Sapanisertib(Sapanisertib) - 药物靶点：mTORC1 x mTORC2_在研适应症：子宫内膜癌，癌肉瘤，卵巢子宫内膜样癌_专利_临床

概要

基本信息

药物类型

小分子化药

别名

MLN0128、Sapanisertib (USAN/INN)

+ [7]

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

子宫内膜癌癌肉瘤卵巢子宫内膜样癌+ [53]

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+ [28]

原研机构

Takeda Pharmaceutical Co., Ltd.

在研机构

National Cancer InstituteTakeda Pharmaceuticals International, Inc.

Takeda Pharmaceutical Co., Ltd.

+ [4]

非在研机构

Pivotal SL

Millennium Pharmaceuticals, Inc.

Dartmouth-Hitchcock Medical Center

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评快速通道 (美国)

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结构

分子式C15H15N7O

InChIKeyGYLDXIAOMVERTK-UHFFFAOYSA-N

CAS号1224844-38-5

关联

48

项与 Sapanisertib 相关的临床试验

NCT06463028 / Not yet recruiting临床2期

An Open-label, Multi-Center, Phase 2 Clinical Trial Evaluating Sapanisertib and Serabelisib (PIKTOR) With Paclitaxel, and a Substudy Evaluating PIKTOR With Paclitaxel Plus Diet, in Patients With Advanced or Recurrent Endometrial Cancer

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

开始日期2024-12-31

申办/合作机构

Faeth Therapeutics, Inc.初创企业

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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187

项与 Sapanisertib 相关的文献（医药）

2024-10-01·Clinical Genitourinary Cancer

Dual mTOR1/2 Inhibitor Sapanisertib (FTH-003/TAK-228) in Combination With Weekly Paclitaxel in Patients With Previously Treated Metastatic Urothelial Carcinoma: A Phase II Open-Label Study

Article

作者: Juan, Oscar ; Juanpere, Nuria ; Rodriguez-Vida, Alejo ; Vazquez, Federico ; Bellmunt, Joaquim ; Maroto, Pablo ; Perez-Gracia, Jose Luis ; Hernandez-Prat, Anna ; Bonfill, Teresa ; Hernandez-Llodra, Silvia ; Rovira, Ana

BACKGROUNDThe PI3K/AKT/mTOR pathway is frequently altered at genomic level in metastatic urothelial carcinoma (mUC). Since mTOR is the last protein in the PI3K signaling cascade, it may have the largest impact on the pathway and has been a focus of targeted therapies. Sapanisertib (FTH-003/TAK-228) is an oral highly selective mTOR1 and mTOR2 inhibitor. NFE2L2 mutations have been described as predictive biomarkers of response in patients with advanced squamous cell lung cancer treated with sapanisertib.PATIENTS AND METHODSThis was an open-label, investigator-initiated phase II study evaluating safety and efficacy of sapanisertib plus paclitaxel in patients with mUC who had progressed to prior platinum therapy, and the correlation with NFE2L2 mutations in responders. Primary endpoint was objective response rate (ORR). Secondary endpoints included progression-free survival (PFS), overall survival (OS) and safety. Patients were treated with weekly paclitaxel at dose of 80 mg/m² on days 1, 8, and 15 in combination with sapanisertib 4 mg administered orally 3 days per week on days 2-4, 9-11, 16-18, and 23-25 of a 28-day cycle. NFE2L2 mutations were analyzed by Sanger sequencing in responders.RESULTS22 patients were enrolled from May 2018 to April 2020; the trial was halted early due to slow accrual and the COVID-19 pandemic. ORR was 18.2% (n = 4). Disease control rate was 50% (7 SD and 4 PR). Median PFS was 3.4 months (95% CI: 1.8-6.1) and median OS was 6.1 months (95% CI: 1.8-13.4). Adverse events (AE) of grade 3-4 were seen in 86% of patients, but no patients discontinued treatment due to AEs. NFE2L2 mutations were not found in responders.CONCLUSIONSAlthough the primary endpoint was no met, sapanisertib and paclitaxel combination demonstrated clinical activity in a heavily pretreated population of mUC. This trial generates insight for future combination of sapaniserib with immunotherapy and/or antibody drug conjugates.

