1. Neuronal Signaling
    GPCR/G Protein
    Metabolic Enzyme/Protease
    Autophagy
  2. Cannabinoid Receptor
    Endogenous Metabolite
    Autophagy
  3. Pregnenolone monosulfate

Pregnenolone monosulfate (Synonyms: 3β-Hydroxy-5-pregnen-20-one monosulfate)

Cat. No.: HY-B1739 Purity: >98.0%
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Pregnenolone monosulfate (3β-Hydroxy-5-pregnen-20-one monosulfate) is a powerful neurosteroid, the main precursor of various steroid hormones including steroid ketones. Pregnenolone monosulfate acts as a signaling-specific inhibitor of cannabinoid CB1 receptor, inhibits the effects of tetrahydrocannabinol (THC) that are mediated by the CB1 receptors. Pregnenolone monosulfate can protect the brain from cannabis intoxication.

For research use only. We do not sell to patients.

Pregnenolone monosulfate Chemical Structure

Pregnenolone monosulfate Chemical Structure

CAS No. : 1247-64-9

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10 mM * 1 mL in DMSO USD 55 In-stock
Estimated Time of Arrival: December 31
50 mg USD 50 In-stock
Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

Pregnenolone monosulfate (3β-Hydroxy-5-pregnen-20-one monosulfate) is a powerful neurosteroid, the main precursor of various steroid hormones including steroid ketones. Pregnenolone monosulfate acts as a signaling-specific inhibitor of cannabinoid CB1 receptor, inhibits the effects of tetrahydrocannabinol (THC) that are mediated by the CB1 receptors. Pregnenolone monosulfate can protect the brain from cannabis intoxication[1][2].

IC50 & Target[1]

CB1

 

Human Endogenous Metabolite

 

In Vitro

CB1 receptor stimulation increases brain Pregnenolone levels, which in turn exerts a negative feedback on the activity of the CB1 receptor antagonizing most of the known behavioral and somatic effects of THC. Pregnenolone likely acts as a signaling-specific negative allosteric modulator binding to a site distinct from that occupied by orthosteric ligands. Pregnenolone does not modify agonist binding but only agonist efficacy[1].
The effect of THC is significantly attenuated when slices are pre-treated with Pregnenolone 100 nM (15.1±1.8 % of inhibition). These effects are likely due to a pre-synaptic action of Pregnenolone. Thus, Pregnenolone blocks the increase in paired-pulse ratio (PPR) induced by THC but does not modify either the amplitude or the decay time of miniature EPSC (mEPSC)[1].

In Vivo

Pregnenolone administration (2-6 mg/kg) blocks THC-induced food-intake in Wistar rats and in C57BL/6N mice, and blunts the memory impairment induced by THC in mice, but it does not modify these behaviors per se. Injections of Pregnenolone (2 and 4mg/kg) before each self-administration session reduce the intake of WIN 55,212-2 and reduce the break-point in a progressive ratio schedule[1].

Clinical Trial
Molecular Weight

396.54

Formula

C₂₁H₃₂O₅S

CAS No.

1247-64-9

SMILES
Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
References
Animal Administration
[1]

Mice and Rats[1]
Adult male Wistar rats (weighing 320-340g), Sprague Dawley male rats (weighing 330-350g), C57BL/6N mice (2-3 months) and CD1 mice (weighing 25-30 g at the beginning of the experiments) are used. Pregnenolone is injected subcutaneously (sc). The injection volumes are 1 mL/kg of body weight for rats and 10 mL/kg for mice[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References
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Keywords:

Pregnenolone monosulfate3β-Hydroxy-5-pregnen-20-one monosulfateCannabinoid ReceptorEndogenous MetaboliteAutophagyInhibitorinhibitorinhibit

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