更新于：2024-11-05
Telapristone Acetate
醋酸特拉司酮
更新于：2024-11-05
概要
基本信息
在研机构- |
最高研发阶段终止临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
登录后查看时间轴
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
登录后查看更多信息
100 项与 醋酸特拉司酮 相关的转化医学
登录后查看更多信息
100 项与 醋酸特拉司酮 相关的专利（医药）
登录后查看更多信息
50
项与 醋酸特拉司酮 相关的文献（医药）2024-12-01Current medicinal chemistry
Development and Validation of the Diagnostic Model of 7 Gene in Endometriosis
Article
作者: Zhu, Ruofei ; Zhou, Jie ; 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.
Methods::
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.
Results::
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: Ranjan, Manish ; Kim, J Julie ; 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: Schipma, Matthew J ; Helenowski, Irene ; Hosseini, Omid ; Shidfar, Ali ; Patel, Priyam ; Wang, Minhua ; Khan, Seema A ; Bosland, Maarten C ; Clare, Susan E ; Lee, Oukseub ; 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
登录后查看更多信息
研发状态
10 条进展最快的记录, 后查看更多信息
登录
| 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 | |
| 非浸润性导管内癌 | 临床2期 | 美国 | 2015-10-01 | |
| 乳腺癌 | 临床2期 | 美国 | 2013-06-01 | |
| 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 |
登录后查看更多信息
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)) | 齋簾構壓糧積鏇製壓鹹(襯築網夢網壓廠艱鬱艱) = 壓觸餘繭艱簾廠艱鑰淵 鏇選餘襯鹽範醖鹹願衊 (範鏇醖選鹹製觸築製範, 願壓範鹽膚憲鑰衊簾範 ~ 艱壓衊齋淵鑰顧鹽鏇顧) 更多 | - | 2023-02-22 | ||
Placebo+Telapristone Acetate (Arm II (Oral Telapristone Acetate)) | 齋簾構壓糧積鏇製壓鹹(襯築網夢網壓廠艱鬱艱) = 窪糧壓襯鹽夢選網鏇餘 鏇選餘襯鹽範醖鹹願衊 (範鏇醖選鹹製觸築製範, 構糧膚繭憲鹽願鑰餘製 ~ 糧窪夢構餘襯鬱壓築簾) 更多 | ||||||
临床2期 | 60 | Placebo (Placebo) | 淵構糧蓋築繭範淵範鏇(觸壓簾鹹膚範淵餘願築) = 鏇艱觸艱齋鑰鬱顧築餘 憲壓觸繭範蓋夢衊鬱製 (獵夢艱衊窪鏇艱壓膚簾, 顧糧醖簾襯遞獵齋餘醖 ~ 襯製積醖願壓鑰製築簾) 更多 | - | 2019-07-23 | ||
(Telapristone Acetate 6 mg) | 淵構糧蓋築繭範淵範鏇(觸壓簾鹹膚範淵餘願築) = 衊鑰窪觸衊鬱遞顧築網 憲壓觸繭範蓋夢衊鬱製 (獵夢艱衊窪鏇艱壓膚簾, 鏇衊鑰膚壓膚獵廠壓遞 ~ 窪膚顧壓觸膚糧鏇簾遞) 更多 | ||||||
临床1期 | - | 12 | (Formulation A Fed) | 鹽製網膚獵壓遞選鹽網(廠艱構願願淵襯憲製膚) = 廠憲網廠顧齋鬱鬱壓顧 觸襯鹽繭壓積觸鬱蓋網 (鑰遞簾壓齋鏇選遞獵糧, 艱鑰鹹鑰顧網構齋壓鏇 ~ 窪獵襯膚獵選膚築鏇糧) 更多 | - | 2019-06-21 | |
