Open-Label Umbrella Study to Evaluate Safety and Efficacy of Sapanisertib and Serabelisib (PIKTOR) in Various Combinations in Patients With HR+/HER2- Advanced or Metastatic Breast Cancer

The study is a Phase 1b/2, multi-center, open-label, dose escalation trial evaluating the safety and preliminary efficacy of sapanisertib and serabelisib (PIKTOR) with fulvestrant and/or other anticancer therapies in participants with HR+/HER2- advanced/metastatic breast cancer.

开始日期2026-04-22

申办/合作机构

Faeth Therapeutics LLC

NCT06811116

/ Recruiting临床1/2期IIT

A Phase I/II Trial of Sapanisertib in Combination With Cabozantinib in β-catenin-mutated Hepatocellular Carcinoma (SAPHIRE)

This phase I/II trial studies the side effects and best dose of sapanisertib when given together with cabozantinib, and to see how well they work in treating patients with liver cancer that has spread from where it first started to other places in the body (metastatic) and contains a mutation (change) in the β-catenin gene. Sapanisertib and cabozantinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving sapanisertib and cabozantinib together may work better than giving cabozantinib alone in treating β-catenin-mutated metastatic hepatocellular carcinoma.

开始日期2025-11-17

申办/合作机构

National Cancer Institute

NCT06463028

/ 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 an Insulin-Suppressing 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2024-12-12

申办/合作机构

Faeth Therapeutics LLC

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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项与 Sapanisertib 相关的文献（医药）

2026-05-01·CURRENT OPINION IN UROLOGY

The future of urothelial carcinoma: a 2024–2025 update of early-phase trials of novel therapeutic agents

Review

作者: Wong, Chris Ming-Ho ; Teoh, Jeremy Yuen-Chun ; Liu, Alex Qinyang ; Lee, Yan Hiu Athena

Purpose of review:

The treatment landscape for advanced and non-muscle-invasive urothelial carcinoma (UC) is rapidly evolving beyond platinum chemotherapy and immune checkpoint inhibitors. This review is timely and relevant as it synthesizes recent, impactful data from 2024–2025 early-phase trials, highlighting agents poised to redefine clinical standards.

Recent findings:

Recent studies showcase promising novel strategies. These include next-generation targeted therapies like sapanisertib, novel antibody–drug conjugates (ADCs) and bicycle toxin conjugates (BTCs) such as zelenectide pevedotin (BT8009) and dual-ADC combinations with high response rates, and the approved immunomodulator N-803 for BCG-unresponsive disease. Furthermore, innovative intravesical therapies, including ADCs (disitamab vedotin) and immune checkpoint inhibitors, show transformative potential for localized disease with favorable safety.

Summary:

The findings indicate a shift towards more effective and tailored treatments. Future efforts must focus on biomarker validation, strategic sequencing, and managing combination toxicities to integrate these advances into practice and improve patient outcomes.

2026-03-02·CANCER RESEARCH

Macropinocytosis and Vascularization Determine Response to mTOR Inhibitors in Lung Squamous Cell Carcinoma

Article

作者: Brady, Morgan R. ; Lisberg, Aaron ; Garon, Edward B. ; Momcilovic, Milica ; Matulionis, Nedas ; Christofk, Heather R. ; Shackelford, David B.

Abstract:

The capacity of cancer cells to rewire their cellular metabolism in response to therapeutic pressure confers resistance to treatments targeting key metabolic pathways, which represents a significant challenge in personalized cancer therapy for lung tumors. In this study, we investigated the mechanisms of resistance to the small-molecule mTOR inhibitor TAK228 across lung squamous cell carcinoma (LUSC) models, including cell lines, xenografts, and patient-derived xenografts (PDX). LUSC cells adapted to mTOR inhibition by engaging macropinocytosis, a form of endocytosis that facilitates enhanced uptake of extracellular nutrients, thereby increasing amino acid availability. Coinhibition of both mTOR and macropinocytosis using small-molecule inhibitors effectively reduced tumor growth. Additionally, angiogenesis limited the efficacy of inhibition of mTOR and macropinocytosis by ensuring a sufficient nutrient supply. Notably, inhibiting angiogenesis in combination with inhibitors of mTOR and macropinocytosis reduced tumor growth in xenografts and PDXs. Moreover, prolonged treatment of LUSC PDXs with TAK228 and the glutaminase inhibitor CB-839 led to upregulation of vascularization, which coincided with a rebound in tumor growth despite continued therapeutic administration. These findings highlight adaptive resistance mechanisms to small-molecule inhibitors that target key metabolic pathways, lending insights into potential future clinical strategies for the treatment of LUSC.

Significance::

Macropinocytosis and angiogenesis are adaptive mechanisms that support nutrient uptake and availability to drive resistance to metabolic therapies, providing a promising future therapeutic strategy to overcome metabolic flexibility of lung cancer.

2026-03-01·REPRODUCTIVE TOXICOLOGY

A mouse model of busulfan-induced ovarian toxicity and evidence for attenuation with mTOR inhibition

Article

作者: Inatomi, Ayako ; Tanaka, Yuji ; Nakamura, Akiko ; Takahashi, Akimasa ; Yamanaka, Hiroyuki ; Tsuji, Shunichiro ; Hanada, Tetsuro ; Amano, Tsukuru ; Deguchi, Mari ; Yoneoka, Yutaka

Busulfan, an alkylating agent used in hematopoietic stem cell transplantation conditioning, is associated with a high risk of ovarian toxicity. We established a time-resolved in vivo model of busulfan-induced ovarian injury and tested whether sapanisertib, an mTOR inhibitor, mitigates damage. Mice received busulfan (30 mg/kg, intraperitoneally) or saline; ovaries were assessed at 12, 24, and 72 h and 7 days by hematoxylin and eosin histology, follicle counting, TUNEL, and Ki-67 immunohistochemistry. A separate cohort received daily oral sapanisertib (0.3 mg/kg) from 7 days before busulfan through euthanasia; proliferation was assessed at 24 h, and follicle counts at 7 days. In the busulfan-only group, Ki-67 staining showed an early proliferative surge at 24 h in growing follicles, including primary follicles, whereas loss of primordial follicles and an increased primary-to-primordial follicle ratio were evident by 7 days. Primordial follicles showed no TUNEL-positive cells through 72 h, whereas growing follicles were frequently TUNEL-positive. Relative to busulfan alone, the mTOR inhibitor preserved primordial follicles, shifted the primary-to-primordial ratio toward control values, and reduced the proportion of primary follicles with extensive proliferation at 24 h. These findings are consistent with premature activation of primordial follicles as a proximate contributor to busulfan-induced loss of ovarian reserve and suggest that mTOR inhibition may mitigate this process. A two-time-point assay (24 h for proliferation, 7 days for morphology) provides a practical framework for future studies and translation.

