Dehydroepiandrosterone sulfate (sodium)


CAS No. : 1099-87-2

(Synonyms: DHEA sulfate (sodium); Prasterone sulfate (sodium))

1099-87-2
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Cat. No. : HY-B0765
M.Wt: 390.47
Formula: C19H27NaO5S
Purity: >98 %
Solubility: H2O : 10 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic)
Introduction of 1099-87-2 :

Dehydroepiandrosterone sulfate (DHEA sulfate; Prasterone sulfate) sodium salt is a neurosteroid and the main secretion product of the adrenal gland. Dehydroepiandrosterone sulfate sodium salt has both non-competitive antagonist activity of GABAA receptor and agonist activity of σ1 receptor. Dehydroepiandrosterone sulfate sodium salt can partially penetrate the blood-brain barrier, inhibit GABAA receptor-mediated chloride influx, enhance NMDA receptor activity through σ1 receptors, exert anti-inflammatory, anti-glucocorticoid and antidepressant effects, and increase convulsive sensitivity. Dehydroepiandrosterone sulfate sodium salt participates in neuroprotection, neurite growth regulation and catecholamine secretion regulation, and can be used in the study of depression, post-traumatic stress disorder (PTSD), Alzheimer's disease, etc. Dehydroepiandrosterone sulfate sodium salt may also be a biomarker for cardiovascular disease mortality, and its concentration is independently and negatively correlated with mortality[1][2][3][4]. In Vitro:Dehydroepiandrosterone sulfate sodium salt (0.1 nM-10 μM; 2-24 h) increases neuronal survival in embryonic rat cortical cell hypoxia assay, with significant effects at 10 μM[1].
Dehydroepiandrosterone sulfate sodium salt (0.1-10 μM) protects neurons in rat cerebellar granule cell oxygen-glucose deprivation assay in a dose-dependent manner, with almost complete protection at 10 μM[1].
Dehydroepiandrosterone sulfate sodium salt (DHEAS) (1 μM-1 mM; 48 h) inhibits TNF-α-induced VCAM-1, IL-8, and ICAM-1 expression in human aortic endothelial cell inflammation assay, and inhibits NF-κB activity via activation of PPARα[5].
Dehydroepiandrosterone sulfate sodium salt (DHEAS) (10-7-10-5 M; 96 h) inhibits LIF-induced proliferation of juvenile bovine chromaffin cells and enhances EGF-induced proliferation of adult bovine chromaffin cells in a proliferation assay[6].
In Vivo:Dehydroepiandrosterone sulfate (DHEAS) (1 mg/kg; intravenous injection; single dose) sodium salt reduces the threshold shift of compound action potentials and the amplitude of distortion product otoacoustic emissions in the noise-induced cochlear injury model of albino guinea pigs, and has a protective effect on the cochlea[7].
Dehydroepiandrosterone sulfate (DHEAS) (converted from 2 mg/kg Dehydroepiandrosterone intraperitoneally; once daily; 13 days) can shorten the immobility time in the forced swim test in the male FSL rat model of depression, but when used in combination with electroconvulsive shock (ECS), it offsets the antidepressant effect of ECS[8].
Dehydroepiandrosterone sulfate (DHEAS) (10 mg/kg; subcutaneous injection; once daily; 4 weeks) sodium salt enhances the seizure sensitivity of Laka mice in the pentylenetetrazol-induced seizure model, as shown by a decrease in the half effective dose of seizure (ED50 from 67.6 mg/kg to 48.6 mg/kg) and a shortens seizure latency, an effect that is reversed by Progesterone (HY-N0437) or Dizocilpine (HY-15084B)[9].
Chronic treatment with Dehydroepiandrosterone sulfate sodium salt for 4 weeks significantly reduces the body weight of mice in the pentylenetetrazol-induced seizure model[9].

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