2024-07-15·AIDS

Differential susceptibility of cells infected with defective and intact HIV proviruses to killing by obatoclax and other small molecules

Article

作者: Janssens, Julie ; Telwatte, Sushama ; Wedrychowski, Adam ; Kadiyala, Gayatri Nikhila ; Kim, Sun Jin ; Yukl, Steven A. ; Kim, Peggy ; Wong, Joseph K. ; Deeks, Steven

Objectives:Some drugs that augment cell-intrinsic defenses or modulate cell death/survival pathways have been reported to selectively kill cells infected with HIV or Simian Immunodeficiency Virus (SIV), but comparative studies are lacking. We hypothesized that these drugs may differ in their ability to kill cells infected with intact and defective proviruses.Design:To investigate this hypothesis, drugs were tested ex vivo on peripheral blood mononuclear cells (PBMC) from nine antiretroviral therapy (ART)-suppressed individuals.Methods:We tested drugs currently in clinical use or human trials, including auranofin (p53 modulator), interferon alpha2A, interferon gamma, acitretin (RIG-I inducer), GS-9620/vesatolimod (TLR7 agonist), nivolumab (PD-1 blocker), obatoclax (Bcl-2 inhibitor), birinapant [inhibitor of apoptosis proteins (IAP) inhibitor], bortezomib (proteasome inhibitor), and INK128/sapanisertib [mammalian target of rapamycin mTOR] [c]1/2 inhibitor). After 6 days of treatment, we measured cell counts/viabilities and quantified levels of total, intact, and defective HIV DNA by droplet digital PCR (Intact Proviral DNA Assay).Results:Obatoclax reduced intact HIV DNA [median = 27–30% of dimethyl sulfoxide control (DMSO)] but not defective or total HIV DNA. Other drugs showed no statistically significant effects.Conclusion:Obatoclax and other Bcl-2 inhibitors deserve further study in combination therapies aimed at reducing the intact HIV reservoir in order to achieve a functional cure and/or reduce HIV-associated immune activation.

2024-05-01·Translational Oncology

The highly selective and oral phosphoinositide 3-kinase delta (PI3K-δ) inhibitor roginolisib induces apoptosis in mesothelioma cells and increases immune effector cell composition

Article

作者: Finotello, Francesca ; Kalla, Claudia ; van der Veen, Lars ; Lahn, Michael ; Falkenstern-Ge, Roger ; Ott, German ; Kopecka, Joanna ; Riganti, Chiara ; Conza, Giusy Di ; Niewola-Staszkowska, Karolina ; Schüler, Julia

Targeting aberrantly expressed kinases in malignant pleural mesothelioma (MPM) is a promising therapeutic strategy. We here investigated the effect of the novel and highly selective Phosphoinositide 3-kinase delta (PI3K-δ) inhibitor roginolisib (IOA-244) on MPM cells and on the immune cells in MPM microenvironment. To this aim, we analyzed the expression of PI3K-δ by immunohistochemistry in specimens from primary MPM, cell viability and death in three different MPM cell lines treated with roginolisib alone and in combination with ipatasertib (AKT inhibitor) and sapanisertib (mTOR inhibitor). In a co-culture model of patient-derived MPM cells, autologous peripheral blood mononuclear cells and fibroblasts, the tumor cell viability and changes in immune cell composition were investigated after treatment of roginolisib with nivolumab and cisplatin. PI3K-δ was detected in 66/89 (74%) MPM tumors and was associated with reduced overall survival (12 vs. 25 months, P=0.0452). Roginolisib induced apoptosis in MPM cells and enhanced the anti-tumor efficacy of AKT and mTOR kinase inhibitors by suppressing PI3K-δ/AKT/mTOR and ERK1/2 signaling. Furthermore, the combination of roginolisib with chemotherapy and immunotherapy re-balanced the immune cell composition, increasing effector T-cells and reducing immune suppressive cells. Overall, roginolisib induces apoptosis in MPM cells and increases the antitumor immune cell effector function when combined with nivolumab and cisplatin. These results provide first insights on the potential of roginolisib as a therapeutic agent in patients with MPM and its potential in combination with established immunotherapy regimen.

