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MedChemExpress - Model Betamethasone - ...

MedChemExpress - Model Betamethasone - 378-44-9

Betamethasone is a synthetic glucocorticoid with anti-inflammatory and immunosuppressive activities. Betamethasone accelerates fetal lung maturation and induces gene expression and apoptosis[1][2][3][4].

Betamethasone

MCE China：Betamethasone

Brand：MedChemExpress (MCE)

Cat. No.HY-13570

CAS：378-44-9

Purity：99.88%

Storage：4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Betamethasone is a synthetic glucocorticoid with anti-inflammatory and immunosuppressive activities. Betamethasone accelerates fetal lung maturation and induces gene expression and apoptosis.

In Vitro：Betamethasone (0.1-1 μM; 12 h) induces gene expression in L929 cells[4]. Betamethasone (0.1-1 μM; 48 h) induces CEM C7 T-cells apoptosis[4].

In Vivo：Betamethasone (0.48 mg; i.v.gtt for 48 h) decreases the hypercapnia-induced increase in CBF due to decreased cerebral vasodilatation[1]. Betamethasone (0.05 ml (1 mg/L); topical injection) ameliorates spinal nerve transection induced mechanical allodynia and thermal hyperalgesia, and reduces the activation of NF-κB and elevation of TNFα and IL-1β, and induces the expression of IL-10 in the rats brain[2].

References：

[1]. Schwab M, et, al. Effects of betamethasone administration to the fetal sheep in late gestation on fetal cerebral blood flow. J Physiol. 2000 Nov 1;528(Pt 3):619-32. [Content Brief]

[2]. Xie W, et, al. Betamethasone affects cerebral expressions of NF-kappaB and cytokines that correlate with pain behavior in a rat model of neuropathy. Ann Clin Lab Sci. Winter 2006;36(1):39-46. [Content Brief]

[3]. Kubin ME, et, al. Clinical Efficiency of Topical Calcipotriol/Betamethasone Treatment in Psoriasis Relies on Suppression of the Inflammatory TNFα - IL-23 - IL-17 Axis. Acta Derm Venereol. 2017 Apr 6;97(4):449-455. [Content Brief]

[4]. Hofmann TH, et, al. Various glucocorticoids differ in their ability to induce gene expression, apoptosis and to repress NF-kappaB-dependent transcription. FEBS Lett. 1998 Dec 28;441(3):441-6. [Content Brief]

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