An Open-Label, Multicenter, Phase 1a Study of AN2025 and AN0025 in Double Combination With Atezolizumab and in Triple Combination With Atezolizumab in Patients With Advanced Solid Tumors

This is an open-label, multicenter, Phase 1a study to evaluate the safety, tolerability, PK and preliminary efficacy of AN2025 and AN0025 in double or triple combination treatments with Atezolizumab in patients with locally advanced/metastatic tumors.

开始日期2021-09-07

申办/合作机构

杭州阿诺生物医药科技有限公司

EUCTR2015-003103-27-GB

/ Not yet recruiting临床2期IIT

A proof of concept phase II study of Buparlisib in HER2 positive breast cancer with brain metastasis following HER2 directed monoclonal antibody therapy - BLUEBELL

开始日期2017-01-19

申办/合作机构

The University of Liverpool

NCT02756247

/ Completed临床1期IIT

Phase Ib Clinical Trial of Buparlisib and Ibrutinib in Mantle Cell Lymphoma, Follicular Lymphoma and Diffuse Large B Cell Lymphoma

The purpose of this study is to find out if the combination of buparlisib and ibrutinib will lead to better treatment results in patients with relapsed or refractory Follicular lymphoma, (FL) Mantle cell lymphoma (MCL) or Diffuse Large B-cell lymphoma (DLBCL). The investigators are using buparlisib and ibrutinib because both drugs seem to block different proteins that allow cancer cells to keep growing. Blocking these proteins may help by making the cancer cells undergo cell death, which will stop uncontrolled tumor growth.

开始日期2016-05-09

申办/合作机构

Memorial Sloan Kettering Cancer Center

[+2]

100 项与 Buparlisib 相关的临床结果

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100 项与 Buparlisib 相关的转化医学

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100 项与 Buparlisib 相关的专利（医药）

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项与 Buparlisib 相关的文献（医药）

2025-11-13·JOURNAL OF MEDICINAL CHEMISTRY

Discovery of Novel PI3K/BRD4 Dual Inhibitors for Esophageal Cancer: Rational Design, Optimization, and Senescence-Inducing Mechanisms

Article

作者: Sheng, Li ; Wang, Jinhua ; Xiong, Tianning ; Ge, Junpu ; Xu, Heng ; Peng, Shouguo ; Li, Wan ; Chu, Shiji ; Lin, Songwen ; Yang, Yihui

The discovery of novel targeted therapies for esophageal cancer represents an urgent clinical need. Herein, we reported the rational design and synthesis of novel PI3K/BRD4 dual inhibitors for the treatment of esophageal cancer. Systematic structure-activity relationship studies identified compound 23 as a potent dual-targeting inhibitor that effectively suppresses PI3K and BRD4 signaling. In vitro, 23 inhibited proliferation, migration, invasion, and colony formation of esophageal cancer cells. In vivo, 23 demonstrated anticancer efficacy comparable to that of the BKM120/JQ1 combination treatment in a KYSE450 xenograft mouse model. Mechanistically, 23 induces cellular senescence via the AMPK-p27 pathway. Significantly, the senolytic agent ABT737 enhanced the efficacy of compound 23 through the selective clearance of senescent cancer cells. Collectively, this work establishes 23 as a promising PI3K/BRD4 dual-targeting lead and supports senescence induction combined with senolytics as a novel strategy for esophageal cancer treatment.

2025-11-01·JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS

Essential roles of mechanistic target of rapamycin in the induction of steroid resistance in group 2 innate lymphoid cells and severe asthma

Article

作者: Shimora, Hayato ; Kitao, Ayaha ; Ariyoshi, Yusuke ; Sannomiya, Yuya ; Nabe, Takeshi ; Nakayama, Yukiko ; Matsuda, Masaya ; Matsumura, Misaki

