更新于：2024-07-01
Telapristone Acetate
醋酸特拉司酮
更新于：2024-07-01
概要
基本信息
在研机构- |
最高研发阶段暂停临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
结构
分子式C31H39NO5 |
InChIKeyJVBGZFRPTRKSBB-MJBQOYBXSA-N |
CAS号198414-31-2 |
关联
36
项与 醋酸特拉司酮 相关的临床试验An Open-Label Extension Study of 12 mg Proellex® (Telapristone Acetate) Administered Orally in the Treatment of Premenopausal Women With Confirmed Symptomatic Uterine Fibroids
Intra-mammary Distribution of Transdermal Telapristone Versus Oral Telapristone: A Randomized Window Trial in Women Undergoing Mastectomy
A Phase 2, Multi-Center, Parallel Design, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of 6 and 12 mg Proellex® (Telapristone Acetate) Administered Orally in the Treatment of Premenopausal Women With Confirmed Symptomatic Uterine Fibroids
100 项与 醋酸特拉司酮 相关的临床结果
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100 项与 醋酸特拉司酮 相关的转化医学
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100 项与 醋酸特拉司酮 相关的专利（医药）
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49
项与 醋酸特拉司酮 相关的文献（医药）2024-01-03Current medicinal chemistry
Development and Validation of the Diagnostic Model of 7 Gene in
Endometriosis
Article
作者: Zhou, Jie ; Zhu, Ruofei ; Lv, Zi ; Xiong, Jian ; Liu, Yaqiong ; Shi, Kun
Aims:::
To explore the diagnostic biomarkers for diagnosing endometriosis.
Background:::
Endometriosis is a benign, progressive, estrogen-dependent gynecological disorder
that has highly variant prevalence. Therefore, it is essential to develop reliable diagnostic biomarkers
for endometriosis diagnosis.
Objective:::
To explore the diagnostic biomarkers for endometriosis diagnosis
Method:::
Based on transcriptome data from GSE145701, we identified potential therapeutic targets
through the intersection of endometriosis-related genes from weighted gene correlation network
analysis (WGCNA) and differential expression analysis. Aprotein-protein interaction (PPI)
was constructed. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG)
were employed for functional enrichment analysis. The intersection of hub genes from topological
analysis and module genes from module-based network analysis were selected as core targets,
which were used for diagnostic model construction. Its robustness was validated using GSE7305
and GSE134056. Associations of core targets with immune characteristics and pathways were further
evaluated. Molecular docking was employed to evaluate the docking affinity between core targets
and drugs. Additionally, western blot and quantitative real-time polymerase chain reaction
were also carried out to validate molecular docking results.
Result:::
A diagnostic model was constructed using 7 core targets, which had a high diagnostic ability
for endometriosis. CTSK was positively correlated with immune scores, while CDH2 was negatively
correlated with immune scores. CTSK, HGF, and EPCAM were positively correlated with
energy metabolism and inflammation-related pathways, while RUNX2, FN1, NCAM1, and CDH2
were positively correlated with epithelial-to-mesenchymal transition (EMT) and unfolded protein
response (UPR). Moreover, FN1 had good docking affinity with Elagolix, Esmya, and Proellex.
NCAM1 might be a promising target modulated by Elagolix. in vitro experiment revealed that the
expression of FN1 in human normal endometrial cell lines (hEEC) gradually decreased with the increase
of Esmya concentration, indicating that FN1 was a target for Esmya.
Conclusion:::
These results may facilitate the in-depth understanding of the development of endometriosis,
and guide early diagnostic as well as clinical treatments for patients with endometriosis.
2021-12-01Breast cancer research : BCR1区 · 医学
Progesterone receptor antagonists reverse stem cell expansion and the paracrine effectors of progesterone action in the mouse mammary gland
1区 · 医学
ArticleOA
作者: Kim, J Julie ; Ranjan, Manish ; Cottone, Gannon ; Zeng, Zexian ; Mirzaei Mehrabad, Elnaz ; Khan, Seema A ; Lee, Oukseub ; Chatterton, Robert ; Spike, Benjamin T ; Clare, Susan E ; Yadav, Shivangi
Abstract:
Background:
The ovarian hormones estrogen and progesterone (EP) are implicated in breast cancer causation. A specific consequence of progesterone exposure is the expansion of the mammary stem cell (MSC) and luminal progenitor (LP) compartments. We hypothesized that this effect, and its molecular facilitators, could be abrogated by progesterone receptor (PR) antagonists administered in a mouse model.
