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Purity: ≥98%
Dexamethasone Phosphate disodium, the water-soluble salt form of dexamethasone administered through i.v. injection, is a potent synthetic glucocorticoid class of steroid drugs, and an interleukin receptor modulator with anti-inflammatory and immunosuppressive activities. Dexamethasone has anti-inflammatory and immunosuppressant effects. It is 25-fold more potent than cortisol in its glucocorticoid effect, while having minimal mineralocorticoid effect. Dexamethasone is used for the treatment of many conditions including: rheumatologic problems, a number of skin diseases such as erythema multiforme, severe allergies, asthma.
| Targets |
Glucocorticoid receptor
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|---|---|
| ln Vitro |
Dexamethasone disodium phosphate promotes the activation and inhibition of important genes involved in regulatory responses by regulating a number of regulatory factors, such as activator protein-1, nuclear factor-AT, and nuclear factor-kB [1]. With an EC50 of 2.2 nM, dexamethasone disodium phosphate efficiently controls the release of granulocyte-macrophage colony-stimulating factor (GM-CSF) from A549 cells. At 10-100 times greater concentrations, dexamethasone disodium phosphate (EC50=36 nM) inhibits the release of GM-CSF via sensing β2 infrared receptors and attaching to the DNA of the glucose signal receiving hormone (GR). The inhibition of GM-CSF release is linked to the inhibition of 3×κB (NF-κB, IκBα, and I-κBβ) by dexamethasone disodium phosphate (IC50=0.5 nM) [2].
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| ln Vivo |
Lipopolysaccharide (LPS)-induced receptors were successfully suppressed by treatment with dexamethasone disodium phosphate at a dose of 2 × 5 mg/kg. When mice were exposed to lipopolysaccharide (LPS) and given a single injection of dexamethasone disodium phosphate (10 mg/kg (ip)), it resulted in a significant decrease in both granulocyte recruitment and oxygen freedom in our experimental system. revolutionaries emerging on their own initiative. One hour prior to and one hour following LPS inhalation, the effect was statistically significant. When water aerosols are administered to healthy animals, the number of granulocytes in BALF drops to values similar to those of those animals [3]. In comparison to the chart, rats treated with dexamethasone disodium phosphate devoured less food and weighed less. Even though the dosage of dexamethasone disodium phosphate injections was within food guidelines, the five-day injection period led to notable increases in liver mass (+42%) and liver-to-body weight (+65%). After 5 days of therapy, the muscles of the gastrocnemius were identical, but the animals' body weight was also reduced compared to those fed chow. Wet weight dropped by 20%, but relative weight remained exactly the same (g/100 g body weight), suggesting that weight reduction following surgery was coordinated with weight loss [4].
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| Enzyme Assay |
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].
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| Cell Assay |
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[5].
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| Animal Protocol |
We investigated the role that mitochondrial proton leak may play in the glucocorticoid-induced hypermetabolic state. Sprague-Dawley rats were injected with dexamethasone over a period of 5 days. Liver mitochondria and gastrocnemius subsarcolemmal and intermyofibrillar mitochondria were isolated from dexamethasone-treated, pair-fed and control rats. Respiration and membrane potential were measured simultaneously using electrodes sensitive to oxygen and to the potential-dependent probe triphenylmethylphosphonium, respectively. Five days of dexamethasone injection resulted in a marked increase in the basal proton conductance of liver mitochondria, but not in the muscle mitochondrial populations. This effect would have a modest impact on energy expenditure in rats.[4]
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| References |
[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]. 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. |
| Additional Infomation |
Dexamethasone sodium phosphate is an organic sodium salt which is the disodium salt of dexamethasone phosphate. It has a role as a glucocorticoid receptor agonist. It contains a dexamethasone phosphate(2-).
Dexamethasone Sodium Phosphate is a sodium phosphate salt form of Dexamethasone, 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) See also: Dexamethasone (broader); Dexamethasone sodium phosphate; neomycin sulfate (component of) ... View More ... |
| Exact Mass |
516.13
|
|---|---|
| Elemental Analysis |
C, 51.17; H, 5.47; F, 3.68; Na, 8.90; O, 24.78; P, 6.00
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| CAS # |
2392-39-4
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| Related CAS # |
Dexamethasone;50-02-2;Dexamethasone acetate;1177-87-3;Dexamethasone phosphate;312-93-6
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| PubChem CID |
16961
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| Appearance |
Typically exists as white to off-white solids at room temperature
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| Density |
1.32g/cm3
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| Boiling Point |
669.6ºC at 760 mmHg
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| Melting Point |
233-235 °C
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| Flash Point |
358.7ºC
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| Vapour Pressure |
2.81E-15mmHg at 25°C
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| Index of Refraction |
1.591
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| LogP |
2.889
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
34
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| Complexity |
962
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| Defined Atom Stereocenter Count |
8
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| SMILES |
C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)COP(=O)([O-])[O-])O)C)O)F)C.[Na+].[Na+]
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| InChi Key |
PLCQGRYPOISRTQ-FCJDYXGNSA-L
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| InChi Code |
InChI=1S/C22H30FO8P.2Na/c1-12-8-16-15-5-4-13-9-14(24)6-7-19(13,2)21(15,23)17(25)10-20(16,3)22(12,27)18(26)11-31-32(28,29)30/h6-7,9,12,15-17,25,27H,4-5,8,10-11H2,1-3H3,(H2,28,29,30)/q2*+1/p-2/t12-,15+,16+,17+,19+,20+,21+,22+/m1../s1
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| Chemical Name |
sodium 2-((8S,9R,10S,11S,13S,14S,16R,17R)-9-fluoro-11,17-dihydroxy-10,13,16-trimethyl-3-oxo-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-3H-cyclopenta[a]phenanthren-17-yl)-2-oxoethyl phosphate
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| Synonyms |
Dexamethasone 21-phosphate disodium EGP-437 EGP 437 EGP437 Dex-Phos.
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ≥ 100 mg/mL (~193.65 mM)
DMSO : ~1 mg/mL (~1.94 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (193.65 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT02955641 | UNKNOWN STATUSV | Drug: Dexamethasone Disodium Phosphate 0.1% Drug: Nepafenac 0.1% Drug: Hydroxyethylcellulose 0.19% |
Glaucoma, Angle-Closure Glaucoma, Closed-Angle Glaucoma, Narrow-Angle |
Sheba Medical Center | 2016-11-01 | Not Applicable |
| NCT01004497 | COMPLETED | Drug: Dasatinib Drug: Cyclophosphamide Drug: Vincristine |
Acute Lymphoblastic Leukemia | The Catholic University of Korea | 2010-03 | Phase 2 |
| NCT06437054 | NOT YET RECRUITING | Drug: Dexamethasone Drug: Hyaluronic acid Other: Indocyanine green(ICG) |
Hearing Loss, Sensorineural Hearing Loss, Sudden Intratympanic Injection |
Seoul National University Hospital | 2025-02-15 | Phase 1 Phase 2 |
| NCT03580473 | COMPLETED | Drug: SATURNO II association Drug: Vigadexa® |
Cataract Ocular Inflammation |
EMS | 2020-02-27 | Phase 2 |
| NCT02973880 | COMPLETED | Drug: NETILDEX™ ophthalmic gel Drug: NETILDEX™ eye drops solution |
Cataract Cataract Extraction |
SIFI SpA | 2017-10-15 | Phase 3 |
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