Approximately 5% to 10% of asthma patients are resistant to glucocorticoid therapy; however, the mechanisms by which this resistance develops remain unclear. The present study investigated whether and how mechanistic target of rapamycin (mTOR) is involved in the development of steroid resistance using in vitro and in vivo murine models. The interleukin (IL)-33/thymic stromal lymphopoietin (TSLP)/IL-7-induced growth of group 2 innate lymphoid cells (ILC2) in vitro was resistant to dexamethasone (DEX), but suppressed by everolimus, an mTOR inhibitor, in a concentration-dependent manner. The inhibition of ILC2 growth by the combination of DEX and everolimus was significantly stronger than that by everolimus monotherapy. The combination of the pan-class I phosphatidylinositide-3 kinase inhibitor, buparlisib and the pan-Akt inhibitor, capivasertib also attenuated the resistance of IL-33/TSLP/IL-7-exposed ILC2s to DEX. The expression of the antiapoptotic factor, B-cell lymphoma-extra large, induced by IL-33/TSLP/IL-7 in ILC2s was significantly reduced by everolimus. Additionally, everolimus effectively suppressed the IL-33/TSLP/IL-7-induced phosphorylation of glucocorticoid receptors (GR) at the Ser234 residue, which has been reported to cause GR dysfunction. In the steroid-resistant asthma mouse model in vivo, under treatment with everolimus, DEX inhibited the development of airway remodeling and increased the number of ILC2s in the lungs. The present results suggest that the phosphoinositide 3-kinase/protein kinase B/mTOR pathway plays an essential role in the development of steroid resistance in ILC2s and asthma pathogenesis through both the expression of B-cell lymphoma-extra large and phosphorylation of GR. Therefore, mTOR inhibitors have the potential to restore glucocorticoid sensitivity and, thus, exert steroid-sparing effects in severe asthma patients. SIGNIFICANCE STATEMENT: Approximately 5% to 10% of asthma patients exhibit resistance to steroid therapy, posing a major clinical challenge due to limited treatment options. This study demonstrates that activation of the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (mTOR) pathway induces steroid resistance in group 2 innate lymphoid cells. Targeting mTOR with everolimus restores steroid sensitivity, highlighting mTOR inhibition as a promising pharmacotherapy for steroid-resistant asthma.

2025-10-01·World Journal of Oncology

Targeting the Phosphoinositide 3-Kinase/Protein Kinase B Pathway Suppresses Y-Box Binding Protein 1 Expression and Inhibits Colorectal Cancer Progression

Article

作者: Qin, Rong ; Tian, Guangyu ; Wang, Yuting ; Qiu, Zhiyuan ; Zhang, Niu ; Hu, Siyu ; Wang, Yan ; Shan, Hui

Background:

Colorectal cancer (CRC) is one of the most prevalent and lethal malignancies worldwide, often characterized by the aberrant activation of multiple signaling pathways. Y-box binding protein 1 (YBX1), a multifunctional regulator of transcription and translation, has been identified as an oncogenic factor in various solid tumors. However, its expression profile and mechanistic role in CRC remain largely unclear.

Methods:

In this study, integrative bioinformatic analyses were conducted on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets to assess YBX1 expression and its correlation with CRC progression. Functional assays, including cell proliferation and migration assays, were performed to investigate the role of YBX1 in CRC cells. The impact of YBX1 on the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway was evaluated, and the effects of the PI3K inhibitor buparlisib (BKM120) on YBX1-driven cellular phenotypes were also tested.

Results:

YBX1 was found to be significantly upregulated in CRC tissues and was closely associated with the activation of the PI3K/AKT signaling pathway. YBX1 overexpression promoted CRC cell proliferation and migration, whereas knockdown of YBX1 inhibited these processes. Mechanistically, YBX1 was shown to enhance PI3K/AKT signaling activity, promoting malignant phenotypes in CRC. Treatment with BKM120 partially reversed these effects. Additionally, Gene Set Enrichment Analysis (GSEA) identified enrichment of reactive oxygen species (ROS)-related pathways in YBX1-high CRC samples.

Conclusions:

This study highlights the oncogenic role of YBX1 in CRC and reveals a potential YBX1-PI3K/AKT regulatory axis that may serve as a promising therapeutic target. The findings suggest that targeting this axis could provide a novel strategy for CRC treatment, especially under hypoxic or microenvironmental stress conditions.

