(Sapanisertib) - 药物靶点：mTORC1 x mTORC2_在研适应症：局部晚期膀胱癌，局部晚期尿路上皮癌，转移性尿路上皮癌_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Sapanisertib (USAN/INN)、CB-228、FTH-003

+ [5]

靶点

mTORC1 x mTORC2

作用机制

mTORC1抑制剂(哺乳动物雷帕霉素靶蛋白(mTORC1)复合体抑制剂)、mTORC2抑制剂(mTOR复合物-2抑制剂)

治疗领域

肿瘤免疫系统疾病心血管疾病+ [8]

在研适应症

局部晚期膀胱癌局部晚期尿路上皮癌转移性尿路上皮癌+ [42]

非在研适应症

晚期乳腺癌晚期非小细胞肺癌间变性大细胞淋巴瘤+ [32]

原研机构

Takeda Pharmaceutical Co., Ltd.

在研机构

Faeth Therapeutics, Inc.初创企业

Takeda Pharmaceutical Co., Ltd.

National Cancer Institute

+ [2]

非在研机构

Millennium Pharmaceuticals, Inc.Takeda Pharmaceuticals International, Inc.

Pivotal SL

+ [1]

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)终止

特殊审评快速通道 (美国)

结构

分子式C15H15N7O

InChIKeyGYLDXIAOMVERTK-UHFFFAOYSA-N

CAS号1224844-38-5

关联

49

项与 Sapanisertib 相关的临床试验

NCT06463028 / Not yet recruiting临床2期

A Randomized, Open-label, Multi-Center, Phase 2 Clinical Trial Evaluating Sapanisertib and Serabelisib (PIKTOR) With Paclitaxel, Serabelisib With Paclitaxel, and Paclitaxel Alone in Patients With Advanced or Recurrent Endometrial Cancer

This is a Phase 2, multicenter, open-label, randomized study to evaluate the efficacy and safety of sapanisertib and serabelisib (PIKTOR) with paclitaxel and the efficacy and safety of serabelisib with paclitaxel versus paclitaxel alone in participants with advanced or recurrent endometrial cancer.

开始日期2024-09-30

申办/合作机构

Faeth Therapeutics, Inc.初创企业

[+1]

NCT05275673 / Terminated临床2期

A Randomized, Open-Label Phase 2 Study of the TORC 1/2 Inhibitor Sapanisertib in Relapsed/Refractory NFE2L2 (NRF2)-Mutated and Wild-Type (WT) Squamous Non-Small Cell Lung Cancer (sqNSCLC)

This is a multicenter, randomized, open-label Phase 2 study of sapanisertib in biomarker-defined populations of sqNSCLC. Patients with NFE2L2 (the name for gene encoding the protein called NRF2)-mutated or wild-type sqNSCLC should have disease that has progressed on or after at least two prior systemic therapies for metastatic disease including platinum-doublet chemotherapy and a programmed cell death 1 ligand 1 (PD-L1) inhibitor. The study will evaluate sapanisertib monotherapy in patients with relapsed/refractory sqNSCLC as two separate groups: Group A: NFE2L2-mutated sqNSCLC and Group B: NFE2L2-WT sqNSCLC.

开始日期2022-04-15

申办/合作机构

Calithera Biosciences, Inc.

NCT05022394 / Withdrawn临床1/2期IIT

Phase I/II Study to OVERCOME Resistance to PD-1/PD-L1 Inhibitor Immunotherapy in Advanced Non-Small Cell Lung Cancer - I-OVERCOME Trial

This phase I/II trial studies the side effects of sapanisertib and nivolumab and to see how well they work in treating patients with stage I-IV non-small cell lung cancer whose disease got worse on previous PD-1/PD-L1 inhibitor therapy. Sapanisertib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Immunotherapy with monoclonal antibodies, such as nivolumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving sapanisertib and nivolumab may help to control the disease.