项与 Sapanisertib 相关的新闻（医药）

2026-08-09

·BioSpace

Faeth Therapeutics Announces Inducement Grants Under Nasdaq Listing Rule 5635(c)(4) - August 7, 2026

AUSTIN, Texas--(BUSINESS WIRE)--Faeth Therapeutics, Inc. (Nasdaq: FTH) today announced that the Compensation Committee of Faeth’s Board of Directors granted two new employees options to purchase an aggregate of 11,000 shares of the Company’s common stock in connection with their employment (collectively, the “Option Awards”). The Option Awards were granted effective August 4, 2026, pursuant to the Company’s 2026 Inducement Plan as a material inducement to the individuals entering employment with Faeth in accordance with Nasdaq Listing Rule 5635(c)(4). The Option Awards have an exercise price of $25.50 per share, equal to the closing price of the Company’s common stock on the grant date. The Option Awards will vest, with respect to 25% of the shares subject to each such award, on the first anniversary of the applicable employee’s start date, with the remaining shares vesting in 36 substantially equal monthly installments thereafter, in each case subject to such employee’s continued service with Faeth through each such vesting date. The Option Awards have a term of ten years from the grant date and are otherwise subject to the terms and conditions of the 2026 Inducement Plan and the applicable award agreement. About Faeth Therapeutics Faeth Therapeutics, Inc. (Nasdaq: FTH) is a clinical-stage biotechnology company focused on improving outcomes for cancer patients through multi-node inhibition of critical oncogenic pathways. The Company’s lead program is PIKTOR, an investigational all-oral combination of serabelisib and sapanisertib in development for endometrial and breast cancer. Faeth was co-founded in 2019 by Anand Parikh and Oliver Maddocks, Ph.D., together with scientific founders Lewis Cantley, Ph.D., the discoverer of the PI3K pathway; Siddhartha Mukherjee, M.D., D.Phil.; Karen Vousden, Ph.D.; Scott Lowe, Ph.D.; and Greg Hannon, Ph.D. The Company intends to use its website as a means of disclosing material non-public information and for complying with its disclosure obligations under Regulation FD. For more information, please visit and follow the Company on LinkedIn. ezstandalone.cmd.push(function () { ezstandalone.showAds(131); }); Contacts Investor Contact: Matthew Biegler, SVP, Investor Relations matt@faeththerapeutics.com Media Contact: Patrick Schmidt, Consort Partners faeththerapeutics@consortpartners.com

