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]

NCT04250545 / Recruiting临床1期IIT

A Phase 1 Trial of MLN0128 (Sapanisertib) and CB-839 HCl (Telaglenastat) in Advanced NSCLC Patients

This phase I/Ib trial studies the side effects and best dose of CB-839 HCl when given together with sapanisertib in treating patients with non-small cell lung cancer that has spread to other places in the body (advanced). CB-839 HCl and sapanisertib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

开始日期2020-10-26

申办/合作机构

National Cancer Institute

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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181

项与 Sapanisertib 相关的文献（医药）

2024-02-06·Cells

Different Impacts of DNA-PK and mTOR Kinase Inhibitors in Combination with Ionizing Radiation on HNSCC and Normal Tissue Cells.

Article

作者: Nina Klieber ; Laura S Hildebrand ; Eva Faulhaber ; Julia Symank ; Nicole Häck ; Annamaria Härtl ; Rainer Fietkau ; Luitpold V Distel

Despite substantial advancements in understanding the pathomechanisms of head and neck squamous cell carcinoma (HNSCC), effective therapy remains challenging. The application of kinase inhibitors (KIs) in HNSCC, specifically mTOR and DNA-PK inhibitors, can increase radiosensitivity and therefore presents a promising strategy when used simultaneously with ionizing radiation (IR) in cancer treatment. Our study focused on the selective DNA-PK-inhibitor AZD7648; the selective mTOR-inhibitor Sapanisertib; and CC-115, a dual inhibitor targeting both mTOR and DNA-PK. The impact of these KIs on HNSCC and normal tissue cells was assessed using various analytical methods including cell death studies, cell cycle analysis, real-time microscopy, colony-forming assays and immunohistochemical staining for γH2AX and downstream mTOR protein p-S6. We detected a strong inhibition of IR-induced DNA double-strand break (DSB) repair, particularly in AZD7648-treated HNSCC, whereas normal tissue cells repaired DNA DSB more efficiently. Additionally, AZD7648 + IR treatment showed a synergistic decline in cell proliferation and clonogenicity, along with an elevated G2/M arrest and cell death in the majority of HNSCC cell lines. CC-115 + IR treatment led to an elevation in G2/M arrest, increased cell death, and a synergistic reduction in cell proliferation, though the effect was notably lower compared to the AZD7648 + IR- treated group. Sapanisertib led to a high cellular toxicity in both HNSCC and normal tissue cells, even in non-irradiated cells. Regarding cell proliferation and the induction of apoptosis and necrosis, Sapanisertib + IR was beneficial only in HPV⁺ HNSCC. Overall, this study highlights the potential of AZD7648 as a radiosensitizing agent in advanced-stage HPV-positive and negative HNSCC, offering a promising therapeutic strategy. However, the dual mTOR/DNA-PK-I CC-115 did not provide a distinct advantage over the use of selective KIs in our investigations, suggesting limited benefits for its application in KI + IR therapy. Notably, the selective mTOR-inhibitor Sapanisertib was only beneficial in HPV⁺ HNSCC and should not be applied in HPV^- cases.

2024-02-01·Cancer medicine

Phase I study of sapanisertib (CB-228/TAK-228/MLN0128) in combination with ziv-aflibercept in patients with advanced solid tumors.

Article

作者: Niamh Coleman ; Bettzy Stephen ; Siqing Fu ; Daniel Karp ; Vivek Subbiah ; Jordi Rodon Ahnert ; Sarina A Piha-Paul ; John Wright ; Senait N Fessahaye ; Fengying Ouyang ; Bulent Yilmaz ; Funda Meric-Bernstam ; Aung Naing

BACKGROUND:

Sapanisertib is a potent ATP-competitive, dual inhibitor of mTORC1/2. Ziv-aflibercept is a recombinant fusion protein comprising human VEGF receptor extracellular domains fused to human immunoglobulin G1. HIF-1α inhibition in combination with anti-angiogenic therapy is a promising anti-tumor strategy. This Phase 1 dose-escalation/expansion study assessed safety/ tolerability of sapanisertib in combination with ziv-aflibercept in advanced solid tumors.

