Glucocorticoid receptor (likely mediates transcriptional regulation of tight junction proteins; no IC50/Ki/EC50/DC50 values reported). [1]
Dexamethasone Sodium Phosphate targets the glucocorticoid receptor (GR). After hydrolysis to dexamethasone, it binds to the glucocorticoid receptor with high affinity. This binding leads to the translocation of the receptor complex into the nucleus, where it modulates the transcription of glucocorticoid-responsive genes. This results in both transactivation (increasing the synthesis of certain anti-inflammatory proteins) and transrepression (inhibiting the synthesis of pro-inflammatory proteins). The compound has a potent anti-inflammatory effect by inhibiting the production of prostaglandins and leukotrienes, and by suppressing the immune response. It has negligible mineralocorticoid activity.

Dexamethasone inhibits COX-2 mRNA expression induced by IL-1 in human articular chondrocytes. Dexamethasone suppresses the cyclooxygenase-2 induction by tumor necrosis factor α (TNFα) with an IC50 of 1 nM in MC3T3-E1 cells. Dexamethasone binds to the glucocorticoid receptor and then to the glucocorticoid response element. Dexamethasone (10 μM) induces osteoblastic differentiation of rat bone marrow stromal cell cultures with elevated mRNA expression of alkaline phosphatase osteopontin, bone sialoprotein, and osteocalcin. Dexamethasone (5 μM) treatment decreases proliferation of adult hippocampal neural progenitor cells and SRE-driven gene expression.

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Treatment of GPNT cells with 1 μM Dexamethasone Sodium Phosphate (as dexamethasone) from seeding decreased paracellular permeability to [14C]sucrose by 39±7% and to fluorescein by 47±7% (Pe values: sucrose control 7.373±0.617 ×10^{-3} cm/min, treated 4.496±0.530; fluorescein control 5.210±0.472, treated 2.781±0.395 ×10^{-3} cm/min). Permeability to FITC-dextrans of 4, 10, 20, 40, 70, 150 kDa was also reduced, with significant reduction for FD20 (20 kDa) from 0.333±0.031 to 0.156±0.013 ×10^{-3} cm/min. [1]
Pore analysis indicated a decrease in number of large pores (~185 Å radius) and reduction of small pore radius from ~14.5 Å to ~8.3 Å following treatment. [1]
Western blot analysis showed increased expression of tight junction proteins ZO-1 (225 kDa) and occludin (65 kDa) in treated cells. No change in expression of α-, β-, γ-catenin or p100/p120. [1]
Immunofluorescence revealed improved continuity of ZO-1 at cell-cell contacts; occludin remained low but became detectable at junctions after treatment. [1]
TRITC-phalloidin staining showed redistribution of F-actin from cytoplasmic stress fibers to cell periphery; cortactin similarly relocalized to cell-cell contacts. [1]
No change in expression of actin-binding proteins cortactin, ezrin, or tyrosine kinase c-Src was observed by Western blot. [1]
Dexamethasone Sodium Phosphate treatment did not alter transendothelial electrical resistance (remained ~66±3 Ω cm²). [1]
In vitro, Dexamethasone Sodium Phosphate is used to study glucocorticoid receptor signaling and its effects on various cell types. It is a potent inducer of apoptosis in certain cell lines, such as thymocytes and some leukemic cells. It also suppresses the production of pro-inflammatory cytokines like TNF-α, IL-1, and IL-6 in activated macrophages and other immune cells. The compound is routinely used in cell culture to study the effects of glucocorticoids on gene expression, cell proliferation, and differentiation. Its water-soluble nature makes it convenient for use in aqueous cell culture media.