2026-08-07

·乳腺王医生Tumour Time

PI3K/AKT/mTOR信号通路的活化机制、靶向药物与临床研究进展

引言磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）/哺乳动物雷帕霉素靶蛋白（mTOR）通路——简称PAM通路——是高等真核细胞中高度保守的信号转导网络，在促进细胞存活、生长和增殖中发挥着核心作用。该通路响应外部生长因子等刺激信号，通过级联磷酸化反应将信号从细胞膜传递至细胞核，调控细胞代谢、蛋白质合成、自噬、凋亡及免疫调节等一系列关键生物学过程。然而，PAM通路也是人类癌症中最常被异常激活的信号通路。据估计，约50%的肿瘤中存在PAM通路的异常改变。通路的过度激活不仅驱动肿瘤的发生与进展，还广泛参与治疗耐药的产生。正因如此，PAM通路的三个关键节点——PI3K、AKT和mTOR——已成为抗肿瘤药物研发中最受关注的靶点之一。本文将从活化机制、靶向药物及临床试验三个维度，系统梳理PAM通路的研究现状。一、PAM通路的活化机制1.1 通路的启动：PI3K的激活 PAM通路的激活始于细胞膜水平。当生长因子（如胰岛素、胰岛素样生长因子、表皮生长因子等）与细胞表面的受体酪氨酸激酶（RTK）或G蛋白偶联受体结合后，受体发生二聚化和自磷酸化，产生磷酸化酪氨酸位点。这些位点成为PI3K的p85调节亚基的SH2结构域的结合平台，将PI3K的p110催化亚基招募至细胞膜附近。 PI3K家族中，I类PI3K是PAM通路激活的核心成员。I类PI3K由调节亚基（p85）和催化亚基（p110，包括p110α、p110β、p110δ和p110γ四种异构体）组成。被招募至细胞膜的PI3K催化磷脂酰肌醇-4,5-二磷酸（PIP₂）转化为磷脂酰肌醇-3,4,5-三磷酸（PIP₃）。PIP₃作为第二信使，在细胞膜上形成“停靠位点”，招募含有PH结构域的蛋白，其中最重要的便是AKT和PDK1。值得注意的是，PIP₃的水平受到PTEN（磷酸酶与张力蛋白同源物）的负向调控——PTEN将PIP₃去磷酸化回PIP₂，从而终止信号传导。PTEN的功能缺失是PAM通路异常激活的最常见机制之一。1.2 信号的中枢：AKT的磷酸化与活化 AKT（又称PKB）是PAM通路的核心激酶，在哺乳动物中存在AKT1、AKT2和AKT3三种亚型。AKT通过其PH结构域与细胞膜上的PIP₃结合，被招募至细胞膜。在细胞膜上，AKT首先在Thr308位点被PDK1磷酸化，随后在Ser473位点被mTORC2磷酸化。两个位点的完全磷酸化才能使AKT达到最大活性。活化的AKT从细胞膜释放至细胞质和细胞核，通过磷酸化超过100种底物来调控广泛的生物学功能。这些底物包括：促进细胞存活的BAD和Caspase-9（抑制凋亡）、调控代谢的GSK3β和FoxO转录因子、以及最重要的——激活下游mTOR信号通路的TSC2和PRAS40。1.3 信号的执行：mTOR复合物的功能 mTOR是PAM通路的终端效应器，以两种不同的复合物形式存在：mTORC1和mTORC2。 mTORC1对雷帕霉素敏感，由mTOR、Raptor、mLST8等亚基组成，主要调控细胞生长和代谢。AKT通过磷酸化并抑制TSC1/TSC2复合物（TSC2是mTORC1的负调控因子），以及磷酸化PRAS40（解除其对mTORC1的抑制），双重机制激活mTORC1。活化的mTORC1磷酸化其下游两个关键底物——S6K1和4E-BP1，从而促进核糖体生物合成和蛋白质翻译，驱动细胞生长和增殖。 mTORC2对雷帕霉素不敏感，由mTOR、Rictor、mLST8等亚基组成，主要调控细胞增殖、存活和迁移。mTORC2的主要功能之一是磷酸化AKT的Ser473位点，构成一个正反馈环路。此外，mTORC2还参与调控细胞骨架组织和细胞存活。1.4 通路异常激活的分子机制 PAM通路在癌症中的异常激活主要通过以下几种机制实现： PIK3CA功能获得性突变：PIK3CA基因编码p110α催化亚基，其突变导致PI3Kα持续活化。PIK3CA突变在乳腺癌（尤其是HR+/HER2-亚型）、卵巢透明细胞癌、子宫内膜癌和结直肠癌中高频出现。 PTEN功能缺失：PTEN是PAM通路最重要的负调控因子，其失活导致PIP₃堆积和AKT过度激活。 AKT的激活突变或扩增：AKT1的E17K突变可导致AKT持续定位于细胞膜并被异常激活。上游RTK的过表达或激活突变。1.5 通路的负反馈调控与耐药机制 PAM通路内部存在复杂的负反馈调节网络，这也是靶向治疗耐药的重要机制之一。当使用mTOR抑制剂（如依维莫司）抑制mTORC1时，会解除对上游PI3K的负反馈抑制，导致AKT反馈性过度激活，从而削弱抗肿瘤效果。类似地，AKT抑制剂单药治疗时，mTOR信号通路的恢复被证实是早期驱动耐药的主要机制。最新研究表明，在PTEN缺失的前列腺癌中，AKT抑制后mTOR信号的恢复可通过多种分子改变实现，导致mTOR负调控因子的缺失，而联合mTOR抑制剂可恢复对AKT抑制的敏感性。此外，抑制PAM通路的反馈环还会导致包括PI3K、AKT和ERK在内的多条代偿通路过度激活，进一步加剧耐药。这些发现为联合靶向策略提供了重要的理论依据。二、基于PAM通路开发的靶向药物基于上述活化机制，研究者针对PI3K、AKT和mTOR三个节点开发了多类抑制剂。截至2026年，已有多个药物获批上市，更多候选药物处于不同阶段的临床开发中。2.1 PI3K抑制剂 PI3K抑制剂根据靶向范围可分为泛PI3K抑制剂和亚型选择性抑制剂。（1）亚型选择性PI3Kα抑制剂 Alpelisib（BYL719 是首个获批的选择性PI3Kα抑制剂，在美国、欧洲和中国获批用于PIK3CA突变的HR+/HER2-晚期乳腺癌。然而，PI3Kα抑制剂存在固有的“类效应”毒性，包括高血糖、腹泻和皮疹等，其中高血糖症尤其限制了糖尿病或糖尿病前期患者的使用。 Inavolisib（伊那利塞）是罗氏开发的新一代PI3Kα抑制剂，于2025年3月在中国获批上市。INAVO120研究数据显示，伊那利塞联合CDK4/6抑制剂和内分泌治疗显著延长了患者的中位无进展生存期，降低了57%的疾病进展或死亡风险。伊那利塞也是中国首个且目前唯一获批的高选择性PI3Kα抑制剂。瑞索利塞（CYH33）是由海和药物自主研发的高选择性PI3Kα抑制剂，于2025年6月获得日本厚生劳动省孤儿药认定，用于治疗携带PIK3CA基因突变的卵巢透明细胞癌（OCCC）。这是全球首个用于OCCC的单药靶向治疗药物。其上市许可申请基于CYH33-G201关键II期研究的有效性和安全性数据。临床前研究显示，CYH33可高效、特异地抑制PI3Kα激酶活性，对PIK3CA突变的肿瘤模型具有强效抗肿瘤作用。 Tersolisib（LY4064809/STX-478）是一种口服、变构、可穿透中枢神经系统的泛突变选择性PI3Kα抑制剂。PIKALO-1试验的最新数据显示，截至2026年1月6日，共193例PIK3CA突变的HR+/HER2-晚期乳腺癌患者接受了治疗。值得注意的是，54%的患者伴有糖尿病或糖尿病前期。Tersolisib单药或联合氟维司群±CDK4/6抑制剂展现了良好的耐受性，PI3K抑制剂类毒性（皮疹和口腔炎）发生率较低，且在基线血糖正常的患者中未观察到3级高血糖事件。