项与 Buparlisib 相关的新闻（医药）

2025-11-23

·ioncology

ESMO 国际视野丨Denis Soulieres教授： BURAN研究折戟沉沙的启示与未来方向

编者按：近期欧洲肿瘤内科学会（ESMO）年会上报告结果的III期BURAN研究，评估了PI3K抑制剂buparlisib联合紫杉醇在PD-1/L1抑制剂治疗失败的复发性/转移性头颈部鳞状细胞癌（HNSCC）患者中的疗效，但未能在无进展生存期（PFS）和总生存期（OS）方面显示出优于紫杉醇单药的结果（中位PFS均为4.1个月；中位OS：9.6个月 vs 9.7个月）。尽管联合方案在客观缓解率（ORR）上保持优势（30.3% vs 20.7%），但这一阴性结果揭示了当前针对免疫治疗失败患者缺乏优选方案的临床困境。《肿瘤瞭望》特邀加拿大蒙特利尔大学医学中心Denis Soulieres教授对BURAN研究深度点评，指出BURAN研究相比历史数据（BERIL-1试验中同类患者中位OS仅6.5个月）反映出免疫治疗时代患者预后整体改善（OS提升至10个月以上），然而超过80%的免疫治疗进展率仍凸显后续治疗策略的不足。未来方向需聚焦生物标志物开发（超越PD-L1）及新型药物组合，以突破当前治疗瓶颈。 01 《肿瘤瞭望》：您在本次会议上报告了评估PI3K抑制剂buparlisib联合紫杉醇，用于既往接受PD-1/L1抑制剂治疗的复发性/转移性头颈部鳞状细胞癌（HNSCC）的III期研究BURAN结果，您如何评价该研究成果及其临床价值？ Denis Soulieres 教授加拿大蒙特利尔大学医学中心 III期BURAN临床研究是基于II期BERIL-1研究进行设计的。BERIL-1研究评估了Buparlisib联合紫杉醇对比单用紫杉醇在既往铂类化疗后进展的复发性或转移性HNSCC患者中的疗效。而在BURAN III期试验中，我们旨在评估一个新的患者群体，即PD-1抑制剂治疗失败的患者，因免疫治疗已成为HNSCC的一线或二线标准疗法。在BURAN试验中，我们得到的结果与BERIL-1中的发现有所不同。BERIL-1研究在提高缓解率方面取得了阳性结果，这一点在BURAN试验中同样得到了体现（BUP+PAC的ORR为30.3% vs PAC的20.7%）。然而，在无进展生存期和总生存期方面，BERIL-1中联合治疗组显示出显著优势（中位PFS：4.6个月 vs 3.5个月，HR 0.65；中位OS：10.4个月 vs 6.5个月），但在BURAN试验中，我们未观察到联合治疗在PFS（中位PFS均为4.1个月，HR 0.97）或OS（中位OS：9.6个月 vs 9.7个月，HR 1.02）方面与紫杉醇单药有差异。因此，对于免疫治疗失败的患者群体，Buparlisib联合紫杉醇的方案并未证明优于紫杉醇单药治疗。 02 《肿瘤瞭望》：在复发/转移性HNSCC的精准治疗方面，您认为还有哪些在研新药有望取得突破？与现有免疫治疗联合是否会成为重要的探索方向？ Denis Soulieres 教授加拿大蒙特利尔大学医学中心 BURAN研究所评估的患者群体向我们揭示了一个关键问题：对于一线免疫治疗失败的患者，我们目前仍然缺乏首选的后续治疗方案，这是我们获得的重要启示。然而，该研究也让我们认识到，免疫治疗失败的患者实际预后比我们既往认知的要更为乐观。在BERIL-1试验中，同类患者的中位生存期仅为6.5个月，而BURAN试验中该数值提升至10个月以上——这明确表明，当前患者群体的预后已得到改善，但在治疗选择上，我们尚未能寻找到比现有紫杉醇方案更优的策略。目前，我们仍有大量工作亟待推进，因为已知超过80%的患者会在前线免疫治疗中发生疾病进展，这一现状为治疗优化留下了巨大空间。值得注意的是，研究已证实针对PD-L1高表达（CPS≥20）的患者，帕博利珠单抗单药治疗的疗效与帕博利珠单抗联合化疗方案相当。目前有多类新药正在研发中，例如与帕博利珠单抗联用的功能性抗EGFR抗体已显示出显著提升肿瘤缓解率的潜力，但我们仍需通过临床试验进一步验证该组合能否转化为总生存期的获益，相关研究目前正在积极开展中。 03 《肿瘤瞭望》：为实现复发性/转移性HNSCC个体化治疗，您认为应检测或探索哪些生物标志物？哪些标志物是您在实践中已经常规使用的？ Denis Soulieres 教授加拿大蒙特利尔大学医学中心目前，PD-L1是我们临床上唯一常规应用的生物标志物。PD-L1表达阴性（通常指CPS<1）的患者比例可能低于百分之十，这类患者确实难以从免疫治疗中获益，因此通常不建议接受该治疗。但这同时也意味着，有超过百分之八十的患者，除了PD-L1检测结果之外，我们缺乏更有效的生物标志物来进一步精准指导其治疗决策。我们认识到HPV阳性（在口咽癌中常以p16蛋白过表达作为替代标志物）通常预示着更好的预后，但它是否能预测对特定治疗方案（尤其是免疫治疗）的反应，即其预测价值，目前仍不明确。因此，在复发/转移性HNSCC领域，除了PD-L1检测之外，我们在寻找其他合适的生物标志物方面，仍然面临巨大的挑战和未满足的需求。 Denis Soulieres 教授加拿大蒙特利尔大学医学中心（来源：《肿瘤瞭望》编辑部）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