Dexamethasone (2 mg/kg) reduces the number of the BrdU-labeled hepatocytes by 80% in male Fischer F344 rats. Dexamethasone (2 mg/kg) pretreatment suppresses the expression of both TNF and IL-6 after partial hepatectomy and significantly reduces the proliferative response of the hepatocytes in male Fischer F344 rats. Dexamethasone also severely diminishes the induction and expansion of oval cells induced by the 2-acetylaminofluorene/partial hepatectomy (AAF/PH) protocol but does not have any effect on the proliferation of the bile duct cells stimulated by bile duct ligation. Dexamethasone (100 μg/kg) produces a significant decrease 59.2% of BrdU(+) hippocampal progenitor cells in Sprague–Dawley rats. Dexamethasone (100 μg/kg) decreases ERK activation in granule cell layer in Sprague–Dawley rats.
Dexamethasone Sodium Phosphate is a potent anti-inflammatory and immunosuppressive agent in vivo. After administration, it is rapidly hydrolyzed to dexamethasone, which exerts its systemic effects. It is used to reduce inflammation in a variety of conditions, including arthritis, dermatitis, and respiratory diseases. It suppresses the immune response and is used in the management of autoimmune diseases and organ transplantation. It is also used as an antiemetic in cancer patients receiving chemotherapy. Its effects are dose-dependent and can be seen within hours of administration.

Non-cellular receptor binding assays for Dexamethasone Sodium Phosphate involve measuring its affinity for the glucocorticoid receptor. These assays typically use cytosolic preparations from tissues rich in GR or purified receptor protein. The compound's ability to displace a labeled ligand, such as [3H]-dexamethasone, is measured to determine its binding affinity (Ki or IC50). These assays are essential for characterizing its potency as a glucocorticoid receptor agonist. After hydrolysis to dexamethasone, its binding affinity is well-characterized.

Dexamethasone Sodium Phosphate (as dexamethasone) was used in cell-based assays only. GPNT cells (immortalized rat brain endothelial line) were grown to confluence on collagen-coated Transwell-Clear inserts (polyester, 12 mm diameter, 0.4 μm pore size) or six-well plates in DMEM:Ham's F12 (1:1) medium containing 10% fetal calf serum, 10 mM HEPES, 100 U/mL penicillin, 100 μg/mL streptomycin, with or without 1 μM Dexamethasone Sodium Phosphate added from seeding. [1]
Paracellular permeability measurement: Monolayers on Transwell inserts were incubated with tracer markers ([14C]sucrose, fluorescein, FITC-dextrans of 4,10,20,40,70,150 kDa) in the apical compartment. Samples were taken from basolateral compartment at timed intervals. Permeability coefficients (Pe) were calculated from the slope of cleared volume vs. time curves. Values were corrected for unconjugated fluorescein in dextran preparations. [1]
Transendothelial electrical resistance (TEER) measurement: Confluent GPNT monolayers on Transwell inserts were measured using an Endohm 12 chamber and Endohmeter; resistance was 66±3 Ω cm², unchanged by dexamethasone. [1]
Immunofluorescence: Cells were fixed and stained with antibodies against ZO-1, occludin, β-catenin, p100/p120, and TRITC-phalloidin for F-actin, and anti-cortactin. Images were acquired. [1]
Western blot: Whole cell lysates were prepared by replacing culture medium with hot SDS sample buffer, heated at 95°C for 5 min. Extracts were resolved by SDS-PAGE, transferred to nitrocellulose, blocked with 5% non-fat milk, probed with primary antibodies (anti-ZO-1, anti-occludin, anti-α/β/γ-catenin, anti-p100/p120, anti-cortactin, anti-ezrin, anti-c-Src), then HRP-conjugated secondary antibodies, and detected by enhanced chemiluminescence. [1]
In vitro cell-based assays for Dexamethasone Sodium Phosphate are used to study its effects on cell function and gene expression. These assays often use immune cells like lymphocytes or macrophages to measure its ability to suppress cytokine production. Reporter gene assays, where cells are transfected with a plasmid containing a glucocorticoid-responsive element linked to a reporter gene, are also used to quantify its transcriptional activity. The compound's effects on cell viability, proliferation, and apoptosis are also assessed in various cell lines.