在疗效方面，Tersolisib联合氟维司群的客观缓解率达35%，疾病控制率达87%。基于这些积极数据，III期PIKALO-2试验（NCT07174336）正在计划中。 JYP0035 是嘉越医药研发的新一代高选择性PI3Kα抑制剂，其独特之处在于兼具PI3Kα抑制剂和突变型PI3Kα降解剂的双重功能。这种机制有望通过降低对野生型PI3Kα的影响来减少高血糖等副作用。2025年3月，JYP0035联合氟维司群（伴或不伴哌柏西利）治疗PIK3CA突变、HR+/HER2-乳腺癌的临床试验获NMPA批准。 JS105 是君实生物与润佳医药合作开发的PI3Kα口服小分子抑制剂，主要用于PIK3CA突变的实体瘤治疗，包括乳腺癌、宫颈癌等妇科肿瘤。 ETX-636 是昂胜医药开发的泛突变选择性PI3Kα抑制剂，其全球I/II期临床研究已在中国完成首例患者给药，用于评估其在携带PIK3CA突变的晚期实体瘤患者中的安全性、耐受性、药代动力学和初步疗效。（2）PI3Kδ选择性抑制剂 Leniolisib（CDZ173）是PI3Kδ选择性抑制剂，主要用于活化PI3Kδ综合征（APDS）的治疗，已在美国获批用于12岁及以上APDS患者。2.2 AKT抑制剂 AKT处于PAM通路的核心枢纽位置，抑制AKT可同时阻断上游PI3K信号和下游mTOR信号。 Capivasertib（卡匹色替，Truqap）是全球首个获批的AKT激酶抑制剂，可同时抑制AKT1、AKT2和AKT3三种亚型。其获批适应症为PIK3CA/AKT1/PTEN基因改变的HR+/HER2-晚期乳腺癌。2026年6月12日，美国FDA进一步批准Capivasertib联合阿比特龙和泼尼松用于PTEN缺陷的转移性激素敏感性前列腺癌（mHSPC）成人患者，使其成为首个且唯一获批用于该适应症的靶向治疗药物。常见不良反应包括血糖升高、腹泻及皮肤反应，多为1～2级，总体可耐受。2025年12月，卡匹色替被纳入中国国家医保目录。 Afuresertib（LAE002）是一种口服AKT强效抑制剂，可抑制所有三种AKT亚型（AKT1、AKT2及AKT3），是全球两种处于晚期临床开发阶段的针对乳腺癌的AKT抑制剂之一。其III期临床试验AFFIRM-205（联合氟维司群治疗HR+/HER2-局部晚期或转移性乳腺癌伴PIK3CA/AKT1/PTEN基因改变患者）已于2025年12月完成入组。来凯医药计划于2026年上半年公布顶线数据，并于同年提交新药上市申请。2025年11月，来凯医药与齐鲁制药签订了最高可达20.45亿元的中国地区独家许可协议。Afuresertib有望成为首个国产AKT抑制剂。 Ipatasertib（GDC-0068）是另一种泛AKT抑制剂。TAKTIC Ib期研究探索了Ipatasertib联合氟维司群和哌柏西利在CDK4/6抑制剂经治的HR+/HER2-转移性乳腺癌中的疗效。研究显示，中位无进展生存期为5.5个月，联合方案显示了初步临床疗效及可接受的安全性。此外，NCI-MATCH试验的子方案Z1K正在评估Ipatasertib在携带AKT基因突变癌症患者中的疗效。 TAS-117（Pifusertib）是一种口服、选择性、非ATP竞争性变构AKT抑制剂，在I期研究中显示出令人鼓舞的抗肿瘤活性。其II期研究在携带胚系PTEN失活突变的晚期实体瘤患者中评估了安全性和临床获益，推荐II期剂量为16 mg每日一次。 MK-2206 是变构性AKT抑制剂，在急性髓系白血病的临床前研究中显示出活性，但单药临床抗白血病活性不足。 ATV-1601 是Atavistik Bio开发的变构选择性AKT1 E17K抑制剂，专门针对携带AKT1 E17K突变的实体瘤患者，已于2025年启动I期临床试验。2.3 mTOR抑制剂（1）第一代mTOR抑制剂（雷帕霉素类似物） Everolimus（依维莫司）和Temsirolimus（替西罗莫司）是雷帕霉素的衍生物，主要抑制mTORC1。Everolimus联合内分泌治疗在HR+乳腺癌中显示了临床获益（基于BOLERO-2试验）。Temsirolimus已在美国和欧洲获批用于晚期肾细胞癌的治疗。此外，mTOR抑制剂在结节性硬化症（TSC）相关难治性癫痫的治疗中也显示出潜力。值得关注的是，mTOR抑制剂在延缓衰老、预防慢性疾病和延长健康寿命方面的潜力也正在被积极探索。（2）第二代mTOR抑制剂（ATP竞争性抑制剂，靶向mTORC1/2） TAK228（Sapanisertib）是一种强效、高选择性的ATP竞争性mTORC1/mTORC2抑制剂。在铂耐药卵巢癌中，早期研究提示TAK228与紫杉醇存在协同作用。DICE试验正在评估TAK228联合紫杉醇周疗在晚期/复发性上皮性卵巢癌中的疗效。此外，多节点抑制策略提示同时靶向mTORC1、mTORC2和PI3Kα可能是更优的选择。 Onatasertib（ATG-008）是口服mTORC1/2双重抑制剂，在TORCH-2试验中联合特瑞普利单抗治疗CPI耐药宫颈癌患者，客观缓解率达22.2%，疾病控制率达85.2%。最新研究进一步显示，mTORC1/2抑制剂联合PD-1抗体在晚期实体瘤中具有协同增效作用，且在宫颈癌等适应症中显示出优势。（3）mTORC1选择性抑制剂 RMC-5552 是一种双作用（bi-steric）、mTORC1选择性抑制剂，可强效抑制mTORC1底物4E-BP1和S6K的磷酸化，同时对mTORC2具有选择性。其I期临床试验已在晚期实体瘤中完成。研究验证了RMC-5552在临床中选择性抑制mTORC1的可行性，克服了传统mTOR抑制剂因mTORC2抑制导致的高血糖副作用。未来需进一步在II期试验中评估其单药或联合治疗的疗效。2.4 多靶点PAM通路抑制剂 Gedatolisib 是一种强效的多靶点PAM通路抑制剂，可同时靶向所有四种I类PI3K亚型（α、β、δ、γ）以及mTORC1和mTORC2，实现PAM通路的全面阻断。与仅靶向通路中单一节点的药物相比，Gedatolisib具有更优越的临床前效力和细胞毒性。目前，Gedatolisib已在美国递交新药申请（NDA），用于治疗HR+/HER2-/PIK3CA野生型晚期乳腺癌患者，FDA预计于2026年7月17日做出审评决定。 Paxalisib 是一种具有血脑屏障穿透性的PI3K/mTOR双重抑制剂，正在开发用于多种脑部肿瘤的治疗。此外，该药也在探索联合奥拉帕利或帕博利珠单抗治疗晚期乳腺癌。 Omipalisib（GSK2126458）是PI3K/mTOR双重抑制剂，已完成I期临床试验。三、关键临床试验进展3.1 PI3K抑制剂相关临床试验 INAVO120 是伊那利塞的关键III期试验，基于该研究中无进展生存期具有统计学意义和临床意义的显著改善，FDA和NMPA批准了伊那利塞联合哌柏西利和氟维司群用于PIK3CA突变的HR+/HER2-晚期乳腺癌。伊那利塞进入临床实践后，正在改变PIK3CA突变乳腺癌的治疗格局。此外，INAVO123研究正在探索伊那利塞在已扩散的乳腺癌中的疗效。 