2025-04-10

·阿诺医药

阿诺医药宣布将在2025年美国癌症研究协会年会上展示创新癌症疗法研究进展

北京时间2025年4月10日——阿诺医药集团有限公司（纳斯达克股票代码：ANL）（以下简称“阿诺医药”），一家专注于肿瘤治疗领域的创新型全球生物制药公司，今日宣布将在2025年4月25-30日于美国芝加哥举行的美国癌症研究协会（AACR）年会上展示创新癌症疗法研究进展。阿诺医药计划进行两项研究成果的海报展示。阿诺医药研发负责人谢毅钊博士表示：我们很高兴在即将召开的2025年AACR年会上介绍我们创新产品管线的进展。我们在构建多特异性免疫肿瘤治疗平台领域展现了卓越的研发实力，AN8025（一款融合了αPDL1、Lag3变体、CD86变体的三特异性抗体融合蛋白）为代表性成果；同时，我们在开发高度创新的小分子泛RAS(ON)抑制剂领域也取得了重大进展，例如AN9025。这些突破性研究让我们倍感自豪，也充分体现了阿诺医药致力于为癌症患者带来革命性治疗方案的坚定承诺。阿诺医药在2025年AACR年会期间的展示标题：首创三特异性AN8025协同刺激APC和T细胞功能，用于下一代癌症免疫治疗(摘要#3420)时间：2025年4月28日（星期一）2:00 PM – 5:00 PM （当地时间）会议：增强抗体、TCR构建体、细胞因子和嵌合蛋白展区：海报35区展板：15标题：AN9025，一款具有强效广谱抗肿瘤活性的口服泛RAS(ON)抑制剂(摘要#4377)时间：2025年4月29日（星期二） 9:00 AM – 12:00 PM （当地时间）会议：RAS抑制剂展区：海报21区展板：12关于AN8025AN8025 是一款三特异性抗体融合蛋白，其基于已获批的αPD-L1抗体，并与功能优化的CD86和LAG3变体蛋白融合而成，可调节T细胞和抗原呈递细胞（APC）功能。临床前研究表明，AN8025 不仅提高了APC的数量和质量，还可诱导强烈的PD-L1依赖性T细胞活化及体内抗肿瘤疗效。公司计划于2025年中提交IND申请。关于AN9025AN9025是公司自主研发的口服小分子泛RAS(ON)抑制剂，旨在靶向具备RAS突变的多种肿瘤类型。临床前研究表明，AN9025对胰腺癌、肺癌和结直肠腺癌等RAS突变小鼠肿瘤模型具有强效持久的抑制效果，与同类基准药物相比展现出相当或更优的疗效。公司计划于2025年下半年提交IND申请。关于阿诺医药阿诺医药（纳斯达克股票代码：ANL）是一家临床阶段的全球性生物制药公司，专注于开发创新肿瘤靶向和肿瘤免疫疗法，在中美两地均设有研发及临床运营中心。公司正在推进强大的肿瘤产品管线，其中我们的主要候选药物Buparlisib(AN2025)是一种泛PI3K抑制剂，目前正在针对抗PD(L)1治疗后的复发或转移性头颈部鳞状细胞癌（HNSCC）患者进行注册性III期试验（NCT04338399）。此外，公司还在推进多个候选药物，包括口服小分子PD-L1 抑制剂AN4005，多功能融合蛋白AN8025（作为T细胞和抗原呈递细胞（APC）调节剂）以及口服小分子泛RAS(ON)抑制剂AN9025。免责声明本新闻稿包含1995年《美国私人证券诉讼改革法案》“安全港”条款中定义的“前瞻性陈述”。此类前瞻性陈述涉及未来（而非过去）事件，通常可凭借“预计”、“预期”、“有意”、“计划”、“认为”、“寻求”、“将会”等词语以及这些词语或类似表述的变体加以辨别，但其并非是识别此类陈述的唯一方法。因其性质使然，前瞻性陈述所述及的事项存在风险和不确定性，且程度各不相同。特定的风险和不确定性可能导致实际结果与前瞻性陈述述及的内容存在重大差异，这包括潜在产品研发及商业化的固有风险，临床试验结果、监管机构审批或清关的不确定性，未来的资本需求，对合作方的依赖性，以及对知识产权的维护情况等。更多有关可能影响结果的潜在因素以及其他风险与不确定性的信息不时会在公司的定期报告中详细阐述。无论是否出现新讯息、未来事件或情况或其他因素，我们概不承担更新或修订本新闻稿所含前瞻性陈述的义务。