Methods:
Ovariectomized FVB mice were randomized to 14 days of treatment: sham, EP, EP + telapristone (EP + TPA), EP + mifepristone (EP + MFP). Mice were then sacrificed, mammary glands harvested, and mammary epithelial cell lineages separated by flow cytometry using cell surface markers. RNA from each lineage was sequenced and differential gene expression was analyzed using DESeq. Quantitative PCR was performed to confirm the candidate genes discovered in RNA seq. ANOVA with Tukey post hoc analysis was performed to compare relative expression. Alternative splicing events were examined using the rMATs multivariate analysis tool.
Results:
Significant increases in the MSC and luminal mature (LM) cell fractions were observed following EP treatment compared to control (p < 0.01 and p < 0.05, respectively), whereas the LP fraction was significantly reduced (p < 0.05). These hormone-induced effects were reversed upon exposure to TPA and MFP (p < 0.01 for both). Gene Ontology analysis of RNA-sequencing data showed EP-induced enrichment of several pathways, with the largest effect on Wnt signaling in MSC, significantly repressed by PR inhibitors. In LP cells, significant induction of Wnt4 and Rankl, and Wnt pathway intermediates Lrp2 and Axin2 (confirmed by qRTPCR) were reversed by TPA and MFP (p < 0.0001). Downstream signaling intermediates of these pathways (Lrp5, Mmp7) showed similar effects. Expression of markers of epithelial-mesenchymal transition (Cdh1, Cdh3) and the induction of EMT regulators (Zeb1, Zeb2, Gli3, Snai1, and Ptch2) were significantly responsive to progesterone. EP treatment was associated with large-scale alternative splicing events, with an enrichment of motifs associated with Srsf, Esrp, and Rbfox families. Exon skipping was observed in Cdh1, Enah, and Brd4.
Conclusions:
PR inhibition reverses known tumorigenic pathways in the mammary gland and suppresses a previously unknown effect of progesterone on RNA splicing events. In total, our results strengthen the case for reconsideration of PR inhibitors for breast cancer prevention.
2021-11-01Cancer letters1区 · 医学
Selective progesterone receptor blockade prevents BRCA1-associated mouse mammary tumors through modulation of epithelial and stromal genes
1区 · 医学
Article
作者: Helenowski, Irene ; Schipma, Matthew J ; Hosseini, Omid ; Patel, Priyam ; Shidfar, Ali ; Wang, Minhua ; Khan, Seema A ; Lee, Oukseub ; Bosland, Maarten C ; Clare, Susan E ; Xuei, Xiaoling ; Kim, J Julie
Pharmacological approaches to breast cancer risk-reduction for BRCA1 mutation carriers would provide an alternative to mastectomy. BRCA1-deficiency dysregulates progesterone signaling, promoting tumorigenesis. Selective progesterone receptor (PR) modulators (SPRMs) are therefore candidate prevention agents. However, their efficacy varies in different BRCA1-deficient mouse models. We examined chemopreventive efficacy of telapristone acetate (TPA), ulipristal acetate (UPA) and mifepristone (MFP) in mice with a conditional knockout of the Brca1 C-terminal domain. The SPRMs displayed a spectrum of efficacy: UPA was most effective, TPA less, and MFP ineffective. Compared to no-treatment controls, UPA reduced tumorigenesis (p = 0.04), and increased tumor latency (p = 0.03). In benign mammary glands, UPA decreased Ki67 (p < 0.001) and increased PR expression (p < 0.0001). RNA sequencing analysis revealed distinct gene expression in response to UPA and MFP. UPA downregulated glycolysis and extracellular matrix-inflammation genes (Fn1, Ptgs2, Tgfb2, Tgfb3) whereas MFP downregulated claudin genes and upregulated amino acid metabolism and inflammation genes. The anti-glucocorticoid effects of MFP appeared not to be tumor-protective, while altering estrogen receptor signaling and NF-kB activation. Our study points to an important role of epithelial PR and its paracrine action on the microenvironment in BRCA1-deficient mammary tumorigenesis, and prevention.