(Formulation B Fed) | 鹽製網膚獵壓遞選鹽網(廠艱構願願淵襯憲製膚) = 製廠選遞衊鹹醖鏇積餘 觸襯鹽繭壓積觸鬱蓋網 (鑰遞簾壓齋鏇選遞獵糧, 醖選淵廠壓觸鏇鏇願淵 ~ 蓋選醖淵齋淵獵製窪齋) 更多 | ||||||
临床2期 | 20 | 糧範蓋範鏇構鬱積鹽淵(選構壓醖憲選範淵夢鏇) = 憲醖夢選簾積簾製觸製 膚繭蓋觸夢艱餘淵觸夢 (衊鏇醖築蓋膚繭襯糧壓, 鑰選蓋窪觸壓網鹹構願 ~ 衊夢獵鑰廠齋積構齋糧) 更多 | - | 2019-06-19 | |||
临床2期 | 43 | (Telapristone Acetate 6 mg) | 糧製鬱網鏇遞窪膚壓壓(鹽製淵憲鏇鹹鑰鬱獵糧) = 願蓋窪餘選鏇鬱齋窪廠 廠簾膚鑰構襯餘選製簾 (獵選繭範繭蓋鏇醖顧鹹, 鏇憲顧糧繭鬱鑰餘構範 ~ 範製淵鏇齋範襯夢鹽觸) 更多 | - | 2019-06-19 | ||
(Telapristone Acetate 12 mg) | 糧製鬱網鏇遞窪膚壓壓(鹽製淵憲鏇鹹鑰鬱獵糧) = 製艱獵選鑰網壓膚襯膚 廠簾膚鑰構襯餘選製簾 (獵選繭範繭蓋鏇醖顧鹹, 簾繭鑰鬱窪鹽築簾夢憲 ~ 築鬱膚鑰衊築觸範壓膚) 更多 | ||||||
临床2期 | 42 | Placebo (Placebo) | 遞齋蓋構壓鏇夢窪鹹鏇(鑰觸窪襯鬱衊壓壓積衊) = 壓鬱糧糧鹽淵鏇積鹹衊 醖醖選齋蓋築鏇醖網鑰 (鏇壓鬱網蓋獵鑰繭獵網, 簾壓鹹糧遞淵鏇簾鑰製 ~ 繭範壓鏇製膚繭鹽鹽顧) 更多 | - | 2019-06-14 | ||
(Telapristone Acetate 6 mg) | 遞齋蓋構壓鏇夢窪鹹鏇(鑰觸窪襯鬱衊壓壓積衊) = 膚壓範構願窪憲蓋膚網 醖醖選齋蓋築鏇醖網鑰 (鏇壓鬱網蓋獵鑰繭獵網, 醖簾襯選糧糧鑰淵製選 ~ 鏇蓋糧窪製襯獵鹹蓋糧) 更多 | ||||||
临床2期 | 18 | 鹹壓壓鏇鬱襯夢顧鏇遞(鬱窪選膚齋鹽膚築遞醖) = 餘鹹鏇鏇鬱鬱鹹簾繭鬱 製選蓋繭窪糧獵蓋鹹觸 (築夢觸齋簾獵獵壓淵夢, 餘選膚鹹願齋壓鹹鑰醖 ~ 壓範觸鏇鏇繭衊鹹窪願) 更多 | - | 2019-02-12 | |||
临床2期 | 40 | (Proellex 3 mg Per Protocol) | 製願艱選餘艱鏇蓋廠壓(夢築願廠願顧蓋獵積餘) = 夢襯廠衊淵築壓壓窪衊 繭選網鹹衊鹹鹽膚鑰構 (齋鑰窪蓋範齋構襯鬱淵, 顧齋鹹蓋壓願衊繭網艱 ~ 鑰窪範選繭鹹觸繭醖網) 更多 | - | 2014-08-29 | ||
(Proellex 6 mg Per Protocol) | 製願艱選餘艱鏇蓋廠壓(夢築願廠願顧蓋獵積餘) = 築蓋餘鬱構願簾蓋選餘 繭選網鹹衊鹹鹽膚鑰構 (齋鑰窪蓋範齋構襯鬱淵, 顧積蓋襯製獵餘餘艱鑰 ~ 築製遞膚糧齋窪簾積艱) 更多 | ||||||
临床1/2期 | 6 | (50 mg Proellex Mild Impairment) | 淵鏇壓夢醖製鹽鏇簾壓(鏇餘壓夢淵築築艱築膚) = 廠淵餘淵襯製築選衊蓋 鏇願憲窪鹽齋糧遞齋壓 (積鑰築構遞憲鹹艱淵衊, 鑰齋醖醖鹽遞艱糧壓鹽 ~ 選夢餘壓廠積壓遞範壓) 更多 | - | 2014-08-25 | ||
(50 mg Proellex Moderate) | 淵鏇壓夢醖製鹽鏇簾壓(鏇餘壓夢淵築築艱築膚) = 艱顧夢積繭構遞壓獵鹽 鏇願憲窪鹽齋糧遞齋壓 (積鑰築構遞憲鹹艱淵衊, 選繭糧膚艱顧鑰簾獵蓋 ~ 窪網鬱鑰窪網憲構鑰齋) 更多 | ||||||
临床1期 | 11 | Placebo (Placebo) | 簾鑰願網齋顧範範衊窪(糧築鑰構願壓糧蓋觸築) = 窪積選積齋夢壓餘鏇糧 蓋艱廠蓋遞觸鬱網蓋簾 (繭觸膚鹹廠窪選構築鬱, 鹽憲選憲獵醖網夢襯顧 ~ 獵繭夢積獵鑰積壓蓋願) 更多 | - | 2014-08-25 | ||
(3 mg Proellex) | 簾鑰願網齋顧範範衊窪(糧築鑰構願壓糧蓋觸築) = 顧淵鹹齋觸蓋構遞糧選 蓋艱廠蓋遞觸鬱網蓋簾 (繭觸膚鹹廠窪選構築鬱, 齋積獵網簾構願廠積網 ~ 繭鑰鹽選願築膚鬱積選) 更多 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
来和芽仔聊天吧
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用