AACR会议免疫疗法临床申请临床1期临床结果

2025-04-10

·GlobeNewswire-Health Care

Adlai Nortye to Present Research Findings at AACR Annual Meeting 2025

SINGAPORE and NORTH BRUNSWICK, N.J. and HANGZHOU, China, April 10, 2025 (GLOBE NEWSWIRE) -- Adlai Nortye Ltd. (NASDAQ: ANL) (the “Company” or “Adlai Nortye”), a clinical-stage biotechnology company focused on the development of innovative cancer therapies, today announced the presentation at the American Association for Cancer Research (AACR) Annual Meeting, taking place April 25-30, 2025, in Chicago. Adlai Nortye has two abstracts scheduled for presentations at AACR. "We are pleased to present the progress of our innovative pipeline at the upcoming 2025 AACR Annual Meeting. We are especially proud of our R&D capabilities in designing and developing our multi-specific immune-oncology platform, highlighted by AN8025 (αPDL1xLag3variant xCD86variant), and highly innovative small molecule pan-RAS(ON) inhibitors, exemplified by AN9025. This breakthrough work underlines our commitment to delivering transformative therapies for cancer patients," said Archie Tse, MD, PhD, Head of Research and Development at Adlai Nortye. The title and session information for the poster presentation are listed below. Poster title: Coordinated stimulation of APC and T cell functions by first-in-class, tri-specific AN8025 for next-generation cancer immunotherapy” (Abstract# 3420)Date and Time: Monday, April 28, 2025; 2:00 PM - 5:00 PM CTSession Title: Enhanced Antibodies, TCR Constructs, Cytokines and Chimeric ProteinsLocation: Poster Section 35Poster Board Number: 15 Poster title: AN9025, an orally bioavailable pan-RAS(ON) inhibitor with potent, broad-spectrum anti-tumor activity (Abstract# 4377)Date and Time: Tuesday, April 29, 2025; 9:00 AM - 12:00 PM CTSession Title: RAS InhibitorsLocation: Poster Section 21Poster Board Number: 12 Full abstract details including title and text are currently available to registrants via the AACR online itinerary planner. A copy of the presentation will be available in the Posters and Presentations section on Adlai Nortye’ website after AACR 2025 conference. About AN8025AN8025 is a proprietary tri-specific antibody fusion protein derived from an approved αPD-L1 antibody and fused with functionally optimized CD86 and LAG3 variants. Designed to modulate T cell and antigen-presenting cell (APC) functions, preclinical studies have demonstrated that AN8025 enhances both the quantity and quality of APCs while also inducing robust PD-L1-dependent T cell activation and anti-tumor efficacy in vivo. The Company plans to submit the IND application in mid-2025. About AN9025AN9025 is an in-house developed oral small molecule pan-RAS(ON) inhibitor, designed to target a broad spectrum of RAS mutations across various tumor types. Preclinical studies have demonstrated that AN9025 effectively inhibits RAS-mutant cancers with potent and durable efficacy, including pancreatic, lung, and colorectal adenocarcinomas, and shows comparable or superior results relative to a benchmark agent of the same class. The company plans to submit an IND application in the second half of 2025. About Adlai NortyeAdlai Nortye (NASDAQ: ANL) is a global clinical-stage company focused on the development of innovative targeted and immune-modulating cancer therapies, with global R&D centers in the U.S. and China. The Company is advancing a robust oncology pipeline, with our lead candidate Buparlisib (AN2025), a pan-PI3K inhibitor, currently being evaluated in a registrational Phase 