METHODS:

Fifty-five patients with heavily pre-treated advanced metastatic solid tumors resistant or refractory to standard treatment received treatment on a range of dose levels.

RESULTS:

Fifty-five patients were enrolled and treated across a range of dose levels. Forty were female (73%), median age was 62 (range: 21-79), and ECOG PS was 0 (9, 16%) or 1 (46, 84%). Most common tumor types included ovarian (8), colorectal (8), sarcoma (8), breast (3), cervical (4), and endometrial (4). Median number of prior lines of therapy was 4 (range 2-11). Sapanisertib 4 mg orally 3 days on and 4 days off plus 3 mg/kg ziv-aflibercept IV every 2 weeks on a 28-day cycle was defined as the maximum tolerated dose. Most frequent treatment-related grade ≥2 adverse events included hypertension, fatigue, anorexia, hypertriglyceridemia, diarrhea, nausea, mucositis, and serum lipase increase. There were no grade 5 events. In patients with evaluable disease (n = 50), 37 patients (74%) achieved stable disease (SD) as best response, two patients (4%) achieved a confirmed partial response (PR); disease control rate (DCR) (CR + SD + PR) was 78%.

CONCLUSION:

The combination of sapanisertib and ziv-aflibercept was generally tolerable and demonstrated anti-tumor activity in heavily pre-treated patients with advanced malignancies.

2023-12-21·Cancer research communications

Phase I study of mTORC1/2 inhibitor sapanisertib in combination with metformin in patients with mTOR/AKT/PI3K pathway alterations and advanced solid malignancies.

Article

作者: Vivek Subbiah ; Niamh Coleman ; Sarina A Piha-Paul ; Apostolia M Tsimberidou ; Filip Janku ; Jordi Rodon ; Shubham Pant ; Ecaterina E Dumbrava ; Siqing Fu ; David S Hong ; Shizhen Zhang ; Ming Sun ; Yunfang Jiang ; Jason Roszik ; Juhee Song ; Ying Yuan ; Funda Meric-Bernstam ; Aung Naing

BACKGROUND:

Sapanisertib (CB-228/TAK-228) is a potent, selective ATP-competitive, dual inhibitor of mTORC1/2. We report preliminary safety, and efficacy of sapanisertib in combination with metformin.

METHODS:

Patients with advanced metastatic solid tumors refractory to standard treatment, with/without mTOR/AKT/PI3Kpathway alterations, received sapanisertib 3mg or 4mg daily together with metformin once to three times daily (500mg - 1500mg).

RESULTS:

30 pts were enrolled across 4 cohorts (3mg/500mg; 3mg/1000mg, 4mg/1000mg; 4mg/1500mg). 19 were female (63%), median age was 57 (range: 30-77). Tumor types included sarcoma (6), breast (4), ovarian (4) among others. Most common genomic alterations included PIK3CA (27%), PTEN(17%), AKT1/2 (10%), mTOR (10%). Of 30 pts evaluable for response, 4 pts achieved partial response (PR); 15 pts achieved stable disease (SD) as best response. Disease control rate (PR+SD) was 63%. Of the responders in PR, 3/4pts had documented PTEN mutations (3/5 pts enrolled with PTEN mutations had PR); 2/4 of pts in PR had co-mutations (pt with leiomyosarcoma had both PTEN and TSC; pt with breast cancer had both PTEN and STK11); 1/4 pts in PR had AKT and mTOR mutation. Grade (G) 3-5 treatment-related adverse events included hyperglycemia (4/30; 13%) fatigue (2/30; 7%) hypertriglyceridemia (1/30; 3%) rash (2/20; 7%), diarrhea (2/30; 7%), creatinine increase (1/30; 3%), acidosis (1/30; 3%). 4mg/1000mg was defined as the maximum tolerated dose.

CONCLUSIONS:

The safety profile of mTORC1/2 inhibitor sapanisertib in combination with metformin was generally tolerable, with anti-tumor activity observed in patients with advanced malignancies harboring PTEN/ AKT/mTOR pathway alterations.