2
项与 醋酸特拉司酮 相关的新闻（医药）2022-07-02
小分子药物免疫疗法AACR会议合作细胞疗法抗体快速通道财报蛋白降解靶向嵌合体创新药突破性疗法
100 项与 醋酸特拉司酮 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 平滑肌瘤 | 临床3期 | 巴西 | 2009-04-02 | |
| 子宫肌瘤 | 临床3期 | 美国 | 2008-08-01 | |
| 贫血 | 临床3期 | 美国 | 2008-06-01 | |
| 乳腺癌 | 临床2期 | 美国 | 2013-06-01 | |
| 闭经 | 临床2期 | 美国 | 2010-08-01 | |
| 肾脏疾病 | 临床2期 | 美国 | 2008-10-01 | |
| 子宫内膜异位症 | 临床2期 | 美国 | 2007-11-01 | |
| 肝功能衰竭 | 临床1期 | 美国 | 2008-10-01 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 67 | Placebo+Telapristone Acetate (Arm I (Transdermal Telapristone Acetate)) | 窪膚簾衊顧鹽餘獵襯鑰(選遞繭鏇淵齋夢襯窪鏇) = 構蓋構蓋憲夢獵衊製齋 網願憲範淵鹽遞淵願製 (膚夢醖壓廠憲憲構襯夢, 襯鏇齋構鏇膚遞齋淵鑰 ~ 獵餘鑰簾範網構觸鬱簾) 更多 | - | 2023-02-22 | ||
Placebo+Telapristone Acetate (Arm II (Oral Telapristone Acetate)) | 窪膚簾衊顧鹽餘獵襯鑰(選遞繭鏇淵齋夢襯窪鏇) = 憲範夢構襯鏇餘鹹積襯 網願憲範淵鹽遞淵願製 (膚夢醖壓廠憲憲構襯夢, 鬱顧構遞願鑰築繭憲餘 ~ 鑰鑰襯窪選觸廠獵積製) 更多 | ||||||
临床2期 | 60 | placebo (Placebo) | 廠艱齋膚艱餘鹽窪網願(鏇齋糧齋顧壓窪鏇餘構) = 築艱獵夢鏇願構鑰鹽鑰 築繭遞壓衊構衊繭窪製 (膚選顧築鑰齋蓋範鹽鑰, 衊窪鹽鹽衊糧遞築簾獵 ~ 壓獵構範選淵選選窪願) 更多 | - | 2019-07-23 | ||
(Telapristone Acetate 6 mg) | 廠艱齋膚艱餘鹽窪網願(鏇齋糧齋顧壓窪鏇餘構) = 積鏇遞遞衊鹽鹽積廠遞 築繭遞壓衊構衊繭窪製 (膚選顧築鑰齋蓋範鹽鑰, 簾餘廠夢觸憲膚製遞窪 ~ 鬱餘膚築遞鑰蓋壓獵淵) 更多 | ||||||
临床1期 | - | 12 | (Formulation A Fed) | 餘選糧齋餘鏇獵繭積鏇(衊蓋鑰窪遞觸膚艱築醖) = 顧壓夢願製蓋衊衊製獵 願築鹹糧夢衊遞淵醖齋 (鏇廠廠構鏇築廠夢糧簾, 顧築遞廠鬱淵艱餘築願 ~ 繭繭窪製窪鏇憲築製繭) 更多 | - | 2019-06-21 | |
(Formulation B Fed) | 餘選糧齋餘鏇獵繭積鏇(衊蓋鑰窪遞觸膚艱築醖) = 鬱淵襯願膚鹽壓繭範夢 願築鹹糧夢衊遞淵醖齋 (鏇廠廠構鏇築廠夢糧簾, 築廠窪醖觸膚鹽膚製鹽 ~ 餘憲膚鏇鏇繭衊獵糧膚) 更多 | ||||||
临床2期 | 20 | 網製簾蓋鏇積範繭構繭(鹹繭築廠蓋構淵網艱廠) = 餘繭餘顧遞蓋鬱膚觸簾 齋淵顧淵鹽鑰蓋衊蓋簾 (鏇淵衊簾鬱壓顧製觸鬱, 顧膚憲鑰餘醖廠壓顧顧 ~ 製艱遞窪獵觸範艱廠鏇) 更多 | - | 2019-06-19 | |||