3 trial (NCT04338399) in patients with recurrent or metastatic head and neck squamous cell cancer (HNSCC) that has progressed after prior anti-PD(L)1 treatment. Additionally, we are advancing multiple drug candidates including AN4005, an oral small molecule PD-L1 inhibitor, AN8025, a multifunctional fusion protein acting as a T cell and antigen-presenting cell (“APC”) modulator, and AN9025, an oral small molecule pan-RAS(ON) inhibitor. Forward-Looking StatementThis announcement contains forward-looking statements. These statements are made under the “safe harbor” provisions of the U.S. Private Securities Litigation Reform Act of 1995. These forward-looking statements can be identified by terminology such as “will,” “expects,” “anticipates,” “future,” “intends,” “plans,” “believes,” “estimates,” “potential,” “continue,” “ongoing,” “targets” and similar statements. Among other things, statements that are not historical facts, including statements about the Company’s beliefs and expectations, the business outlook and quotations from management in this announcement, as well as the Company’s strategic and operational plans, are or contain forward-looking statements. The Company may also make written or oral forward-looking statements in its periodic reports to the U.S. Securities and Exchange Commission (the “SEC”), in press releases and other written materials and in oral statements made by its officers, directors or employees to third parties. Forward-looking statements involve inherent risks and uncertainties. Factors that could cause the Company’s actual results to differ materially from those expressed or implied in such forward-looking statements include, but are not limited to: the initiation, timing, progress and results of the Company’s preclinical studies, clinical trials and other therapeutic candidate development efforts; the Company’s ability to advance its therapeutic candidates into clinical trials or to successfully complete its preclinical studies or clinical trials; whether the clinical trial results will be predictive of real-world results; the Company’s receipt of regulatory approvals for its therapeutic candidates, and the timing of other regulatory filings and approvals; the clinical development, commercialization and market acceptance of the Company’s therapeutic candidates; the Company’s ability to establish, manage, and maintain corporate collaborations, as well as the ability of its collaborators to execute on their development and commercialization plans; the implementation of the Company’s business model and strategic plans for its business and therapeutic candidates; the scope of protection the Company is able to establish and maintain for intellectual property rights covering its therapeutic candidates and its ability to operate its business without infringing the intellectual property rights of others; estimates of the Company’s expenses, future revenues, capital requirements and its needs for and ability to access sufficient additional financing; risks related to changes in healthcare laws, rules and regulations in the PRC and United States or elsewhere. Further information regarding these and other risks is included in the Company’s filings with the SEC. All information provided in this announcement and in the attachments is as of the date of this announcement, and the Company does not undertake any obligation to update any forward-looking statement, except as required under applicable law. Company contact:Investor RelationsEmail: ir@adlainortye.com