EPIK-O/ENGOT-ov61（NCT04729387）是一项III期临床试验，旨在评估Alpelisib联合奥拉帕利对比单药化疗在铂耐药或难治、无BRCA突变的高级别浆液性卵巢癌中的疗效。该试验于2025年报告了主要分析结果。 CYH33-G201 是一项多国、多中心、开放的II期单臂临床试验，评估瑞索利塞（CYH33）用于既往化疗后进展或复发的PIK3CA突变卵巢透明细胞癌患者的疗效和安全性。基于该研究的积极数据，瑞索利塞已在日本申请上市许可。 PIKALO-1 是一项I/II期试验，评估Tersolisib在PIK3CA突变晚期实体瘤中的安全性和疗效。截至2026年1月6日，193例患者接受了治疗，Tersolisib展现了良好的耐受性和有前景的临床活性，支持进入III期PIKALO-2试验。 JYP0035联合用药试验于2025年3月获NMPA批准，将评估JYP0035联合氟维司群（伴或不伴哌柏西利）治疗PIK3CA突变、HR+/HER2-乳腺癌的疗效与安全性。3.2 AKT抑制剂相关临床试验 CAPItello-291 是一项全球、多中心、双盲、随机对照的III期临床试验，共纳入708例HR+/HER2-晚期乳腺癌患者。结果显示，在总人群中，卡匹色替联合氟维司群组中位PFS为7.2个月，而安慰剂联合氟维司群组为3.6个月（HR=0.60，p＜0.001）。在伴有AKT通路改变的患者中，两组中位PFS分别为7.3个月和3.1个月（HR=0.50）。基于此研究，Capivasertib获得FDA和NMPA批准。2025年12月，卡匹色替被纳入中国国家医保目录。 CAPItello-281 是基于CAPItello-291研究的积极结果，支持了Capivasertib在PTEN缺陷的前列腺癌中的进一步探索。2026年6月12日，FDA正式批准Capivasertib联合阿比特龙和泼尼松用于PTEN缺陷的转移性激素敏感性前列腺癌。 FAKTION研究是一项II期试验，评估卡匹色替联合氟维司群治疗ER+/HER2-晚期乳腺癌。在ITT人群中，中位PFS分别为10.3个月和4.8个月（HR=0.56）；在PIK3CA/AKT1/PTEN基因改变的患者中，中位PFS分别为12.8个月和4.6个月（HR=0.44）。 AFFIRM-205 是Afuresertib（LAE002）的关键III期临床试验，评估其联合氟维司群治疗HR+/HER2-局部晚期或转移性乳腺癌伴PIK3CA/AKT1/PTEN基因改变患者。该试验已于2025年12月完成入组，计划于2026年上半年公布顶线数据。Afuresertib有望成为首个国产AKT抑制剂。 TAKTIC研究是一项Ib期临床研究，评估Ipatasertib联合抗雌激素药物（联合或不联合哌柏西利）治疗CDK4/6抑制剂经治的HR+/HER2-转移性乳腺癌。结果显示，推荐II期剂量为Ipatasertib 400 mg联合哌柏西利100 mg和氟维司群，中位PFS为5.5个月。该研究发表于《Lancet Oncology》。 IPATential150 是一项III期试验，评估Ipatasertib联合阿比特龙治疗转移性去势抵抗性前列腺癌。在PTEN缺失的患者中，联合治疗显著降低了疾病进展风险。 NCI-MATCH（Z1K）是一项II期治疗试验，测试Ipatasertib在携带AKT基因突变癌症患者中的疗效。3.3 mTOR抑制剂相关临床试验 BOLERO-2 是Everolimus的关键III期试验，证实了依维莫司联合内分泌治疗在HR+晚期乳腺癌中的获益。 evERA（NCT05306340）是一项III期试验，评估口服SERD药物Giredestrant联合Everolimus对比标准内分泌治疗联合Everolimus在ER+/HER2-晚期乳腺癌中的疗效。该试验于2025年ESMO大会报告了结果，显示Giredestrant联合Everolimus显著改善了PFS，尤其在ESR1突变患者中获益更为明显。 UNIRAD试验评估了在高危早期luminal乳腺癌患者中，内分泌治疗基础上加用2年Everolimus的辅助治疗效果，但未能显示总体获益。 DICE试验是一项国际多中心随机II期研究，在134例铂耐药卵巢癌患者中比较紫杉醇周疗联合TAK228与紫杉醇周疗单药的疗效。主要终点为PFS。 TORCH-2试验评估ATG-008（mTORC1/2抑制剂）联合特瑞普利单抗治疗CPI耐药宫颈癌，ORR达22.2%，DCR达85.2%。最新研究进一步证实了mTORC1/2抑制剂联合PD-1抗体在晚期实体瘤中的协同增效作用。 RMC-5552 I期试验评估了双作用mTORC1选择性抑制剂RMC-5552在晚期实体瘤中的安全性、耐受性和初步疗效。研究验证了选择性抑制mTORC1的可行性，并显示其克服了传统mTOR抑制剂因mTORC2抑制导致的高血糖副作用。3.4 多靶点PAM通路抑制剂临床试验 VIKTORIA-1 是Gedatolisib的关键III期临床试验，也是首个证明全面阻断PAM通路相较于仅靶向单一节点可显著改善患者预后的III期研究。 PIK3CA野生型队列的结果于2025年ESMO大会首次公布。该队列共纳入392例HR+/HER2-/PIK3CA野生型晚期乳腺癌患者。中位随访10.1个月。三联方案（Gedatolisib+哌柏西利+氟维司群）组中位PFS为9.3个月，而氟维司群单药组为2.0个月（HR=0.24，p＜0.0001）。双联方案（Gedatolisib+氟维司群）组中位PFS为7.4个月（HR=0.33，p＜0.0001）。客观缓解率在三联组为32%（含1例完全缓解），双联组为28.3%，而单药组仅为1%。中期总生存期分析显示，三联组HR为0.69，双联组HR为0.74。安全性方面，≥3级治疗相关不良事件包括中性粒细胞减少症（三联组62.3% vs. 双联组0.8%）、口腔炎（19.2% vs. 12.3%）、皮疹（4.6% vs. 5.4%）和高血糖症（两组均为2.3%）。因治疗相关不良事件停药率较低（三联组2.3%，双联组3.1%）。这些数据支持Gedatolisib联合方案可能成为HR+/HER2-/PIK3CA野生型晚期乳腺癌二线治疗的新标准。 PIK3CA突变队列的结果于2026年ASCO年会公布。该队列共入组700多例患者。双联方案（Gedatolisib+氟维司群）组中位PFS为11.3个月，而标准治疗（Alpelisib+氟维司群）组为5.6个月（HR=0.51，即疾病进展或死亡风险降低49%）。三联方案（Gedatolisib+哌柏西利+氟维司群）组中位PFS为11.1个月（HR=0.50）。客观缓解率方面，双联组为35.7%，三联组为48.9%，而标准治疗组为26.0%。中位缓解持续时间在双联组为24.2个月，三联组为15.7个月，标准治疗组为7.5个月。安全性方面，因治疗相关不良事件导致停药的比例在三联方案组为2.6%，两联方案组为3.8%，均低于Alpelisib组的7.1%。Jefferies分析师指出，这种程度的PFS改善“将改变临床实践”。Celcuity公司已向FDA递交gedatolisib的上市申请，预计2026年7月17日做出审评决定。 