Home Endocrinology & Hormones Estrogen/progestogen Receptor agonist - Progesterone Receptor agonist Medroxyprogesterone

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Medroxyprogesterone Estrogen/progestogen Receptor agonist

Cat.No.S3635

Medroxyprogesterone (MP) is a synthetic pregnane steroid and a derivative of progesterone. It is a potent progesterone receptor agonist.
Medroxyprogesterone Estrogen/progestogen Receptor agonist Chemical Structure

Chemical Structure

Molecular Weight: 344.49

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Chemical Information, Storage & Stability

Molecular Weight 344.49 Formula

C22H32O3

 Storage (From the date of receipt)
CAS No. 520-85-4 Download SDF Storage of Stock Solutions

Synonyms MP Smiles CC1CC2C(CCC3(C2CCC3(C(=O)C)O)C)C4(C1=CC(=O)CC4)C

Solubility

In vitro
Batch:

DMSO : 68 mg/mL (197.39 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 14 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Mechanism of Action

In vitro
Medroxyprogesterone acetate (MPA, 10 nM) treatment for 48 h induces proliferation of the cells (1.6-fold induction). MPA induces cyclin D1 expression (3.3-fold induction). MPA increases both the protein level (2.2-fold induction) and promoter activity (2.7-fold induction) of cyclin D1 in MCF-7 cells transfected with PRB but not with PRA. Although MPA transcriptionally activates cyclin D1 expression, cyclin D1 promoter does not have progesterone-responsive element-related sequence. MPA induces the transient phosphorylation of Akt (2.7-fold induction at 5 min) and also phosphorylation of inhibitor of NFkappaBalpha (IkappaBalpha) (2.3-fold induction)[1]. MPA activates glucocorticoid receptors, which could mimic part of the anti-atherosclerotic effects of glucocorticoids, and has, on the other hand, also anti-androgenic activity, which might diminish protective oestrogen effects[2].
In vivo
Long-term treatment with MPA and MPA + E2 increases arterial thrombosis despite inhibitory effects of MPA on atherosclerosis in ApoE-deficient mice. Increased thrombin formation, reduced smooth muscle content and remodelling of non-collagenous plaque matrix may be involved in the pro-thrombotic effects. Thus, MPA exhibits differential effects on arterial thrombosis and on atherosclerosis. In monkeys, MPA interferes with anti-atherosclerotic oestrogen effects whereas progesterone does not[2].
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05188222 Not yet recruiting
Left Ventricular Dysfunction|Quality of Recovery|Right Ventricular Dysfunction
Jewish General Hospital
 September 1 2024 Phase 4
NCT06325293 Not yet recruiting
Community Acquired Pneumonia in Children|Mycoplasma Pneumoniae|Mycoplasma Pneumoniae Pneumonia
Christoph Berger|University Children''s Hospital Zurich
 July 1 2024 Not Applicable

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