Dissolved in saline; 100 μg/kg; i.p. injection Sprague-Dawley rats
In vivo animal studies for Dexamethasone Sodium Phosphate are standard for evaluating its anti-inflammatory and immunosuppressive effects. The compound is typically administered orally, intravenously, or intramuscularly to animal models of inflammation or autoimmune disease. Endpoints include measuring inflammatory markers, assessing clinical signs of disease, and evaluating histopathological changes. Its efficacy in reducing inflammation and suppressing the immune response has been demonstrated in numerous animal models.

Dexamethasone Sodium Phosphate is a water-soluble prodrug that is rapidly hydrolyzed to dexamethasone after administration. It has a molecular weight of 516.41 g/mol. The compound is available in various formulations for different routes of administration. Its pharmacokinetic profile is similar to that of dexamethasone, with a rapid onset of action and a duration of effect that depends on the dose and route of administration. It is metabolized in the liver and excreted by the kidneys.

Dexamethasone Sodium Phosphate has a well-established safety profile from decades of clinical use. It is generally well-tolerated at therapeutic doses, but its use is associated with side effects related to its glucocorticoid activity, especially with long-term use. These include hyperglycemia, osteoporosis, weight gain, adrenal suppression, and increased susceptibility to infections. The risk of side effects is dose- and duration-dependent. Dexamethasone Sodium Phosphate is an approved drug available by prescription.

Neurosci Lett.2003 Jun 26;344(2):112-6;J Physiol.2003 Feb 15;547(Pt 1):61-6.

Dexamethasone sodium phosphate is an organosodium salt, the disodium salt of dexamethasone phosphate. It is a glucocorticoid receptor agonist. It contains the dexamethasone (2-) ion. Dexamethasone sodium phosphate is the sodium phosphate form of dexamethasone, a synthetic adrenocortical hormone with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone can interfere with NF-κB activation and apoptosis pathways. Compared to other related adrenal hormones, this drug does not have sodium-retaining effects. (NCI04) See also: Dexamethasone (broadly defined); Dexamethasone sodium phosphate; Neomycin sulfate (ingredient)... See more...

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Dexamethasone Sodium Phosphate (as dexamethasone) is a synthetic corticosteroid that modulates tight junction permeability in brain endothelial cells via glucocorticoid receptor-mediated transcriptional regulation. It may upregulate ZO-1 and occludin gene expression or downregulate mediators that increase permeability (e.g., MMP-9, VEGF). The effect is cell-type specific; similar observations have been reported in retinal endothelial cells with hydrocortisone, but not in mammary epithelial cells where actin/ZO-1 distribution was unchanged. [1]
Dexamethasone Sodium Phosphate is a water-soluble prodrug of the potent glucocorticoid dexamethasone. It is used clinically for its potent anti-inflammatory and immunosuppressant properties in a wide range of conditions. It is available in various formulations for multiple routes of administration. Its use is associated with well-known glucocorticoid side effects, especially with long-term therapy. Dexamethasone Sodium Phosphate is an approved drug.

C22H30FO8P.2NA

516.4

516.13

55203-24-2

16961

Typically exists as solid at room temperature

2.889

2

9

3

34

962

8

O=C1C=C2CC[C@H]3[C@@H]4C[C@@H](C)[C@@](C(COP([O-])([O-])=O)=O)(O)[C@@]4(C)C[C@H](O)[C@]3(F)[C@@]2(C)C=C1.[Na+].[Na+]

PLCQGRYPOISRTQ-FCJDYXGNSA-L

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);;/q;2*+1/p-2/t12-,15+,16+,17+,19+,20+,21+,22+;;/m1../s1

disodium;[2-[(8S,9R,10S,11S,13S,14S,16R,17R)-9-fluoro-11,17-dihydroxy-10,13,16-trimethyl-3-oxo-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-17-yl]-2-oxoethyl] phosphate

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)