VIKTORIA-2（NCT06757634）是另一项正在进行的III期临床试验，旨在评估Gedatolisib联合CDK4/6抑制剂和氟维司群作为HR+/HER2-晚期乳腺癌一线治疗的疗效。 CELC-G-201 是一项I/II期试验，评估Gedatolisib联合雄激素受体通路抑制剂Darolutamide治疗转移性去势抵抗性前列腺癌。PAM通路抑制剂与雄激素受体通路抑制剂的联合可能在前列腺癌中产生协同抗肿瘤效应。 NTQ1062 是中国生物制药旗下南京正大天晴开发的AKT抑制剂，已于2026年3月完成III期临床首例患者入组给药。随着精准治疗的发展，NCCN/CSCO指南均推荐CDK4/6抑制剂经治后患者按PAM通路突变状态进行后线治疗。结语 PI3K/AKT/mTOR信号通路作为细胞生命活动的核心调控网络，其在肿瘤中的异常激活为靶向治疗提供了坚实的理论基础。从PI3K抑制剂Alpelisib、Inavolisib、瑞索利塞、Tersolisib，到AKT抑制剂Capivasertib、Afuresertib、Ipatasertib，再到mTOR抑制剂Everolimus、TAK228、RMC-5552，以及多靶点抑制剂Gedatolisib，针对PAM通路的药物研发已从“单个节点阻断”走向“全面通路抑制”的新阶段。VIKTORIA-1研究的成功标志着全面阻断PAM通路的治疗策略在临床上获得了验证。 2025年至2026年，PAM通路靶向治疗迎来了多个里程碑式的进展：Capivasertib获批用于PTEN缺陷前列腺癌；伊那利塞和卡匹色替被纳入中国国家医保目录；Gedatolisib在PIK3CA突变和野生型两个队列中均取得阳性结果；Afuresertib完成III期入组，有望成为首个国产AKT抑制剂；Tersolisib等新一代PI3Kα抑制剂展现了更优的安全性特征。然而，PAM通路抑制剂仍面临诸多挑战：固有的“类效应”毒性（如高血糖、皮疹、腹泻）限制了药物的耐受性和治疗窗口；通路内和通路间的代偿性反馈激活导致耐药性的产生；以及如何通过生物标志物精准筛选获益人群。未来，开发更具选择性的新一代抑制剂（如突变选择性PI3Kα抑制剂和mTORC1选择性抑制剂）、探索合理的联合治疗策略、以及基于基因检测指导下的精准治疗，将是PAM通路靶向治疗的研究重点。参考文献 1. He Y, Sun MM, Zhang GG, et al. PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer. *Molecular Cancer*, 2023, 22: 138. 2. The PI3K/Akt/mTOR Signaling Pathway: An In-depth Technical Guide to Its Role in Human Diseases. BenchChem, 2025. 3. PI3K/Akt/mTOR信号通路在调控细胞增殖、分化等关键生物学过程中的作用. *中南药学*. 4. 史蕤, 张艳华. 乳腺癌治疗新药AKT抑制药——Capivasertib. *中国临床药理学杂志*, 2025(06): 886-889. 5. 海和药物高选择性PI3Kα抑制剂瑞索利塞出海——正式申请日本上市许可. *phirda.com*, 2025. 6. 嘉越医药新一代PI3Kα抑制剂JYP0035胶囊联合用药临床试验获批准. *pharnexcloud.com*, 2025. 7. 临研寻踪丨吹尽狂沙始到金，从临床研究看卡匹色替的乳腺癌探索之路. *medlive.cn*, 2025. 8. Hurvitz SA, et al. Gedatolisib + fulvestrant ± palbociclib vs fulvestrant in HR+/HER2-/PIK3CA wild-type advanced breast cancer: First results from VIKTORIA-1. *Annals of Oncology*, 2025, 36(Suppl 2): S1562-S1563. 9. 激素受体阳性/HER2阴性/PIK3CA野生型晚期乳腺癌 gedatolisib联合氟维司群加或不加哌柏西利治疗均获益. *J Clin Oncol*, 2026年3月9日在线版. 10. Gedatolisib + fulvestrant ± palbociclib vs standard of care in HR+/HER2−/PIK3CA-mutant advanced breast cancer (VIKTORIA-1 Study 2). ASCO, 2026. 11. Jhaveri K, et al. A phase 1/2 trial of tersolisib (LY4064809/STX-478), a pan-mutant-selective PI3Kα inhibitor, in PIK3CA-mutant advanced solid tumors: Updated results from PIKALO-1. ASCO, 2026. 12. 来凯LAE002 (AFURESERTIB) III期临床试验完成入组. *pharnexcloud.com*, 2025. 13. Wander SA, et al. TAKTIC study: Ipatasertib plus fulvestrant and palbociclib in heavily pretreated HR+/HER2− metastatic breast cancer. *Lancet Oncol*, 2026, 27: 580. 14. FDA approves capivasertib with abiraterone and prednisone for PTEN-deficient prostate cancer. FDA, 2026. 15. Uncoupling of Akt and mTOR signaling drives resistance to Akt inhibition in PTEN loss prostate cancers. *Science*, 2025. 16. Schram AM, Naqash AR, Haura EB, et al. The Bi-steric, mTORC1-Selective Inhibitor, RMC-5552, in Advanced Solid Tumors: A Phase 1 Trial. *Clin Cancer Res*, 2025. 17. HR+晚期乳腺癌后CDK4/6i时代，从机制到临床研究看靶向PI3K-AKT-mTOR的治疗格局. *medlive.cn*, 2024. 18. PI3K/AKT/mTOR信号通路抑制剂相关高血糖的管理. *medlive.cn*, 2026. 19. 医药生物行业靶向PAM通路潜在百亿美元市场. *stock.finance.sina.com.cn*, 2026. 20. 中国生物制药NTQ1062完成Ⅲ期临床首例患者入组给药. *bydrug.pharmcube.com*, 2026.

