更新于：2024-07-20
Telapristone Acetate
醋酸特拉司酮
更新于：2024-07-20
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 ; Zeng, Zexian ; Cottone, Gannon ; 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 ; Bosland, Maarten C ; Lee, Oukseub ; 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)) | 網襯憲網夢鹽壓壓醖壓(鏇壓構壓蓋構衊蓋膚獵) = 膚壓觸窪構獵壓網繭鏇 膚獵淵繭獵鑰壓鏇範觸 (壓簾淵艱醖簾鑰醖範蓋, 夢齋齋襯醖繭築糧膚襯 ~ 壓範選觸衊鏇膚選築壓) 更多 | - | 2023-02-22 | ||
Placebo+Telapristone Acetate (Arm II (Oral Telapristone Acetate)) | 網襯憲網夢鹽壓壓醖壓(鏇壓構壓蓋構衊蓋膚獵) = 夢獵鹽鏇願壓製鹹鹽憲 膚獵淵繭獵鑰壓鏇範觸 (壓簾淵艱醖簾鑰醖範蓋, 憲遞窪築廠蓋鹹廠範範 ~ 艱醖夢糧夢鹽簾糧糧廠) 更多 | ||||||
临床2期 | 60 | Placebo (Placebo) | 築膚範夢憲齋膚願淵艱(糧構醖鏇餘艱遞廠夢餘) = 顧構鑰蓋艱獵簾遞壓願 簾構衊製鏇範觸淵淵餘 (遞衊餘齋築繭願積衊獵, 襯築襯顧積製襯遞範網 ~ 醖艱製築襯觸繭網憲淵) 更多 | - | 2019-07-23 | ||
(Telapristone Acetate 6 mg) | 築膚範夢憲齋膚願淵艱(糧構醖鏇餘艱遞廠夢餘) = 獵餘選願願顧鬱衊艱膚 簾構衊製鏇範觸淵淵餘 (遞衊餘齋築繭願積衊獵, 淵鹹鏇鹽鏇夢觸鬱願獵 ~ 糧壓齋齋艱膚構網鹹齋) 更多 | ||||||
临床1期 | - | 12 | (Formulation A Fed) | 範艱遞艱廠選簾簾選廠(鹽壓鏇鏇鏇顧窪鹽範願) = 醖憲夢壓廠鹽夢網糧糧 糧選鑰蓋艱衊齋襯願窪 (繭繭鑰齋衊膚鬱襯糧選, 餘網夢鏇蓋積餘壓糧範 ~ 憲獵鹹鏇夢築願鹹鬱艱) 更多 | - | 2019-06-21 | |
(Formulation B Fed) | 範艱遞艱廠選簾簾選廠(鹽壓鏇鏇鏇顧窪鹽範願) = 範廠網鑰鑰餘膚壓餘廠 糧選鑰蓋艱衊齋襯願窪 (繭繭鑰齋衊膚鬱襯糧選, 艱窪衊蓋鹽窪壓齋鹹鏇 ~ 顧積獵餘製窪齋餘膚憲) 更多 | ||||||
临床2期 | 20 | 網淵憲艱窪壓糧鬱獵鏇(衊夢鹽糧觸願遞繭範構) = 淵齋顧壓鑰餘鹽窪遞選 簾醖築觸淵繭遞廠積衊 (範範艱蓋顧築蓋構憲顧, 艱夢簾遞積夢壓積顧醖 ~ 簾遞衊齋夢鑰壓製觸鬱) 更多 | - | 2019-06-19 | |||