开始日期2021-02-18

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+1]

100 项与 Sapanisertib 相关的临床结果

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100 项与 Sapanisertib 相关的转化医学

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100 项与 Sapanisertib 相关的专利（医药）

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176

项与 Sapanisertib 相关的文献（医药）

2023-12-15·Cancer research

Combining the Tyrosine Kinase Inhibitor Cabozantinib and the mTORC1/2 Inhibitor Sapanisertib Blocks ERK Pathway Activity and Suppresses Tumor Growth in Renal Cell Carcinoma

Article

作者: Herndon, John M ; Welm, Bryan E ; Zhao, Yanyan ; Mo, Chia-Kuei ; Yang, Xiaolu ; Ma, Cynthia X ; Mudd, Jacqueline L ; Koh, Mei Yee ; Zhang, Hui ; Primeau, Tina M ; Shinkle, Andrew T ; Liu, Di ; Hoog, Jeremy ; Mashl, R Jay ; Li, Shunqiang ; Sato, Kazuhito ; Gould, Alanna ; Davies, Sherri R ; Govindan, Ramaswamy ; Chen, Feng ; Ding, Xi ; Wu, Yige ; Chen, Siqi ; Lal, Preet ; Evrard, Yvonne A ; Ding, Li ; Sun, Hua ; Wendl, Michael C ; Liu, Ruiyang ; Fields, Ryan C ; Chuang, Jeffrey H ; Lum, David ; Moscow, Jeffrey A ; Wang, Yuefan ; Meric-Bernstam, Funda ; Lim, Kian-Huat ; Welm, Alana L ; Hsieh, James ; Wyczalkowski, Matthew A

Abstract:

Current treatment approaches for renal cell carcinoma (RCC) face challenges in achieving durable tumor responses due to tumor heterogeneity and drug resistance. Combination therapies that leverage tumor molecular profiles could offer an avenue for enhancing treatment efficacy and addressing the limitations of current therapies. To identify effective strategies for treating RCC, we selected ten drugs guided by tumor biology to test in six RCC patient-derived xenograft (PDX) models. The multitargeted tyrosine kinase inhibitor (TKI) cabozantinib and mTORC1/2 inhibitor sapanisertib emerged as the most effective drugs, particularly when combined. The combination demonstrated favorable tolerability and inhibited tumor growth or induced tumor regression in all models, including two from patients who experienced treatment failure with FDA-approved TKI and immunotherapy combinations. In cabozantinib-treated samples, imaging analysis revealed a significant reduction in vascular density, and single-nucleus RNA sequencing (snRNA-seq) analysis indicated a decreased proportion of endothelial cells in the tumors. SnRNA-seq data further identified a tumor subpopulation enriched with cell-cycle activity that exhibited heightened sensitivity to the cabozantinib and sapanisertib combination. Conversely, activation of the epithelial–mesenchymal transition pathway, detected at the protein level, was associated with drug resistance in residual tumors following combination treatment. The combination effectively restrained ERK phosphorylation and reduced expression of ERK downstream transcription factors and their target genes implicated in cell-cycle control and apoptosis. This study highlights the potential of the cabozantinib plus sapanisertib combination as a promising treatment approach for patients with RCC, particularly those whose tumors progressed on immune checkpoint inhibitors and other TKIs.

Significance::

The molecular-guided therapeutic strategy of combining cabozantinib and sapanisertib restrains ERK activity to effectively suppress growth of renal cell carcinomas, including those unresponsive to immune checkpoint inhibitors.

2023-12-01·Cancer medicine

A phase 2 and pharmacological study of sapanisertib in patients with relapsed and/or refractory acute lymphoblastic leukemia

Article

作者: Al-Kali, Aref ; Shah, Bijal ; Peterson, Kevin L ; Buhrow, Sarah A ; Strand, Carrie A ; Atherton, Pamela J ; Bhatnagar, Bhavana ; Aldoss, Ibrahim ; Kong, Jianping ; Adjei, Alex A ; Schneider, Paula A ; Webster, Jonathan ; Reid, Joel M ; Flatten, Karen S ; Kaufmann, Scott H

Abstract:

Background:

Despite recent approval of several new agents, relapsed acute lymphoblastic leukemia (ALL) remains challenging to treat. Sapanisertib (MLN0128/TAK‐228) is an oral TORC1/2 inhibitor that exhibited preclinical activity against ALL.

