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Dexamethasone (Water Soluble)


CAS No. : 50-02-2

(Synonyms: Dexamethasone cyclodextrin complex)

50-02-2
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25mg $85 In-stock
50mg $135 In-stock
100mg $215 In-stock
500mg $450 In-stock
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Cat. No. : HY-14648C
M.Wt: 1000.00
Formula: N/A
Purity: >98 %
Solubility: H2O : ≥ 100 mg/mL
Introduction of 50-02-2 :

Dexamethasone (Hexadecadrol) Water Soluble is a water-soluble form of Dexamethasone (HY-14648). Dexamethasone is a glucocorticoid receptor agonist, apoptosis inducer, and a common disease inducer in experimental animals. It can be used to construct models of muscle atrophy, hypertension, and depression. Dexamethasone can inhibit the production of inflammatory miRNA-155 exosomes in macrophages and significantly reduce the expression of inflammatory factors in neutrophils and monocytes. Dexamethasone also has the potential to be used in COVID-19 research[1].(Sale size is the weight of dexamethasone) In Vitro:Note:
Product is approximately 65 mg of Dexamethasone per gram containing a balance of Methyl-β-cyclodextrin (HY-101461). Solubility in H2O: ≥ 100 mg/mL indicates that 100 mg of the weighed total product (not the effective weight) dissolves in 1 mL of water.

Dexamethasone (Hexadecadrol) regulates several transcription factors, including activator protein-1, nuclear factor-AT, and nuclear factor-kB, leading to the activation and repression of key genes involved in the inflammatory response[1].
Dexamethasone potently inhibits granulocyte-macrophage colony stimulating factor (GM-CSF) release from A549 cells with EC50 of 2.2 nM. Dexamethasone (EC50=36 nM) induces transcription of the β2-receptor is found to correlate with glucocorticoid receptor (GR) DNA binding and occurred at 10-100 fold higher concentrations than the inhibition of GM-CSF release. Dexamethasone (IC50=0.5 nM) inhibits a 3×κB (NF-κB, IκBα, and I-κBβ), which is associated with inhibition of GM-CSF release[2].
In Vivo:

Based on blood and multi-tissue concentration-time profiles of Dexamethasone (DEX), no significant sex differences were found in its tissue distribution. Blood cell to plasma partitioning (0.664) and plasma free fraction (0.175) were moderate, with widespread distribution in the liver (Kp=6.76). Possibly due to P-glycoprotein-mediated efflux, the concentration of DEX in the brain is very low compared to the expected high permeability[5].
Dexamethasone (DEX) can be used in animal modeling to construct models of muscle atrophy, hypertension and depression.

1. Induction of muscle atrophy[6][7]
Background
Glucocorticoids are important mediators of skeletal muscle protein degradation and upregulation of the ubiquitin-proteasome pathway. Dexamethasone induces tibialis anterior muscle protein degradation by binding to the glucocorticoid receptor, resulting in muscle atrophy.
Specific Modeling Methods
Mice: C57BL/6 • male • 6-week-old
Administration: 5 mg/kg • ip • once daily for 2 weeks
Modeling Indicators
Molecular changes: Increased indicators: C2C12 ubiquitin ligase, MuRF1, Atrogin-1, Cbl-b, p-Foxo1, p-Foxo3a. Resulted C2C12 myotube protein degradation, and Glucocorticoid receptor translocation to the nucleus
Phenotypic observation: Decreased indicators: The weight of the anterior muscles, gastrocnemius, quadriceps and soleus muscles. The ratio of skeletal muscle to body weight decreases.
Correlated Product(s): Betamethasone (HY-13570)
Opposite Product(s): Glabridin (HY-N0393)
2. Induction of hypertension[8][9]
Background
The underlying mechanisms that induce hypertension (HT) are unknown.
Specific Modeling Methods
Rat: Sprague-Dawley • Male • 200-300 g
Administration: 20 μg • sc • once daily from days 5 to 16 • control rats: saline with 0.1 mL/100 g/day from days 1 to 16 (po) or 0.2 mL/rat/day (sc).
Dog: 10.1-19.1 kg • average=13.7 kg
Administration: 0.5 mg/kg • po • once daily for 10 days
Modeling Indicators
Hemodynamics: MAP, systolic blood pressure, diastolic blood pressure, TPR levels increased in central hemodynamics. Total peripheral resistance, blood pressure, atrial natriuretic peptide, and the pressor response to norepinephrine, are significantly increased in Systemic and renal hemodynamics.
Behavior: The dog showed obvious natriuresis and diuresis.
Opposite Product(s): Saralasin (HY-P0205); Prazosin (HY-B0193)
3. Induction of depressive behavior[10][11]
Background
Astrocytes are a key feature of major depressive disorder (MD), and reduced expression by glucocorticoids results in reduced astrocyte numbers. Long-term treatment with Dexamethasone can cause a series of depression-like symptoms in rodents.
Specific Modeling Methods
Rat: Sprague-Dawley • Male • 200-250 g
Administration: 1 mg/kg • po • once daily every other day for 5 months
Note
(1) Prepare a 3% (w/v) treatment solution and filter through a 0.45 μm cellulose acetate filter.
(2) Rats should not be exposed to any other water source for 4 days before starting treatment.
(3) On the 4th day, change the treatment solution to water and feed for 3 days to allow the mice to recover temporarily. Weigh and conduct behavioral experiments on day 7.
Mice: C57BL/6 • Male • 9-10 weeks old • 23-25 g
Administration: 4 mg/kg • ip • once dailly for 21 days
Modeling Indicators
Metabolism changes: Serum cortisol levels in rats ↑.
Behavior: Immobility time during the forced swim test (FST) &uarr. Preference for sucrose &darr in the sucrose preference test.
Opposite Product(s): Amitriptyline (HY-B0527)

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