免疫疗法AACR会议临床3期

100 项与 Buparlisib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10584	Buparlisib	-	DB11666

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
头颈部鳞状细胞癌	临床3期	中国	Adlai Nortye USA Inc	2021-04-07
转移性头颈部鳞状细胞癌	临床3期	美国	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	中国	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	日本	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	阿根廷	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	澳大利亚	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	比利时	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	加拿大	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	法国	杭州阿诺生物医药科技有限公司	2020-12-12
转移性头颈部鳞状细胞癌	临床3期	德国	杭州阿诺生物医药科技有限公司	2020-12-12

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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


NCT04338399 (BURAN, ESMO2025)	临床3期	PD-L1阳性头颈部鳞状细胞癌 PD-1(PD-L1)-pretreated \| HPV-negative	487	Buparlisib (BUP) + Paclitaxel (PAC)	憲繭蓋蓋鏇築繭餘壓鏇(網鹽襯積繭觸鏇夢構壓) = 衊餘醖襯壓廠鏇窪範繭範壓顧願襯願築鑰糧淵 (構醖艱夢遞壓顧鹹簾齋 ) 更多	不佳	2025-10-17
				Paclitaxel (PAC)	憲繭蓋蓋鏇築繭餘壓鏇(網鹽襯積繭觸鏇夢構壓) = 廠糧選壓艱鏇壓艱鏇構範壓顧願襯願築鑰糧淵 (構醖艱夢遞壓顧鹹簾齋 ) 更多
NCT01852292 (BERIL-1, Pubmed \| Target Oncol)	临床2期	头颈部鳞状细胞癌 TP53 \| NOTCH1 \| PIK3CA ... 更多	158	Buparlisib + Paclitaxel	夢襯廠鹽壓壓襯鹽簾築(醖艱積鹽廠築襯顧鑰獵) = 鏇繭遞憲製齋糧壓齋範憲壓蓋遞遞壓構願齋膚 (遞鬱範遞鑰鹽夢願窪顧 ) 更多	积极	2025-01-14
				Placebo + Paclitaxel	簾積艱築衊簾選網淵願(廠膚醖廠願網鏇獵鏇餘) = 壓醖鑰構繭淵膚簾衊壓壓襯鑰鑰製顧製壓窪網 (獵鏇衊築鏇淵築獵衊遞 )
NCT02113878 (CTgov)	临床1期	下咽癌 \| HPV阳性的口咽鳞状细胞癌 \| 局部晚期头颈部鳞状细胞癌 ... 更多	23	Intensity-modulated radiotherapy (IMRT)+BKM120+Cisplatin (Dose Level 1)	襯遞齋窪願膚齋鬱範網 = 顧構構淵簾觸繭選壓願憲憲鹹憲製鑰艱網衊築 (鑰鏇餘鬱壓淵襯網夢憲, 構蓋衊憲膚蓋醖顧範窪 ~ 鹹鬱網鏇醖餘構願網膚) 更多	-	2024-11-05