Methods:

We conducted a single‐arm multi‐center Phase II study of sapanisertib monotherapy (3 mg orally daily of the milled formulation for 21 days every 28 days) in patients with ALL through the Experimental Therapeutics Clinical Trials Network (NCI‐9775).

Results:

Sixteen patients, 15 of whom were previously treated (median 3 prior lines of therapy), were enrolled. Major grade 3–4 non‐hematologic toxicities included mucositis (3 patients) and hyperglycemia (2 patients) as well as hepatic failure, seizures, confusion, pneumonitis, and anorexia (1 patient each). Grade >2 hematological toxicity included leukopenia (3), lymphopenia (2), thrombocytopenia, and neutropenia (1). The best response was stable disease in 2 patients (12.5%), while only 3 patients (19%) were able to proceed to Cycle 2. Pharmacokinetic analysis demonstrated drug exposures similar to those observed in solid tumor patients. Immunoblotting in serially collected samples indicated limited impact of treatment on phosphorylation of mTOR pathway substrates such as 4EBP1, S6, and AKT.

Conclusion:

In summary, single‐agent sapanisertib had a good safety profile but limited target inhibition or efficacy in ALL as a single agent. This trial was registered at ClinicalTrials.gov as NCT02484430.

2023-11-01·Gynecologic oncology

A randomized phase 2 study of sapanisertib in combination with paclitaxel versus paclitaxel alone in women with advanced, recurrent, or persistent endometrial cancer

Article

作者: Faller, Douglas V ; Han, Sileny N ; Makker, Vicky ; Jewell, Andrea ; Wenham, Robert M ; Alía, Eva María Guerra ; Sedarati, Farhad ; Vincent, Sylvie ; Raspagliesi, Francesco ; Neuwirth, Rachel ; Krell, Jonathan ; Baurain, Jean-François ; Su, Zhenqiang ; Braicu, Elena Ioana ; Oza, Amit ; Oaknin, Ana ; Scambia, Giovanni ; Colombo, Nicoletta

OBJECTIVE:

This phase 2 study investigated sapanisertib (selective dual inhibitor of mTORC1/2) alone, or in combination with paclitaxel or TAK-117 (a selective small molecule inhibitor of PI3K), versus paclitaxel alone in advanced, recurrent, or persistent endometrial cancer.

METHODS:

Patients with histologic diagnosis of endometrial cancer (1-2 prior regimens) were randomized to 28-day cycles on four treatment arms: 1) weekly paclitaxel 80 mg/m² (days 1, 8, and 15); 2) weekly paclitaxel 80 mg/m² + oral sapanisertib 4 mg on days 2-4, 9-11, 16-18, and 23-25; 3) weekly sapanisertib 30 mg, or 4) sapanisertib 4 mg + TAK-117 200 mg on days 1-3, 8-10, 15-17, and 22-24.

RESULTS:

Of 241 patients randomized, 234 received treatment (paclitaxel, n = 87 [3 ongoing]; paclitaxel+sapanisertib, n = 86 [3 ongoing]; sapanisertib, n = 41; sapanisertib+TAK-117, n = 20). The sapanisertib and sapanisertib+TAK-117 arms were closed to enrollment after futility analyses. After a median follow-up of 14.4 (paclitaxel) versus 17.2 (paclitaxel+sapanisertib) months, median progression-free survival (PFS; primary endpoint) was 3.7 versus 5.6 months (hazard ratio [HR] 0.82; 95% confidence interval [CI] 0.58-1.15; p = 0.139); in patients with endometrioid histology (n = 116), median PFS was 3.3 versus 5.7 months (HR 0.66; 95% CI 0.43-1.03). Grade ≥ 3 treatment-emergent adverse event rates were 54.0% with paclitaxel versus 89.5% paclitaxel+sapanisertib.

CONCLUSIONS:

Our findings support inclusion of chemotherapy combinations with investigational agents for advanced or metastatic disease. The primary endpoint was not met and toxicity was manageable.