2026-08-07

·BioSpace

Faeth Therapeutics to Present PK/PD Modeling That Informed PIKTOR Dose Selection in Ongoing FTH-PIK-201 Trial at Upcoming Scientific Conference

— The data will be presented at the 2026 Summit for Novel Therapeutics in Oncology and Precision Medicine in Cancer conference on August 8 — These data collectively informed PIKTOR dose selection in the ongoing Phase 2 trial in second-line advanced endometrial cancer (Study FTH-PIK-201) AUSTIN, Texas--(BUSINESS WIRE)--Faeth Therapeutics (Nasdaq: FTH), a clinical-stage oncology company developing PIKTOR, an investigational all-oral, multi-node inhibitor of the PI3K/AKT/mTOR pathway, will present translational data and pharmacokinetic/pharmacodynamic (PK/PD) analysis for PIKTOR, its oral combination of serabelisib and sapanisertib, at the 2026 Summit for Novel Therapeutics in Oncology & Precision Medicine in Cancer (STOP Cancer), held August 7-8 in New York. The poster titled "Exposure/Response Analysis of an Oral Multi-Node PI3K/AKT/mTOR Pathway Inhibitor Combination of Serabelisib and Sapanisertib" will be presented on August 8 between 10:25 and 11:30 AM at the New York Marriott Marquis in New York, NY (Poster #9). ezstandalone.cmd.push(function () { ezstandalone.showAds(131); }); Data to be reported include a PK/PD analysis that integrates skin biopsy data and PK modeling from earlier third-party clinical trials of serabelisib and sapanisertib. Together, these data informed selection of 3 mg sapanisertib and 200 mg serabelisib three days a week as the recommended Phase 2 dose for PIKTOR in the ongoing Phase 2 trial in second-line advanced endometrial cancer, Study FTH-PIK-201 (NCT06463028). A copy of the poster will be made available in the Investors section of Faeth's website at the start of the poster session. About PIKTOR PIKTOR is an investigational, proprietary, all-oral combination of serabelisib, a selective PI3K-alpha inhibitor, and sapanisertib, an mTORC1/mTORC2 inhibitor, designed to inhibit multiple nodes of the PI3K/AKT/mTOR pathway. According to published literature, this pathway is dysregulated in up to 50% of all solid tumors, making it one of the most prevalent therapeutic targets in oncology. PIKTOR is being evaluated in a Phase 2 trial in second-line advanced endometrial cancer (Study FTH-PIK-201), with topline data anticipated by year-end 2026. PIKTOR is also being evaluated in a Phase 1b/2 trial in HR+/HER2- advanced breast cancer (Study FTH-PIK-101), in which the first patient was dosed in April 2026 and interim data is anticipated in 2027. About Faeth Therapeutics Faeth Therapeutics, Inc. (Nasdaq: FTH) is a clinical-stage biotechnology company focused on improving outcomes for cancer patients through multi-node inhibition of critical oncogenic pathways. The Company’s lead program is PIKTOR, an investigational all-oral combination of serabelisib and sapanisertib in development for endometrial and breast cancer. Faeth was co-founded in 2019 by Anand Parikh and Oliver Maddocks, Ph.D., together with scientific founders Lewis Cantley, Ph.D., the discoverer of the PI3K pathway; Siddhartha Mukherjee, M.D., D.Phil.; Karen Vousden, Ph.D.; Scott Lowe, Ph.D.; and Greg Hannon, Ph.D. For more information, please visit and follow the Company on LinkedIn . Cautionary Note Regarding Forward-Looking Statements This press release contains “forward-looking statements” within the meaning of the federal securities laws, including the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements include all statements that are not historical facts and may be identified by words such as “anticipate,” “believe,” “expect,” “intend,” “plan,” “may,” “will,” “would,” “could,” “should,” “estimate,” “potential,” “target,” “on track” and similar expressions, although not all forward-looking statements contain these words. These statements include, but are not limited to, statements regarding: the content, timing and presentation of data at the STOP Cancer conference; the Company’s interpretation of preclinical, pharmacokinetic and pharmacodynamic data and the conclusions the Company draws from that data, including with respect to dose and schedule selection for PIKTOR; the Company’s expectations regarding its pipeline and development plans, including the Phase 2 trial of PIKTOR in advanced endometrial cancer and the anticipated timing of topline data, and the Phase 1b/2 trial of PIKTOR in HR+/HER2- advanced breast cancer and the anticipated timing of interim data; and the potential therapeutic benefits, tolerability pro differentiation of PIKTOR. Forward-looking statements are based on management’s current expectations and assumptions and are subject to a number of risks and uncertainties, many of which are beyond the Company’s control, that could cause actual results to differ materially from those expressed or implied. These risks and uncertainties include, among others, risks related to clinical development and the conduct, timing and results of clinical trials; the risk that results from preclinical studies, earlier clinical trials, modeling or other exploratory analyses may not be predictive of results in ongoing or future clinical trials; the Company’s need for additional financing; its limited operating history and history of operating losses; risks related to the integration of Faeth; the Company’s ability to satisfy applicable Nasdaq listing requirements and to maintain the listing of its common stock; and the other risks and uncertainties described under the headings “Risk Factors” and “Summary of Risk Factors” in the Company’s Annual Report on Form 10-K filed with the Securities and Exchange Commission (the “SEC”) on March 30, 2026, its Quarterly Report on Form 10-Q filed with the SEC on August 4, 2026, and its definitive proxy statement filed with the SEC on April 27, 2026, as well as in the Company’s subsequent filings. Forward-looking statements speak only as of the date of this press release, and the Company undertakes no obligation to update any forward-looking statement, except as required by law. Contacts Investor Contact: Matthew Biegler, SVP, Investor Relations matt@faeththerapeutics.com Media Contact: Patrick Schmidt, Consort Partners faeththerapeutics@consortpartners.com

临床2期ASCO会议临床1期

100 项与 Sapanisertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11183	Sapanisertib	-	DB11836

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
HER2 阴性乳腺癌	临床2期	美国	Faeth Therapeutics LLC	2026-04-22
HR阳性/HER2阴性乳腺癌	临床2期	美国	Faeth Therapeutics LLC	2026-04-22
HER2阳性转移性乳腺癌	临床2期	美国	Faeth Therapeutics LLC	2026-04-22
晚期肝细胞癌	临床2期	美国	National Cancer Institute	2025-11-17
子宫内膜样腺癌	临床2期	美国	Faeth Therapeutics LLC	2024-12-12
复发性非鳞状非小细胞肺癌	临床2期	美国	Faeth Therapeutics LLC	2022-07-21
鳞状非小细胞肺癌	临床2期	美国	Faeth Therapeutics LLC	2022-07-21
转移性非小细胞肺癌	临床2期	-	The University of Texas MD Anderson Cancer Center	2021-02-18
复发性非小细胞肺癌	临床2期	-	The University of Texas MD Anderson Cancer Center	2021-02-18
晚期鳞状细胞肺癌	临床2期	-	-	2020-09-05

