch Dis Child Fetal Neonatal Ed. 2004 Jan;89(1):F76-83.
[6]. Heidi Ledford. et al. Coronavirus Breakthrough: Dexamethasone Is First Drug Shown to Save Lives. Nature. 2020 Jun 16.
[7]. Yun Chen, et al. Glucocorticoids inhibit production of exosomes containing inflammatory microRNA-155 in lipopolysaccharide-induced macrophage inflammatory responses. Int J Clin Exp Pathol 2018;11(7):3391-3397.
[8]. Dexamethasone premedication suppresses vaccine-induced immune responses against cancer. Oncoimmunology. 2020; 9(1): 1758004.

Dexamethazone is an odorless white to off-white crystalline powder with a slightly bitter taste. (NTP, 1992)
Dexamethasone is a fluorinated steroid that is 9-fluoropregna-1,4-diene substituted by hydroxy groups at positions 11, 17 and 21, a methyl group at position 16 and oxo groups at positions 3 and 20. It is a synthetic member of the class of glucocorticoids. It has a role as an adrenergic agent, an antiemetic, an antineoplastic agent, an environmental contaminant, a xenobiotic, an immunosuppressive agent and an anti-inflammatory drug. It is a fluorinated steroid, a 3-oxo-Delta(1),Delta(4)-steroid, a glucocorticoid, a 20-oxo steroid, an 11beta-hydroxy steroid, a 17alpha-hydroxy steroid and a 21-hydroxy steroid. It derives from a hydride of a pregnane.
Dexamethasone, or MK-125, is a corticosteroid fluorinated at position 9 used to treat endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, gastrointestinal, respiratory, hematologic, neoplastic, edematous, and other conditions. Developed in 1957, it is structurally similar to other corticosteroids like [hydrocortisone] and [prednisolone]. Dexamethasone was granted FDA approval on 30 October 1958. In a press release for the Randomized Evaluation of COVID-19 Therapy (RECOVERY) trial on 16 June 2020, dexamethasone was recommended for use in COVID-19 patients with severe respiratory symptoms. Dexamethasone reduced deaths by approximately one third in patients requiring ventilation and by one fifth in those requiring oxygen.
Dexamethasone is a Corticosteroid. The mechanism of action of dexamethasone is as a Corticosteroid Hormone Receptor Agonist.
Dexamethasone has been reported in Aspergillus ochraceopetaliformis, Penicillium chrysogenum, and other organisms with data available.
Dexamethasone is a synthetic adrenal corticosteroid with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone also interferes with NF-kB activation and apoptotic pathways. This agent lacks the salt-retaining properties of other related adrenal hormones. (NCI04)
An anti-inflammatory 9-fluoro-glucocorticoid. [PubChem]
An anti-inflammatory 9-fluoro-glucocorticoid.
See also: Dexamethasone Sodium Phosphate (narrower); Dexamethasone Isonicotinate (is active moiety of); Dexamethasone Dipropionate (is active moiety of) ... View More ...

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Drug Indication
Dexamethasone and [ciprofloxacin] otic suspension is indicated for bacterial infections with inflammation in acute otitis media and acute otitis externa. Intramuscular and intravenous injections are indicated for a number of endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, gastrointestinal, respiratory, hematologic, neoplastic, edematous, and other conditions. Oral tablets are indicated for the treatment of multiple myeloma. An intravitreal implant is indicated for some forms of macular edema and non-infectious posterior uveitis affecting the posterior of the eye. Various ophthalmic formulations are indicated for inflammatory conditions of the eye.
FDA Label
Ozurdex is indicated for the treatment of adult patients with macular oedema following either branch retinal-vein occlusion (BRVO) or central retinal-vein occlusion (CRVO). Ozurdex is indicated for the treatment of adult patients with inflammation of the posterior segment of the eye presenting as noninfectious uveitis. Ozurdex is indicated for the treatment of adult patients with visual impairment due to diabetic macular oedema (DME) who are pseudophakic or who are considered insufficiently responsive to, or unsuitable for non-corticosteroid therapy.
Treatment of multiple myeloma.
Treatment of postoperative pain and inflammation associated with ophthalmic surgery
Treatment of diabetic macular oedema
Chronic non-infectious intermediate or posterior uveitis
Other retinal vascular occlusion

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Mechanism of Action
The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.
Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA, and stimulate transcription of mRNA and subsequent protein synthesis of enzymes ultimately responsible for anti-inflammatory effects of topical application of corticosteroids to the eye. In high concentrations which may be achieved after topical application, corticosteroids may exert direct membrane effects. Corticosteroids decrease cellular and fibrinous exudation and tissue infiltration, inhibit fibroblastic and collagen-forming activity, retard epithelial regeneration, diminish postinflammatory neovascularization and reduce toward normal levels the excessive permeability of inflamed capillaries. /Corticosteroids (Otic)/
Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/
Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocttes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. The overall actions of topical corticosteroids are catabolic. /Corticosteroids (topical)/

C22H29FO5

392.46

392.199

C, 67.33; H, 7.45; F, 4.84; O, 20.38

50-02-2

3936-02-5 (metasulfobenzoate sodium);3800-84-8 (sodium succinate);1177-87-3 (acetate);150587-07-8 (beloxil); 132245-57-9 (cipecilate); 2265-64-7 (isonicotinate); 14899-36-6 (palmitate); 312-93-6 (phosphate); 2392-39-4 (sodium phosphate);

5743

Crystals from ether
WHITE TO PRACTICALLY WHITE CRYSTALLINE POWDER

1.3±0.1 g/cm3

568.2±50.0 °C at 760 mmHg

255-264ºC

297.5±30.1 °C

0.0±3.5 mmHg at 25°C

1.592

1.87

3

6

2

28

805

8

F[C@@]12[C@]3(C=CC(C=C3CC[C@@]1([H])[C@]1([H])C[C@@H](C)[C@](O)(C(=O)CO)[C@]1(C[C@@H]2O)C)=O)C

UREBDLICKHMUKA-CXSFZGCWSA-N

InChI=1S/C22H29FO5/c1-12-8-16-15-5-4-13-9-14(25)6-7-19(13,2)21(15,23)17(26)10-20(16,3)22(12,28)18(27)11-24/h6-7,9,12,15-17,24,26,28H,4-5,8,10-11H2,1-3H3/t12-,15+,16+,17+,19+,20+,21+,22+/m1/s1

(8S,9R,10S,11S,13S,14S,16R,17R)-9-fluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13,16-trimethyl-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-3-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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: ≥ 2.5 mg/mL (6.37 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
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 2: ≥ 2.08 mg/mL (5.30 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 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 3: ≥ 2.08 mg/mL (5.30 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 4: ≥ 2.08 mg/mL (5.30 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 20.8 mg/mL clear DMSO stock solution to 900 μL corn oil and mix evenly.

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Solubility in Formulation 5: 30% PEG400+0.5% Tween80+5% Propylene glycol : 30mg/kg

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Solubility in Formulation 6: 18.18 mg/mL (46.32 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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