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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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
肝癌	临床2期	-	Takeda Pharmaceutical Co., Ltd.	-
甲状腺癌	临床2期	-	Takeda Pharmaceutical Co., Ltd.	-
ER阳性/HER2阴性乳腺癌	临床1期	法国	Calithera Biosciences, Inc.	2014-02-13
ER阳性/HER2阴性乳腺癌	临床1期	美国	Calithera Biosciences, Inc.	2014-02-13
ER阳性/HER2阴性乳腺癌	临床1期	比利时	Calithera Biosciences, Inc.	2014-02-13
BRAF V600E 突变阳性甲状腺未分化癌	临床前	美国	Dana-Farber Cancer Institute, Inc.	2015-07-01
BRAF V600E 突变阳性甲状腺未分化癌	临床前	美国	Millennium Pharmaceuticals, Inc.	2015-07-01
ER阳性/HER2阴性乳腺癌	临床前	美国	Calithera Biosciences, Inc.	2014-02-13
ER阳性/HER2阴性乳腺癌	临床前	比利时	Calithera Biosciences, Inc.	2014-02-13
ER阳性/HER2阴性乳腺癌	临床前	法国	Calithera Biosciences, Inc.	2014-02-13

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临床结果

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


NCT03154294 (CTgov)	临床1期	晚期恶性实体瘤	19	paclitaxel+TAK-117+TAK-228 (Cohort 1)	鏇範鏇齋網醖夢糧築選(艱艱構窪鏇鹽製繭衊範) = 鏇窪襯糧夢襯鏇遞淵鏇壓遞衊糧蓋夢艱淵襯淵 (膚鹹壓遞網窪選遞積獵, 夢鹹衊餘觸鏇壓鑰糧簾 ~ 鏇蓋選餘顧醖鬱壓衊齋) 更多	-	2024-07-26
NCT03154294 (CTgov)	临床1期	晚期恶性实体瘤	19	paclitaxel+TAK-117+TAK-228 (Cohort 2)	鏇範鏇齋網醖夢糧築選(艱艱構窪鏇鹽製繭衊範) = 淵製襯簾網獵觸顧廠遞壓遞衊糧蓋夢艱淵襯淵 (膚鹹壓遞網窪選遞積獵, 糧鹽憲構構壓簾餘鬱積 ~ 選壓鹹築蓋襯廠艱糧壓) 更多	-	2024-07-26
NCT02244463 (phase I/II trial of sapanisertib, Pubmed)	临床1/2期	分化型甲状腺癌 PI3 K/AKT/mTOR pathway	46	Sapanisertib 5 mg	構鹹壓鏇衊壓積簾積鹽(範壓顧糧糧艱鹽廠遞襯) = 鬱製膚夢觸壓選餘艱鏇觸廠鬱壓顧壓膚構鹹糧 (窪鹹壓範壓憲壓範蓋遞 ) 更多	不佳	2024-06-29
NCT02244463 (phase I/II trial of sapanisertib, Pubmed)	临床1/2期	分化型甲状腺癌 PI3 K/AKT/mTOR pathway	46	Placebo	積鬱獵鹹繭願鹹蓋鬱夢(鑰襯鬱製醖築壓選鬱醖) = 窪遞糧鑰齋鹽簾夢膚糧膚簾糧範遞鏇鬱鑰構觸 (繭壓鑰鏇壓憲範艱襯範 ) 更多	不佳	2024-06-29
