Last update 21 Nov 2024

Promegestone

Last update 21 Nov 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Promegestone (INN)

+ [2]

Target

Mechanism

PR agonists(Progesterone receptor agonists)

Therapeutic Areas

Nervous System DiseasesEndocrinology and Metabolic DiseaseOther Diseases

Active Indication

Endocrine System DiseasesMastodyniaMenstruation Disturbances

Inactive Indication-

Originator Organization-

Active Organization-

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date-

Regulation-

Structure

Molecular FormulaC22H30O2

InChIKeyQFFCYTLOTYIJMR-XMGTWHOFSA-N

CAS Registry34184-77-5

100 Clinical Results associated with Promegestone

100 Translational Medicine associated with Promegestone

100 Patents (Medical) associated with Promegestone

734

Literatures (Medical) associated with Promegestone

01 Jan 2024·Advances in Protein Chemistry and Structural Biology

Exploring the role of estrogen and progestins in breast cancer: A genomic approach to diagnosis

Review

Author: Elavarasu, Santhosh Mudipalli ; Dhanushkumar, T ; George Priya Doss, C ; Vasudevan, Karthick ; Selvam, Prasanna Kumar

Breast cancer (BC) is the most common cancer among women and a major cause of death from cancer. The role of estrogen and progestins, including synthetic hormones like R5020, in the development of BC has been highlighted in numerous studies. In our study, we employed machine learning and advanced bioinformatics to identify genes that could serve as diagnostic markers for BC. We thoroughly analyzed the transcriptomic data of two BC cell lines, T47D and UDC4, and performed differential gene expression analysis. We also conducted functional enrichment analysis to understand the biological functions influenced by these genes. Our study identified several diagnostic genes strongly associated with BC, including MIR6728, ENO1-IT1, ENO1-AS1, RNU6-304P, HMGN2P17, RP3-477M7.5, RP3-477M7.6, and CA6. The genes MIR6728, ENO1-IT1, ENO1-AS1, and HMGN2P17 are involved in cancer control, glycolysis, and DNA-related processes, while CA6 is associated with apoptosis and cancer development. These genes could potentially serve as predictors for BC, paving the way for more precise diagnostic methods and personalized treatment plans. This research enhances our understanding of BC and offers promising avenues for improving patient care in the future.

13 Oct 2023·Biology of reproduction

Exposure to a phthalate mixture disrupts ovulatory progesterone receptor signaling in human granulosa cells in vitro†.

Article

Author: Hannon, Patrick R ; Akin, James W ; Curry, Thomas E

Exposure to phthalates disrupts ovarian function. However, limited studies have investigated the effects of phthalate mixtures on ovulation, especially in women. Human granulosa cells were used to test the hypothesis that exposure to a phthalate mixture (PHTmix) disrupts progesterone (P4)/progesterone receptor (PGR) signaling, which is a crucial pathway for ovulation. In addition, progestin and cyclic adenosine 3', 5'-monophosphate (cAMP) supplementation were tested as methods to circumvent phthalate toxicity. Granulosa cells from women undergoing in vitro fertilization were acclimated in culture to regain responsiveness to human chorionic gonadotropin (hCG; clinical luteinizing hormone analogue). Granulosa cells were treated with or without hCG, and with or without PHTmix (1-500 μg/ml; dimethylsulfoxide = vehicle control) for 0.5-36 h. In the supplementation experiments, cells were treated with or without R5020 (stable progestin), and with or without 8-Br-cAMP (stable cAMP analogue). Exposure to hCG + PHTmix decreased P4 levels and mRNA levels of steroidogenic factors when compared to hCG. This was accompanied by decreased mRNA levels of PGR and downstream P4/PGR ovulatory mediators (ADAM metallopeptidase with thrombospondin type 1 motif 1 (ADAMTS1), C-X-C motif chemokine receptor 4 (CXCR4), pentraxin 3 (PTX3), and regulator of G protein signaling 2 (RGS2)) in the hCG + PHTmix groups compared to hCG. Exposure to hCG + PHTmix 500 μg/ml decreased cAMP levels and protein kinase A activity compared to hCG. Supplementation with progestin in the hCG + PHTmix 500 μg/ml group did not rescue toxicity, while supplementation with cAMP restored PGR levels and downstream P4/PGR mediator levels to hCG levels. These findings suggest that phthalate mixture exposure inhibits P4/PGR signaling in human granulosa cells via decreased steroidogenesis, cAMP levels, and protein kinase A activity. Restored P4/PGR signaling with cAMP supplementation provides a potential cellular target for intervention of phthalate-induced ovulatory dysfunction in women.

01 Oct 2023·Journal of the Chinese Medical Association

The rapid activation of cPKCβII by progesterone results in the negative regulation of Ca2+ influx in human resting T cells

Article

Author: Chien, Angela ; Lin, Veronica Hui-Chen ; Chien, Eileen Jea

Background:Progesterone-stimulated rapid suppression of phytohemagglutinin (PHA)-activated sustained membrane Ca2+ influx is revealed by Mn2+ quenching fura-2 fluorescence. Ca2+ influx suppression results in immunosuppression of T-cell proliferation. Downregulation of protein kinase C (PKC) activity by phorbol 12-myristate 13-acetate (PMA) enhances the PHA-activated increase in sustained intracellular Ca2+ concentration ([Ca2+]i) via Ca2+ influx in T cells. Conventional PKC (cPKC) inhibitors also enhance the [Ca2+]i increase in resting T cells caused by progesterone. This study explores whether cPKC activation by progesterone results in suppression of Ca2+ influx in resting T cells.Methods:Progesterone, its analogs (R5020/Org OD 02-0), and plasma membrane-impermeable progesterone-bovine serum albumin conjugate were used to stimulate human resting T cells. Inhibitors and PKC downregulation by PMA were used to investigate whether cPKC affects Ca2+ influx.Results:Progesterone and analogs dose-dependently suppressed Ca2+ influx in T cells. One cPKC inhibitor, Ro318220, attenuated Ca2+ influx suppression, and enhanced the increase in [Ca2+]i caused by progesterone and analogs. U73122 did not affect Ca2+ influx suppression but did decrease the [Ca2+]i increase. Ca2+ influx suppression was not attenuated by the cPKCα/βI isoform-selective inhibitor, Go6976, nevertheless, a cPKCβI/βII isoform-selective inhibitor, LY333531 did. Ca2+ influx suppression was attenuated by the cPKCβII-specific inhibitor CGP53353. After PKC downregulated by PMA, Ca2+ influx suppression by progesterone and analogs was almost abolished in parallel with a massive reduction in cPKCβII expression. This suggests cPKCβII activation by progesterone and analogs mediate Ca2+ influx suppression in resting T cells.Conclusion:Nongenomic membrane activation of cPKCβII by progesterone causes immunosuppression via negative regulation of Ca2+ influx into human resting T cells. This prevents resting T-cell activation and proliferation, which protects the fetus from maternal immune attack while decreasing maternal autoimmune disease flare-ups during pregnancy. Thus, cPKCβII modulators might provide a new therapeutic approach to balancing T-cell tolerance and immunity.

100 Deals associated with Promegestone

External Link

KEGG	Wiki	ATC	Drug Bank
D08431	Promegestone	G03DB07	DB13602

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Endocrine System Diseases	-	-	-
Mastodynia	-	-	-
Menstruation Disturbances	-	-	-

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