项与 Sapanisertib 相关的新闻（医药）

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

2023-01-10

·FierceBiotech

Cash-strapped Calithera closes down in shadow of enrollment delays to cancer trials

"We truly wish the outcome was different today,” Calithera Biosciences CEO Susan Molineaux, Ph.D., said in a release. Calithera Biosciences has kept its head down since a phase 2 fail in 2021 caused layoffs for a third of its workforce. But in the wake of enrollment delays for two lead cancer therapies, the cash-strapped biotech has given up the fight and announced it’s liquidating the business. “The board of directors and management devoted substantial time and effort in identifying and pursuing various opportunities, but we were unable to complete a transaction that would allow us to continue the development of our clinical programs and enhance shareholder value,” CEO Susan Molineaux, Ph.D., said in a release Monday. As a result, all clinical programs will be shut down, with “most” of the company’s employees terminated by the end of this quarter. “Importantly, I would like to sincerely thank our employees and others who have supported Calithera over the years,” Molineaux added in her statement yesterday. “We appreciate your partnership and participation, and we truly wish the outcome was different today.” Money had been tight at the biotech for a while. Calithera had cash and equivalents of $34.1 million at the end of September, which was only expected to last into the second quarter of this year. In November, the company revealed it was “evaluating all options for its programs, including strategic collaboration or licensing agreements and actively considering the sale of certain programs, in order to extend its cash runway.” It can’t have helped that things weren’t quite going to plan for its lead programs, either. Calithera also used its November financial report to reveal that “site activation delays” meant that enrollment for trials of sapanisertib and mivavotinib had been “slower than anticipated.” Still, the company said at the time that initial data from these studies were expected in mid-2023, with sapanisertib having secured an FDA fast-track tag for non-small cell lung cancer in October. The biotech licensed both drugs from Takeda in 2021 after the failure of its own drug telaglenastat in a midstage kidney cancer test prompted Calithera to wield the ax on 35% of staff. Calithera's announcement is just the latest in a string of recent closures for struggling biotechs, with Otonomy winding down in December, followed by Nabriva Therapeutics last week.

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100 项与 Sapanisertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11183	-	-	DB11836

研发状态

适应症	最高研发状态	国家/地区	公司
卵巢癌肉瘤	临床2期	德国更多	Takeda Pharmaceuticals International, Inc. 更多
癌肉瘤	临床2期	英国更多	Takeda Pharmaceuticals International, Inc. 更多
卵巢子宫内膜样癌	临床2期	英国更多	Takeda Pharmaceuticals International, Inc. 更多
鳞状非小细胞肺癌	临床2期	美国更多	Calithera Biosciences, Inc. 更多
卵巢癌	临床2期	英国更多	Takeda Pharmaceutical Co., Ltd. 更多

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临床结果

适应症

分期

评价

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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