NCT02484430 (NCI-9775, Pubmed \| Cancer Med)	临床2期	-	-	Sapanisertib 3 mg	範淵鏇願窪網觸鑰顧網(鹽艱築網壓鬱醖顧鑰鏇) = 1 patient 醖鏇壓簾襯繭積鑰醖鏇 (鬱築願鑰築壓選積衊顧 ) 更多	不佳	2023-12-01
NCT02725268 (phase 2 study of sapanisertib in combination with paclitaxel versus paclitaxel alone in women with advanced, recurrent, or persistent endometrial cancer, Pubmed \| Gynecol Oncol)	临床2期	子宫内膜癌	241	Paclitaxel	(夢糧淵願淵製積築鬱艱) = 遞廠齋鏇淵憲齋鏇壓網醖餘糧鹹觸鹽淵齋壓鹽 (築鹹襯積齋顧壓淵餘簾 )	不佳	2023-11-01
	临床2期	子宫内膜癌	241	Paclitaxel + Sapanisertib	(夢糧淵願淵製積築鬱艱) = 鹽範築窪淵窪鏇醖醖醖醖餘糧鹹觸鹽淵齋壓鹽 (築鹹襯積齋顧壓淵餘簾 )	不佳	2023-11-01
NCT03193853 (CTgov)	临床2期	转移性三阴性乳腺癌	12	Nab Paclitaxel+Cisplatin+Tak-117+Tak-228	(範醖鑰襯蓋夢簾選鹽醖) = 餘憲構廠觸築鹹艱鑰選衊糧窪蓋鑰鹹鹹鏇膚餘 (廠夢夢積艱繭膚艱網齋, 選鑰顧齋艱廠顧鑰範顧 ~ 糧衊繭鑰襯願壓衊餘觸) 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	(範鹽齋襯鬱簾鏇觸淵鬱) = 齋衊鑰製壓齋鹹網鑰艱願齋襯築齋淵廠遞繭襯 (夢廠鹽夢蓋鏇齋鑰壓糧 ) 更多	不佳	2022-10-20
SGO	N/A	晚期癌症	-	Sapanisertib (TAK-228) and Serabelisib (TAK-117) with Paclitaxel	窪網膚遞艱獵鑰鏇憲夢(鏇艱遞蓋網製衊齋糧憲) = 45 (9%) grade 3 or 4 events 製積築觸蓋餘糧選窪膚 (齋衊築鏇鑰願鏇膚製網 ) 更多	-	2022-08-01
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	(製糧淵齋顧鏇獵艱鏇獵) = 9% 艱鏇齋齋鏇觸襯選願餘 (糧築醖襯壓範積憲蓋網 ) 更多	积极	2022-07-14
NCT04479306 (ASCO2022)	临床1期	复发性非小细胞肺癌	40	Osimertinib 80 mg daily + Alisertib 20 mg, 30 mg, and 40 mg daily	(築鬱鹽鹽蓋簾醖衊鬱鏇) = Biomarker analysis is ongoing to identify the molecular determinants of response and resistance to sapasertib 膚餘願衊鏇衊繭遞築夢 (遞顧網範膚鹹遞築鹽憲 ) 更多	-	2022-06-02
NCT04479306 (ASCO2022)	临床1期	复发性非小细胞肺癌	40	Osimertinib 80 mg daily + Sapanisertib 2 mg and 3 mg daily		-	2022-06-02
NCT02719691 (ASCO2022)	临床1期	HR阳性/HER2低表达实体瘤	31	Alisertib + MLN0128	(憲淵網範築積糧壓醖襯) = mucositis, fatigue, hyperglycemia and neutropenia reported as most common 鏇膚範構選構範壓觸憲 (鹹襯艱糧範蓋選鬱築鏇 )	-	2022-06-02