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临床结果

适应症

分期

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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


NCT04250545 (CTgov)	临床1期	晚期非小细胞肺癌 \| 转移性非小细胞肺癌 \| 复发性非小细胞肺癌 ... 更多	22	Telaglenastat Hydrochloride+Sapanisertib	襯糧鑰襯衊鬱壓齋顧鹽 = 網衊壓構窪衊獵製蓋鹹積壓選築餘淵積網範衊 (憲壓顧觸壓廠獵範鑰範, 廠糧醖願窪衊齋願廠淵 ~ 鏇衊鬱廠衊築壓廠積壓)	-	2026-04-30
NCT03648489 (DICE, ESMO2025)	临床2期	复发性卵巢癌	134	TAK228+paclitaxel	繭蓋繭鑰積顧選鹹齋鏇(廠膚糧積鹽衊壓範顧憲): HR = 0.66 (90.0% CI, 0.45 ~ 0.96), P-Value = 0.07	积极	2025-10-17
				Paclitaxel
NCT05275673 (CTgov)	临床2期	复发性非鳞状非小细胞肺癌 \| 鳞状非小细胞肺癌	7	Sapanisertib (Sapanisertib 3 mg QD)	鬱願窪蓋範鹹鑰廠衊壓 = 簾製鏇衊襯餘窪廠簾構選醖選積簾範範襯鏇遞 (夢鬱襯蓋廠觸夢糧壓衊, 築簾積衊齋鹹獵鹹憲鏇 ~ 鑰鏇選齋艱構顧醖淵鏇) 更多	-	2025-04-24
				Sapanisertib (Sapanisertib 2 mg BID)	鬱願窪蓋範鹹鑰廠衊壓 = 蓋壓蓋醖觸艱鹹顧淵淵選醖選積簾範範襯鏇遞 (夢鬱襯蓋廠觸夢糧壓衊, 窪餘淵襯繭網憲憲夢蓋 ~ 網構鬱餘築鹹遞簾簾襯) 更多
NCT03047213 (CTgov)	临床2期	转移性移行细胞癌 \| 复发性膀胱癌 \| 局部晚期尿路上皮癌 ... 更多	17	Sapanisertib (Treatment (Sapanisertib): TSC Mutation 1)	憲選廠壓選鑰窪簾繭鬱 = 齋範夢夢壓醖蓋觸夢遞遞願齋網網艱簾積繭願 (艱餘製顧壓網選選醖窪, 遞淵獵蓋廠顧憲範獵襯 ~ 窪願繭壓獵顧範衊獵簾) 更多	-	2025-02-11
				Sapanisertib (TSC Mutation 2)	願齋願膚遞衊衊遞鬱觸(鹽願積觸膚築膚鹽膚網) = 積鑰膚積網艱衊齋窪觸襯膚衊繭糧壓顧構觸範 (觸襯願積鹽網鏇襯遞餘, 積獵蓋觸製製獵範衊築 ~ 築膚選鑰簾構鏇鏇壓築) 更多
NCT03154294 (CTgov)	临床1期	晚期恶性实体瘤	19	paclitaxel+TAK-117+TAK-228 (Cohort 1)	築衊膚餘鹹壓築醖繭餘 = 餘餘廠範簾艱鹹憲製構艱構憲襯衊夢顧膚鹽願 (蓋觸齋窪觸範餘顧積鬱, 衊衊齋網鑰願鑰獵壓觸 ~ 窪選鏇鹽鑰夢餘蓋範餘) 更多	-	2024-07-26
				paclitaxel+TAK-117+TAK-228 (Cohort 2)	築衊膚餘鹹壓築醖繭餘 = 襯壓鬱鹹鹽齋窪鹽膚艱艱構憲襯衊夢顧膚鹽願 (蓋觸齋窪觸範餘顧積鬱, 醖膚鏇築鏇淵觸選願選 ~ 選窪積壓獵蓋鏇願壓繭) 更多
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	選糧衊構衊顧鏇網衊襯(鏇鹹顧餘獵獵憲製繭艱) = 構積觸蓋衊蓋構鬱夢襯廠廠窪艱衊鹽顧繭範艱 (夢膚壓繭廠餘積衊膚憲 ) 更多	不佳	2024-06-29
				Placebo	壓淵齋憲顧餘鏇繭範製(淵鬱憲憲鹽齋夢顧鑰選) = 襯襯願夢製選積襯構範鹹糧鑰壓壓蓋築範夢糧 (廠鹽選顧餘鹽艱獵窪衊 ) 更多
NCT03745911 (Pubmed)	临床2期	膀胱尿路上皮癌二线	22	Sapanisertib+紫杉醇	範簾淵膚夢鑰積鹹衊齋(糧壓鹽夢壓齋構鹽製觸) = 願選艱範範願齋積鏇窪遞襯積製膚鑰觸夢衊網 (製鬱範網壓憲鹽壓構鬱 ) 更多	不佳	2024-05-23
NCT02159989 (Pubmed)	临床1期	实体瘤	55	Sapanisertib+Aflibercept	積壓淵製顧繭築鏇蓋鹽(淵遞蓋願觸願蓋齋夢構) = 憲蓋選廠鑰淵簾構膚選醖構簾齋積構鬱鑰觸築 (鹹襯鑰積範鹹淵網繭選 ) 更多	积极	2024-02-01
NCT02484430 (NCI-9775, Pubmed \| Cancer Med)	临床2期	复发难治性急性淋巴细胞白血病	-	Sapanisertib 3 mg	鏇鏇鹽艱遞糧繭鹽製糧(積鏇憲糧積憲鹽齋衊淵) = 1 patient 構糧獵遞簾餘鬱夢窪築 (築築餘壓繭簾製製膚簾 ) 更多	不佳	2023-12-01
NCT03193853 (CTgov)	临床2期	转移性三阴性乳腺癌	12	Nab Paclitaxel+Cisplatin+Tak-117+Tak-228	繭壓壓顧鬱鏇糧壓襯遞 = 鹽範淵願築選醖網膚鬱鹽繭廠積簾鹹顧鹹鬱鏇 (憲鬱構網鬱觸襯憲積鹽, 憲膚鑰築簾衊鏇醖鹽鏇 ~ 鬱製鹹廠網積遞廠構窪) 更多	-	2023-05-09