NCT02725268 (ASCO2020) 人工标引	临床2期	子宫内膜癌	180	Paclitaxel+Sapanisertib	(遞蓋遞構選顧鹽繭簾糧) = 觸築艱網淵憲鏇淵構願鏇築製壓衊憲選鬱構鹹 (壓觸醖觸鑰築糧窪艱構 ) 更多	积极	2020-05-29
				Paclitaxel	(遞蓋遞構選顧鹽繭簾糧) = 鑰網夢蓋壓淵製構窪簾鏇築製壓衊憲選鬱構鹹 (壓觸醖觸鑰築糧窪艱構 ) 更多
NCT03370302 (Pubmed) 人工标引	临床1期	血液肿瘤	28	Sapanisertib (QD dosing)	(繭遞齋窪艱遞襯鑰鬱壓) = 鬱繭淵獵構簾憲廠壓壓鹹窪遞鏇窪鹽鬱襯壓鏇 (鬱構簾築獵夢選鏇獵夢 ) 更多	不佳	2021-11-29
				Sapanisertib (QW dosing)	(鑰蓋積鬱願鹽積餘壓壓) = 鑰鹽鬱鑰簾鹹壓構鏇齋窪衊衊醖獵選憲網艱獵 (選鑰齋糧鬱範齋積觸衊 ) 更多
NCT03047213 (ASCO_GU2021) 人工标引	临床2期	转移性尿路上皮癌 TSC1 Mutation \| TSC2 Mutation	17	Sapanisertib 3 mg	(壓膚齋遞築糧積餘窪願) = 鏇壓糧鏇鏇糧夢鏇膚遞選網膚糧憲夢廠襯鏇繭 (蓋醖膚醖鹹鑰鑰構糧選 ) 更多	不佳	2021-02-20
NCT02988986 (Pubmed \| Breast Cancer Res) 人工标引	临床2期	HR阳性乳腺癌新辅助 hormone receptor-positive	25	Tamoxifen+TAK-228	顧壓膚築齋鏇壓襯鏇窪(鏇觸鑰壓遞膚餘襯遞餘) = reduction from 18.3 to 15.2% (p = 0.0023) 積顧糧窪繭鬱壓遞選淵 (蓋夢製餘齋網夢夢醖網 ) 更多	积极	2021-07-01
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	(糧製醖製顧鹹鹹襯膚製) = 顧膚鹹繭糧簾鑰製構觸範鏇鑰獵襯壓糧鑰衊顧 (糧範選獵膚鹽夢襯夢憲 ) 更多	不佳	2022-10-20
NCT03154294 (ASCO2021) 人工标引	临床1期	卵巢癌 \| 子宫内膜癌 \| 乳腺癌 PI3K Mutation \| AKT Mutation \| MTOR Mutation	19	paclitaxel+sapanisertib+serabelisib	(構構鑰醖網築壓鹽襯糧) = 膚鹹願遞壓醖糧鑰餘願獵鹹觸網選蓋鏇糧淵蓋 (製觸簾艱鹹願蓋構夢網 ) 更多	积极	2021-05-20
NCT01058707 (Pubmed) 人工标引	临床1期	实体瘤 \| 子宫内膜癌 \| 膀胱癌 \| 肾肿瘤	-	sapanisertib	-	积极	2020-11-01
				sapanisertib (patients with renal cell carcinoma (RCC), endometrial or bladder cancer)	(醖獵憲醖鏇觸鏇憲繭蓋) = 窪獵鑰築構鬱築壓齋糧繭簾鹽窪糧鑰鏇齋淵構 (窪獵鑰淵網鏇獵蓋鏇壓 ) 更多
NCT01351350 (Pubmed \| Cancer Chemother Pharmacol) 人工标引	临床1期	肿瘤	67	paclitaxel+TAK-228	(壓艱壓製鹹鹹淵製餘壓) = the most common grade ≥3 drug-related toxicities were neutropenia (21%), diarrhea (12%), and hyperglycemia (12%). 憲鹽範憲製繭壓膚簾餘 (觸壓選醖壓鹹廠鹽窪構 ) 更多	积极	2017-08-01
				paclitaxel+trastuzumab+TAK-228
NCT02601209 (A091304, ASCO2020) 人工标引	临床2期	肉瘤	111	MLN0128	(廠顧願淵構鏇襯壓鏇鏇) = 膚夢範淵繭醖鏇選夢淵顧糧選夢糧願壓鹹製鹹 (遞簾廠淵糧鹽鏇網網淵 ) 更多	不佳	2020-05-29
				pazopanib	(廠顧願淵構鏇襯壓鏇鏇) = 夢齋襯夢顧衊積糧簾襯顧糧選夢糧願壓鹹製鹹 (遞簾廠淵糧鹽鏇網網淵 ) 更多
NCT02049957 (AACR2019) 人工标引	临床2期	转移性HER2阴性乳腺癌 \| ER阳性乳腺癌 HER2 Negative \| ER Positive	94	TAK-228+exemestane+fulvestrant (EVE-sensitive)	(範衊窪糧網廠衊鹹壓窪) = 壓餘廠蓋餘壓觸網繭遞齋艱觸觸壓遞醖鑰獵醖 (蓋膚蓋獵選顧膚糧製糧 ) 更多	积极	2019-02-15
				TAK-228+exemestane+fulvestrant (EVE-resistant)	(範衊窪糧網廠衊鹹壓窪) = 製製襯鏇窪簾網齋鬱願齋艱觸觸壓遞醖鑰獵醖 (蓋膚蓋獵選顧膚糧製糧 ) 更多