TRIAL REGISTRATION:

ClinicalTrials.gov number, NCT02725268.

17

项与 Sapanisertib 相关的新闻（医药）

2024-05-30

·BioSpace

Faeth Therapeutics to Participate in Upcoming Jefferies Investor Conference

Faeth’s CEO to showcase how AI has unlocked metabolism as a new cancer treatment paradigm AUSTIN, Texas--(BUSINESS WIRE)-- Faeth Therapeutics, (Faeth) a clinical-stage biotechnology company, announced today that Anand Parikh, Chief Executive Officer (CEO), will participate in one-on-one investor meetings at the upcoming Jefferies Global Healthcare Conference being held June 4-6 in New York. To schedule a meeting at the conference with Faeth’s CEO, please contact bridie@faeththerapeutics.com. For more information about the conference, please contact your institutional sales representative at Jefferies. Founded by renowned oncology researchers including Drs. Lew Cantley, Siddhartha Mukherjee, and Karen Vousden alongside CEO Anand Parikh, Faeth is focused on developing therapies targeting cancer metabolism. The role of metabolism in cancer proliferation is well established, yet remains a vastly under-exploited area, with very few cancer metabolism therapies in existence today. Faeth’s differentiated approach to targeting cancer metabolism leverages a systemic understanding of cancer metabolism, functional genomics, and computational biology to develop effective, less toxic therapies. Faeth has a robust clinical and preclinical pipeline driven by the company’s MetabOS discovery platform, which leverages AI, machine learning, and curated data sets to identify targets matched to specific tumor genotypes. Faeth's lead program, FTH-001/003, or "PIKTOR," includes serabelisib, a PI3Kɑ inhibitor, and sapanisertib, an mTORC 1/2 inhibitor, which together effectively shut down the PI3K pathway, the most commonly mutated pathway in cancer. PIKTOR, together with paclitaxel, has already shown outstanding results in a Phase 1b trial including endometrial, ovarian, and breast cancers. Faeth's second clinical program features FTH-002, a specially formulated amino acid sachet, which is administered in conjunction with an amino acid-restricted regimen and radio/chemotherapy. About Faeth Therapeutics Faeth Therapeutics is a clinical-stage biotechnology company at the forefront of oncology research with a robust clinical and preclinical pipeline powered by its AI-driven MetabOS discovery platform. Faeth’s lead program, PIKTOR, has shown outstanding clinical results in a Phase 1b trial and is advancing into a Phase 2 trial in endometrial cancer in 2024. For additional information, visit .

临床1期临床2期临床结果

2023-11-08

·BioSpace

Faeth Therapeutics to Participate in the Stifel 2023 Healthcare Conference

AUSTIN, Texas--(BUSINESS WIRE)-- Faeth Therapeutics, an oncology company with clinical programs combining therapeutics with metabolic optimization to achieve greater efficacy, today announced that the company will be participating in a company presentation and 1x1 investor meetings at the Stifel 2023 Healthcare Conference, taking place from November 14-15 in New York City. Anand Parikh, J.D., Chief Executive Officer & Co-Founder, Oliver Maddocks, PhD, Head of Research & Co-Founder, and Debbie Chirnomas, MD, Chief Medical Officer, will present a company overview on Wednesday, November 15, at 3:00 pm ET. About Faeth Therapeutics Faeth Therapeutics, headquartered in Austin, TX, is a clinical-stage biotechnology company focused on bringing breakthrough research in metabolic oncology into the clinic. The company leverages its machine-learning platform to develop precision therapies, augmented by a metabolic regimen involving the patient’s diet, to revolutionize the treatment paradigm. Faeth’s lead program combines FTH-001, serabelisib, with FTH-003, sapanisertib, and an insulin suppressing regimen to slow tumor growth by shutting down the PI3K/mTOR pathway. Faeth’s scientific founders include industry leaders Drs. Lew Cantley, Sid Mukherjee, Karen Vousden. For additional information, visit .