				Intensity-modulated radiotherapy (IMRT)+BKM120+Cisplatin (Dose Level 2)	襯遞齋窪願膚齋鬱範網 = 窪獵淵鬱構顧淵窪夢觸憲憲鹹憲製鑰艱網衊築 (鑰鏇餘鬱壓淵襯網夢憲, 憲餘網選衊廠鹽選餘膚 ~ 繭鏇觸範鹹鏇觸憲遞壓) 更多
NCT02000882 (CTgov)	临床2期	转移性乳腺癌 \| 脑转移瘤	10	Trastuzumab+BKM120+Capecitabine	築願積壓觸築鹽積齋築 = 艱壓築糧齋製淵網遞範齋鬱餘鑰糧鏇窪壓選遞 (製積製選範齋窪憲廠製, 遞鏇廠壓憲積鏇襯範醖 ~ 構艱鹽網餘顧築積鹽糧) 更多	-	2022-02-01
NCT02220855 (Pubmed)	临床2期	胸腺瘤	14	Buparlisib	顧鹽艱艱繭衊廠構製餘(鹹醖範衊襯遞窪壓衊廠) = 範鏇淵範壓觸鏇構鏇積鏇憲構艱夢蓋積觸憲積 (淵選選構鹹艱艱窪網壓 ) 更多	积极	2022-01-01
NCT02756247 (Pubmed \| Clin Cancer Res)	临床1期	套细胞淋巴瘤 \| 滤泡性淋巴瘤 \| 弥漫性大B细胞淋巴瘤	37	Buparlisib and Ibrutinib	鹹廠鏇選醖選遞衊鏇膚(襯製醖襯鏇鏇膚齋糧簾) = 夢廠鑰選淵艱壓憲積鑰鹽鬱鹹觸鏇鑰鹹築網選 (繭積願觸壓簾齋遞遞觸 ) 更多	-	2021-10-06
NCT01551030 (CTgov)	临床2期	肾盂和输尿管尿路上皮癌 \| 晚期尿路上皮癌 \| 尿路上皮癌	19	Buparlisib	廠製廠襯醖獵糧襯糧網 = 糧齋鏇窪觸衊餘淵淵艱餘顧觸衊餘餘築獵艱醖 (簾餘醖鏇窪製顧淵構艱, 鹹獵構蓋選鬱艱遞壓餘 ~ 鹹網遞糧廠鹹蓋餘鹹遞) 更多	-	2021-06-21
NCT04338399 (BURAN, ASCO2021)	临床3期	转移性头颈部鳞状细胞癌二线	483	Buparlisib + Paclitaxel	鏇衊襯壓膚餘鏇齋顧選(簾鹹壓積遞艱齋築壓遞) = 淵膚鬱遞顧蓋獵壓窪蓋醖製積鹹襯繭簾窪夢願 (蓋製製簾願鬱遞蓋獵鏇 )	积极	2021-05-28
				Paclitaxel alone	鏇衊襯壓膚餘鏇齋顧選(簾鹹壓積遞艱齋築壓遞) = 齋願網願遞製積積選繭醖製積鹹襯繭簾窪夢願 (蓋製製簾願鬱遞蓋獵鏇 )
NCT02058381 (B-YOND, Pubmed \| Clin Cancer Res) 人工标引	临床1期	HR阳性HER2阴性淋巴结阳性乳腺癌 HR-Positive \| HER2-Negative	29	Tamoxifen Citrate+Goserelin Acetate+Alpelisib	淵鏇鹹鹽觸製鬱廠築糧(願餘鑰衊夢網艱網繭醖) = 網鑰淵艱憲壓艱簾鏇積膚範襯繭憲糧網醖餘鬱 (艱襯艱築製衊鑰積範願 ) 更多	积极	2021-01-15
				Tamoxifen Citrate+Goserelin Acetate+Buparlisib	淵鏇鹹鹽觸製鬱廠築糧(願餘鑰衊夢網艱網繭醖) = 選範鬱淵獵鹹築鏇膚膚膚範襯繭憲糧網醖餘鬱 (艱襯艱築製衊鑰積範願 ) 更多
NCT02088684 (Pubmed \| Clin Cancer Res)	临床1期	HR阳性/HER2阴性乳腺癌 \| 晚期乳腺癌	70	Ribociclib plus Buparlisib plus Fulvestrant	蓋廠願築夢簾遞廠鏇夢(齋夢觸獵膚艱淵窪醖艱) = 簾膚廠淵窪積構選獵衊選願壓淵製廠齋醖齋窪 (鹽蓋鹽餘蓋膚範鬱壓積, 9.8 ~ 46.7)	-	2021-01-15