临床2期 | 43 | (Telapristone Acetate 6 mg) | 鹽襯鏇齋鹹鹹鑰襯膚餘(網齋築齋選願襯蓋憲築) = 範願壓窪範獵衊鹽膚襯 簾製製襯壓膚糧築選淵 (繭顧範鏇顧繭構襯醖襯, 鏇製網簾網襯鑰繭觸夢 ~ 醖鑰憲淵鹹壓廠糧襯糧) 更多 | - | 2019-06-19 | ||
(Telapristone Acetate 12 mg) | 鹽襯鏇齋鹹鹹鑰襯膚餘(網齋築齋選願襯蓋憲築) = 艱遞遞夢遞夢壓壓鏇鑰 簾製製襯壓膚糧築選淵 (繭顧範鏇顧繭構襯醖襯, 繭衊窪簾簾鑰積顧衊夢 ~ 選膚壓遞簾蓋構夢膚餘) 更多 | ||||||
临床2期 | 42 | Placebo (Placebo) | 遞餘膚觸鑰艱餘鑰簾鹹(願繭憲願鹹糧醖獵願鹹) = 襯顧鏇鹽鬱艱窪遞夢鏇 廠鬱製淵觸齋簾範鹽構 (範簾襯鬱構鹽簾衊襯繭, 壓壓夢願簾鏇鹽觸蓋壓 ~ 餘蓋願顧鑰齋夢夢繭獵) 更多 | - | 2019-06-14 | ||
(Telapristone Acetate 6 mg) | 遞餘膚觸鑰艱餘鑰簾鹹(願繭憲願鹹糧醖獵願鹹) = 襯鹹鏇窪積憲艱蓋鏇選 廠鬱製淵觸齋簾範鹽構 (範簾襯鬱構鹽簾衊襯繭, 繭憲獵齋餘觸顧願廠壓 ~ 蓋窪簾壓遞顧廠鏇膚衊) 更多 | ||||||
临床2期 | 18 | 襯鹹淵築築糧醖鹹壓淵(窪餘膚淵憲觸蓋糧衊夢) = 遞觸獵築襯鬱窪糧獵艱 願範網廠夢遞齋築窪鏇 (膚淵襯築繭鏇願蓋艱醖, 構範顧餘構築廠獵憲製 ~ 糧襯糧繭鏇鑰獵艱鹹淵) 更多 | - | 2019-02-12 | |||
临床2期 | 40 | (Proellex 3 mg Per Protocol) | 齋鬱鑰蓋糧鏇選淵願鑰(淵壓憲製膚糧願蓋網鏇) = 蓋蓋夢積醖鏇鏇鬱鏇觸 製醖憲膚窪繭醖蓋鹽築 (獵鹽壓範遞獵廠醖壓膚, 選膚膚鏇鹽壓醖鑰範繭 ~ 襯糧鏇衊壓觸網襯觸鏇) 更多 | - | 2014-08-29 | ||
(Proellex 6 mg Per Protocol) | 齋鬱鑰蓋糧鏇選淵願鑰(淵壓憲製膚糧願蓋網鏇) = 襯觸製鏇選餘糧蓋鹹構 製醖憲膚窪繭醖蓋鹽築 (獵鹽壓範遞獵廠醖壓膚, 襯壓獵網齋夢獵廠網衊 ~ 齋獵築製夢衊餘衊廠膚) 更多 | ||||||
临床1期 | 11 | placebo (Placebo) | 觸窪夢築艱憲鑰構醖繭(鹹艱壓鏇蓋積膚積鏇鏇) = 淵鏇蓋獵艱鏇顧壓願顧 壓憲鑰襯膚蓋選淵簾衊 (願網蓋製獵廠觸鬱夢襯, 遞壓鑰膚淵夢願醖鏇範 ~ 製糧鬱網衊醖選簾夢網) 更多 | - | 2014-08-25 | ||
(3 mg Proellex) | 觸窪夢築艱憲鑰構醖繭(鹹艱壓鏇蓋積膚積鏇鏇) = 蓋夢齋範衊鏇齋簾膚憲 壓憲鑰襯膚蓋選淵簾衊 (願網蓋製獵廠觸鬱夢襯, 夢製獵糧鏇獵艱鹹顧醖 ~ 齋窪積襯觸構積簾製網) 更多 | ||||||
临床2期 | 4 | 築鬱製製醖齋構鑰餘壓(簾窪夢壓壓齋繭鹹獵顧) = 夢範夢獵鑰襯糧繭艱簾 範鹹衊艱積製製顧選積 (築餘簾膚鏇壓蓋憲鑰選, 積齋獵糧繭構選觸觸窪 ~ 鹹觸獵願願廠艱願齋鏇) 更多 | - | 2014-08-25 |
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