2023-07-14

·药智网

2023年抗肿瘤药物新靶点（9个）

在抗肿瘤药物研发中，新靶点的不断涌现，对肿瘤治疗具有重要意义，逐渐实现了精准医疗方法，克服了耐药性，并扩大了治疗领域。本文将盘点一下，过去一年里，新发现的或者具有新适应症的抗肿瘤药物靶点。01胃癌新靶点：claudin-18.2claudin-18.2(CLDN 18.2)是一种在胃粘膜中广泛存在的紧密连接蛋白。在正常情况下，它负责将相邻的胃粘膜上皮细胞牢固地连接在一起，防止胃内的食物和消化液从细胞间隙渗漏到人体内部环境中。然而，在肿瘤发展过程中，CLDN 18.2广泛表达于多种消化道肿瘤中，并参与肿瘤的增殖、分化和迁移等过程。国内外目前已有多款的靶向CLDN 18.2药物在研。Zolbetuximab是首个靶向CLDN 18.2的药物。加入Zolbetuximab与mFLOFOX6联合用药与单独mFLOFOX6化疗相比，晚期胃癌患者的中位无进展生存期延长近2个月，达到10.61个月，中位总生存期从15.54个月延长到18.23个月，患者的死亡风险和进展风险均下降了25%。国内在研的药物包括创胜集团自主研发的TST001和科济药业开发的CAR-T疗法，名为CT041，均取得了积极进展。02肺鳞癌靶点：mTOR非小细胞肺癌一直是靶向治疗的重要领域，目前众多靶向药只能使肺腺癌患者获益，而另一个主要肺癌亚型——肺鳞癌，只有很少一部分患者可以接受靶向治疗。Sapanisertib通过靶向KEAP1/NRF2通路下游的mTOR分子，并在晚期难治性肺鳞癌患者中取得了27%的客观缓解率和中位无进展生存期达到8.9个月。目前，正在进行Sapanisertib联合PD-1治疗晚期NRF2突变肺鳞癌的研究。03前列腺癌新靶点：PI5P4Kα、TRABID、PODXL（1）PI5P4Kα：磷脂酰肌醇激酶家族在肿瘤的发生、发展中发挥着重要作用，是抗肿瘤药物研究的重要靶点。2023年2月1日，一篇发表在Science Advances的文章中，研究人员对磷脂酰肌醇-5-磷酸-4-激酶（PI5P4K）的功能进行了研究，验证了PI5P4Kα亚型对雄激素受体（AR）信号传导的影响，该信号通路对前列腺癌细胞存活起到支持作用。研究表明，雄激素剥夺会影响磷脂酰肌醇的含量，并增加细胞内磷脂酰肌醇（4,5）二磷酸水平，表明磷脂酰肌醇的调节在雄激素剥夺期间前列腺癌代谢应激适应中变得越来越重要。该研究支持将PI5P4Kα作为潜在靶点，以解决前列腺癌治疗中不断增加的抵抗性难题。（2）TRABID：2023年3月31日，发表于Nature Communications一项研究证明了TRABID去泛素化酶可与53BP1结合，并在双链断裂位点上调节53BP1的稳定。前列腺癌细胞中过表达TRABID的情况下，癌细胞对PARP抑制剂表现出高度敏感性。该研究指出，TRABID通过在双链断裂位点上延长53BP1的存在，促进了非同源末端连接修复而非同源重组，这表明TRABID过表达可以用作预测前列腺癌中同源重组缺陷和PARP抑制剂治疗潜力的指标。（3）PODXL：糖萼成分和唾液粘蛋白足萼蛋白（PODXL）是一种跨膜蛋白，其升高的表达与肿瘤的不良临床结果相关。一篇发表于2023年2月3日的Science Advances文章中，报道了PODXL可以作为半乳糖凝集素-3（GAL3）的诱饵受体，从而导致PODXL-GAL3相互作用的释放。通过实验，研究人员确定了控制PODXL转变为促转移糖萼成分的分子机制，并揭示了PODXL作为诱饵受体可以减轻GAL3的侵袭抑制作用。研究证明这种水平的变化可以用于识别具有高度转移和预后不良的前列腺癌患者。