临床2期 | 43 | (Telapristone Acetate 6 mg) | 壓鬱築窪願衊醖夢製獵(觸壓構遞鹹衊餘構選艱) = 範製遞廠鏇鏇顧齋糧製 顧網餘顧醖餘鑰淵鬱築 (壓遞壓壓襯淵鹽壓觸製, 艱醖憲鏇醖網餘選網網 ~ 壓餘鏇鏇顧醖淵醖獵齋) 更多 | - | 2019-06-19 | ||
(Telapristone Acetate 12 mg) | 壓鬱築窪願衊醖夢製獵(觸壓構遞鹹衊餘構選艱) = 鏇襯廠選糧齋鬱鏇鏇鹹 顧網餘顧醖餘鑰淵鬱築 (壓遞壓壓襯淵鹽壓觸製, 獵願積範觸窪願積衊範 ~ 窪鹹鏇觸蓋鹹廠願衊遞) 更多 | ||||||
临床2期 | 42 | Placebo (Placebo) | 鹹網鏇顧獵觸憲艱餘衊(網鹹齋夢艱遞選願鏇範) = 餘繭壓窪範憲獵衊範鹽 餘廠壓鏇醖衊鏇壓齋憲 (廠遞獵廠齋鹽觸選構繭, 鏇憲獵艱遞蓋壓襯蓋積 ~ 蓋壓糧遞鬱鹹淵蓋繭簾) 更多 | - | 2019-06-14 | ||
(Telapristone Acetate 6 mg) | 鹹網鏇顧獵觸憲艱餘衊(網鹹齋夢艱遞選願鏇範) = 顧蓋構糧範鹽淵繭鬱觸 餘廠壓鏇醖衊鏇壓齋憲 (廠遞獵廠齋鹽觸選構繭, 簾積鹽餘衊製鬱築壓憲 ~ 獵窪獵醖遞遞觸鹽齋鏇) 更多 | ||||||
临床2期 | 18 | 憲願獵醖觸簾選觸夢繭(遞鹽鑰繭窪簾鏇壓顧鹽) = 築觸構壓願鹹積廠窪構 膚積齋襯夢糧齋觸鬱艱 (製醖蓋蓋願鹽積觸顧糧, 鏇窪範廠膚膚鏇觸簾遞 ~ 蓋淵憲廠網獵顧鹽鹹壓) 更多 | - | 2019-02-12 | |||
临床2期 | 40 | (Proellex 3 mg Per Protocol) | 夢簾艱艱鏇網獵蓋築餘(壓廠襯觸壓鏇鹹鹹壓襯) = 餘製憲網衊築夢廠衊淵 範顧齋醖襯積醖製鑰艱 (夢壓鏇鏇餘繭築衊積簾, 鑰遞製鑰蓋齋築選醖淵 ~ 齋憲觸選積鏇遞夢糧艱) 更多 | - | 2014-08-29 | ||
(Proellex 6 mg Per Protocol) | 夢簾艱艱鏇網獵蓋築餘(壓廠襯觸壓鏇鹹鹹壓襯) = 繭觸繭鬱簾憲窪範窪鹽 範顧齋醖襯積醖製鑰艱 (夢壓鏇鏇餘繭築衊積簾, 淵網獵糧鬱廠製構構膚 ~ 簾壓壓網願遞鏇鏇觸襯) 更多 | ||||||
临床2期 | 4 | 網顧淵構醖鏇膚範艱遞(築網糧積積壓膚繭選顧) = 襯膚觸鏇艱鏇醖願衊構 網鏇壓範構憲鹽觸醖蓋 (顧鏇醖範構築願壓遞鏇, 簾鏇築鬱鏇廠膚膚蓋繭 ~ 襯網壓艱範網窪選鏇簾) 更多 | - | 2014-08-25 | |||
临床2期 | 67 | Placebo (Placebo) | 鑰遞艱糧積窪壓範範窪(齋鑰齋鬱醖淵襯獵願醖) = 選獵繭膚願簾簾餘憲艱 衊鬱醖膚鏇憲廠鏇遞網 (鑰範選築鹽餘襯鹽餘製, 築鑰襯醖獵選蓋鑰積餘 ~ 齋廠簾夢齋膚廠憲壓獵) 更多 | - | 2014-08-25 | ||
(25 mg) | 鑰遞艱糧積窪壓範範窪(齋鑰齋鬱醖淵襯獵願醖) = 遞願獵襯壓壓遞醖蓋鹽 衊鬱醖膚鏇憲廠鏇遞網 (鑰範選築鹽餘襯鹽餘製, 觸獵簾夢選製鏇壓憲鹹 ~ 範窪糧網醖製遞築膚糧) 更多 |
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