2. Immunology/Inflammation Vitamin D Related/Nuclear Receptor
  3. Glucocorticoid Receptor
  4. RU 43044

RU 43044 is an orally active, selective glucocorticoid receptor inhibitor. RU 43044 blocks glucocorticoid receptor activity and reverses the enhanced dopamine release induced by high potassium in the prefrontal cortex. RU 43044 also inhibits thymocyte receptor down-regulation induced by high-dose glucocorticoids without affecting thymocyte apoptosis or basal receptor expression. RU 43044 is widely applicable to research related to depression.

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RU 43044

RU 43044 Chemical Structure

CAS No. : 136959-96-1

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Description

RU 43044 is an orally active, selective glucocorticoid receptor inhibitor. RU 43044 blocks glucocorticoid receptor activity and reverses the enhanced dopamine release induced by high potassium in the prefrontal cortex. RU 43044 also inhibits thymocyte receptor down-regulation induced by high-dose glucocorticoids without affecting thymocyte apoptosis or basal receptor expression. RU 43044 is widely applicable to research related to depression[1][2][3].

In Vivo

RU 43044 (10-30 mg/kg; p.o.; administered at 23.5, 5, and 1 hours before experiments) produces antidepressant-like effects in chronic corticosterone-treated mice, reversing increased forced swim test immobility and enhanced prefrontal high K+-stimulated dopamine release, without altering motor function[1].
RU 43044 (10-30 mg/kg; p.o.; administered at 23.5, 5, and 1 hours before experiments) produces antidepressant-like effects in isolation-reared mice, reversing increased forced swim test immobility and enhanced prefrontal high K+-stimulated dopamine release, without altering motor function[1].
RU 43044 (1 mg/kg; i.p.; every 12 hours; 2 days) alone has no effect on normal thymocyte development or GCR expression, but it blocks high-dose Dexamethasone (HY-14648) -induced GCR down-regulation in mature single-positive thymocytes[3].

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

Animal Model: ddY mice (male, 5 weeks old at study initiation, chronic corticosterone-induced)[1]
Dosage: 10 mg/kg; 30 mg/kg
Administration: p.o.; administered at 23.5, 5, and 1 hours before experiments
Result: Significantly reversed the increased immobility time in the forced swim test caused by chronic corticosterone treatment at 10 mg/kg and 30 mg/kg.
Reversed the chronic corticosterone-induced enhancement of high K+-stimulated dopamine release in the prefrontal cortex at 30 mg/kg.
Did not affect basal dopamine release, basal serotonin release, or high K+-stimulated serotonin release in chronic corticosterone-treated mice at 30 mg/kg.
Had no effect on spontaneous locomotor activity or rotarod performance in chronic corticosterone-treated mice at 30 mg/kg.
Molecular Weight

414.58

Formula

C29H34O2
CAS No.
SMILES

O=C1CC[C@@]2(C3=CC[C@@]4([C@@](O)(CC[C@]4([C@@]3(CCC2=C1)[H])[H])C#CC)C)CC5=CC=C(C=C5)C
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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RU 43044 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

RU 43044136959-96-1RU43044RU-43044Glucocorticoid Receptorthymocytesglucocorticoid receptordopaminedexamethasoneforced swim testmiceprefrontal cortexdepressioncorticosteronesingle-positive thymocytesInhibitorinhibitorinhibit

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