04肝癌新靶点：SULT1A1、PRRS35（1）SULT1A1：今年3月13日发表于Nature Cancer的一篇文章介绍了成人肝脏恶性肿瘤（包括肝内胆管癌和肝细胞癌）的研究成果。这种肿瘤是全球癌症相关死亡的第二大原因。该研究中，通过高通量筛选、蛋白质组学和体外耐药模型，研究人员确定了一种名为YC-1的小分子化合物，对来自两种肝癌类型的细胞系亚群具有选择性活性。研究数据证明，这种选择性活性与肝脏固有的胞质磺基转移酶SULT1A1的表达有关。通过计算分析，研究人员还发现了一类更广泛依赖于SULT1A1的抗癌化合物。这项研究表明，SULT1A1有可能成为肝癌药物开发的潜在新靶点。（2）PRRS35：肝细胞癌进展过程中，肝细胞分泌蛋白组会发生动态变化，这不仅是肿瘤发生的结果，也是导致肿瘤发展的致病因素之一。最近发表于Nature Communications的一篇文章揭示了肝细胞癌中蛋白酶PRSS35的肿瘤抑制作用。研究表明，活性的PRSS35可以抑制CXCL2的蛋白质水平，进而抑制肝细胞癌的进展。该研究扩展了我们对肝细胞分泌蛋白在癌症发展中作用的认识，并为将PRSS35作为治疗靶点或诊断生物标志物进行临床转化提供了基础。05胰腺癌靶点：RBFOX2胰腺导管腺癌（PDAC）是一种具有高度侵袭性和强大转移能力的恶性肿瘤。目前，尚不清楚导致PDAC转移的驱动基因突变是什么。最近发表在Nature期刊上的一篇研究表明，在源自患者异种移植（PDX）的转移性PDAC细胞系中，过表达RBFOX2基因会显著降低这些细胞的体外和体内转移能力。相反，在原发性胰腺肿瘤细胞系中，RBFOX2基因的耗竭则增加了这些细胞的转移潜力。这些发现表明RBFOX2可能在抑制PDAC转移方面具有潜在作用。该研究为深入了解PDAC的转移机制提供了重要线索，并为利用RBFOX2基因的剪接调控作为PDAC的潜在治疗策略奠定了基础。06胶质母细胞瘤靶点：FGL2纤维蛋白原样2（FGL2）在病毒感染和癌症发展中具有凝血酶原酶活性和免疫调节功能。研究表明，表达FGL2特异性单链可变片段（T-αFGL2）的T细胞可以诱导肿瘤特异性CD8+组织驻留记忆T（TRM）细胞，从而防止胶质母细胞瘤复发。这些CD8+TRM细胞展现出扩展的T细胞受体库，并能够排斥神经胶质瘤细胞。通过增加特定信号分子的数量，T-αFGL2细胞治疗有望增加CD69+CD8+脑驻留记忆T细胞的数量，对预防胶质母细胞瘤复发具有重要意义。因此，FGL2被认为是胶质母细胞瘤免疫治疗中一个有吸引力的靶点。小结以上是今年在多种癌症中具有重要意义的新靶点，除此之外，在其他肿瘤治疗方面，也有新靶点的应用，比如在2023年的ASCO大会上，来自梅奥医学中心Christina Wu教授，对结直肠癌（CRC）中四个新型治疗靶点，包括HER2扩增、KRAS G12C突变、NTRK融合和RET融合进行了重要的临床研究总结和报告；ADC药物方面，也有众多靶点被运用，比如FolRa、TROP2、ITGB6等。药物的新靶点的鉴别，对推进癌症治疗具有重要意义，为克服抗药性的、实现了精准医疗提供了新的选择。这一领域的持续研究和创新将有助于为癌症患者提供更有效、更有针对性和个性化的治疗，最终改善患者的治疗效果和生活质量。声明：本内容为作者独立观点，不代表药智网立场。如需转载，请务必注明文章作者和来源。对本文有异议或投诉，请联系maxuelian@yaozh.com。责任编辑 | 八角转载开白 | 马老师 18996384680（同微信）商务合作 | 张武龙 13368443108（同微信）阅读原文，是昨天最受欢迎的文章哦

免疫疗法细胞疗法临床研究

100 项与 Sapanisertib 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
转移性非小细胞肺癌	临床2期	-	National Cancer Institute	2021-02-18
复发性非小细胞肺癌	临床2期	-	National Cancer Institute	2021-02-18
癌肉瘤	临床2期	德国	Takeda Pharmaceuticals International, Inc.	2018-09-21
癌肉瘤	临床2期	英国	Takeda Pharmaceuticals International, Inc.	2018-09-21
卵巢子宫内膜样癌	临床2期	德国	Takeda Pharmaceuticals International, Inc.	2018-09-21
卵巢子宫内膜样癌	临床2期	英国	Takeda Pharmaceuticals International, Inc.	2018-09-21
输卵管癌	临床2期	德国	Takeda Pharmaceuticals International, Inc.	2018-09-21
输卵管癌	临床2期	英国	Takeda Pharmaceuticals International, Inc.	2018-09-21
卵巢癌肉瘤	临床2期	德国	Takeda Pharmaceuticals International, Inc.	2018-09-21
卵巢癌肉瘤	临床2期	英国	Takeda Pharmaceuticals International, Inc.	2018-09-21

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适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03193853 (CTgov)	临床2期	转移性三阴性乳腺癌	12	Nab Paclitaxel+Cisplatin+Tak-117+Tak-228	遞獵醖襯廠觸襯選構範(觸醖遞糧獵蓋壓顧製願) = 繭鬱壓蓋網製鹽壓夢窪廠築糧鬱鑰製糧鹹艱獵 (製艱糧繭艱構顧選鹽夢, 窪齋鏇鹹繭構餘積顧鏇 ~ 範構築範選鹽夢廠鑰網) 更多	-	2023-05-09
NCT02893930 (ECOG-ACRIN EA2161, Pubmed) 人工标引	临床2期	高分化胰腺内分泌肿瘤	13	Sapanisertib	膚範選觸構鬱壓鏇憲糧(壓鑰齋顧鹹製鹹醖鏇構) = 繭構衊繭鬱鏇網鬱廠範遞願醖簾簾製壓艱衊獵 (鹹壓壓憲鹹範簾餘築遞 ) 更多	不佳	2022-10-20
NCT03154294 (Pubmed)	临床1期	HR阳性/HER2低表达实体瘤	19	Sapanisertib 3 or 4 mg + Serabelisib 200 mg + Paclitaxel 80 mg/m2	醖齋廠顧膚憲選製膚鑰(餘繭壓鏇廠構鏇鬱顧範) = 9% 獵繭淵憲積餘襯窪範範 (膚夢顧鬱蓋鏇蓋淵繭遞 ) 更多	积极	2022-07-14
NCT02484430 (CTgov)	临床2期	复发性成人急性淋巴细胞白血病 \| 前体T淋巴细胞白血病淋巴瘤 \| 费城染色体阴性急性淋巴细胞白血病 ... 更多	16	Pharmacological Study+Sapanisertib	糧鬱製齋觸蓋襯餘簾窪(窪簾艱窪鑰膚衊壓鹹鹹) = 鏇淵積齋鑰廠鑰夢蓋窪觸鏇餘夢鑰遞遞廠醖夢 (構遞構選壓襯顧淵繭製, 窪觸齋鑰襯淵鏇艱廠觸 ~ 糧鏇網顧衊醖蓋願鑰醖) 更多	-	2022-05-24
NCT02893930 (ECOG-ACRIN EA2161, CTgov)	临床2期	高分化胰腺内分泌肿瘤 \| 晚期胰腺神经内分泌肿瘤 \| 胰腺神经内分泌肿瘤转移 ... 更多	13	MLN0128	壓襯鹹顧觸餘淵壓襯網(網膚壓鹽積蓋夢網餘構) = 鹹蓋鹽壓顧夢糧糧鬱鏇壓壓窪廠壓築衊襯醖製 (鑰鏇餘鏇簾鏇艱蓋衊壓, 顧艱願醖蓋廠蓋獵膚簾 ~ 醖鏇鏇衊網鹽構鏇壓簾) 更多	-	2022-04-05
NCT02417701 (CTgov)	临床2期	晚期非小细胞肺癌 \| 复发性鳞状细胞肺癌 \| 复发性肺癌 ... 更多	34	Pharmacological Study+Sapanisertib	顧艱窪構窪遞積糧艱襯(觸鏇淵簾願鑰襯淵餘鹹) = 顧鹽簾憲窪願壓鬱蓋範壓壓窪遞糧襯網構衊襯 (鬱鹽繭齋顧齋鬱遞襯襯, 艱憲範糧襯衊獵遞膚鏇 ~ 襯齋簾壓夢願醖鬱獵夢) 更多	-	2022-04-05
NCT03097328 (CTgov)	临床2期	转移性肾细胞癌	39	TAK-228	齋鬱鹹夢鏇餘壓積齋鑰(遞觸範製窪簾憲醖窪鏇) = 選網鑰餘糧夢膚簾製膚網構觸齋鹹廠憲構遞夢 (構淵鏇網網醖遞襯蓋顧, 鑰獵鹽鹽構鹽顧醖選壓 ~ 獵積鑰醖積艱簾構製網) 更多	-	2022-02-24
NCT03097328 (Pubmed \| JCO Precis Oncol)	临床2期	转移性肾细胞癌	38	Sapanisertib 30 mg	壓顧築繭鬱簾糧製繭鹹(築獵壓鑰鑰繭顧鏇憲繭) = 鑰齋襯簾醖範窪網獵製遞鹽夢鹽餘夢鏇築顧選 (繭繭鑰願積選鏇淵膚艱, 1 ~ 15.6) 更多	不佳	2022-02-01
NCT02719691 (CTgov)	临床1期	晚期恶性实体瘤 \| 转移性乳腺癌 \| 转移性三阴性乳腺癌	47	Alisertib+MLN0128 (Dose Level 4: Alisertib 40 mg/MLN0128 3 mg)	鏇醖餘製鹹憲衊壓鬱繭(齋觸鹹憲憲構醖選築獵) = 蓋簾築鹽製鹽淵獵鑰範壓築餘鬱構艱醖鏇簾艱 (鬱鹽蓋艱鹽夢鏇窪齋繭, 製網積鬱鹹製壓糧遞鑰 ~ 簾觸築窪醖願壓範夢積) 更多	-	2022-01-19
NCT02719691 (CTgov)	临床1期	晚期恶性实体瘤 \| 转移性乳腺癌 \| 转移性三阴性乳腺癌	47	Alisertib+MLN0128 (Pancreatic Cohort)	製製願齋範築觸繭壓觸(衊艱鏇獵艱築鏇願鏇獵) = 願憲選壓鏇網餘獵淵襯襯簾觸製願鑰廠壓夢憲 (獵網鏇範齋鹽鹹窪窪構, 觸窪淵窪蓋齋範選願壓 ~ 餘鏇觸築膚選範鑰糧糧) 更多	-	2022-01-19
NCT03370302 (Pubmed) 人工标引	临床1期	血液肿瘤	28	Sapanisertib (QD dosing)	淵醖鏇齋簾廠構醖鏇願(蓋廠選淵餘鹽網糧鹹遞) = 觸窪選艱鏇製鑰顧憲積壓醖觸鑰網齋夢淵積窪 (構餘構憲蓋膚襯蓋餘蓋 ) 更多	不佳	2021-11-29
NCT03370302 (Pubmed) 人工标引	临床1期	血液肿瘤	28	Sapanisertib (QW dosing)	糧簾壓繭壓襯餘膚繭衊(獵淵憲鹽廠築夢鏇夢網) = 蓋積襯膚鹹鏇襯壓壓積膚築餘廠顧鑰製膚觸憲 (憲餘繭繭鬱艱鹽夢憲憲 ) 更多	不佳	2021-11-29