Patients with metastatic bladder cancer are usually treated with chemotherapy. If their cancers do not progress after chemotherapy, they can be enrolled into this study and receive a standard-of-care immunotherapy medication named avelumab plus a study drug named copanlisib.

开始日期2025-06-02

申办/合作机构

VA Office of Research and Development

[+1]

NCT06218667

/ Withdrawn临床1/2期IIT

CHARIOT: a Phase 1b/2 Study of Androgen Deprivation Therapy and Copanlisib in High-Risk Localized Prostate Cancer Patients Prior to Radical Prostatectomy

The researchers are doing this study to find out whether copanlisib in combination with degarelix, given before standard surgical treatment (radical prostatectomy), is a safe and effective treatment that causes few or mild side effects for people who have localized high-risk prostate cancer.

开始日期2024-01-11

申办/合作机构

Memorial Sloan Kettering Cancer Center

NCT05082025

/ Terminated临床2期IIT

Phase 2 Study of PI3K Inhibitor Copanlisib in Combination With Fulvestrant in Selected ER+ and/or PR+ Cancers With PI3K (PIK3CA, PIK3R1) and/or PTEN Alterations

The purpose of this study is to evaluate the efficacy and safety of copanlisib in combination with fulvestrant in advanced hormone receptor-positive (HR+) solid tumors harboring alterations that activate the Phosphatidylinositol-3 kinase (PI3K) pathway.

开始日期2022-09-27

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+1]

100 项与盐酸可泮利塞相关的临床结果

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100 项与盐酸可泮利塞相关的转化医学

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100 项与盐酸可泮利塞相关的专利（医药）

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304

项与盐酸可泮利塞相关的文献（医药）

2026-09-01·Translational Oncology

Combined inhibition of CDK4/6 and PI3K pathways exhibit highly synergistic activity and translational potential in Ewing sarcoma

Article

作者: Crompton, Brian D ; Finstuen-Magro, Sarah ; Shulman, David S ; McDannell, Brigit ; Blandin, Anne-Florence ; Meyer, Stephanie ; Klega, Kelly ; Shen, Min ; Chakraborty, Advaita ; Zhang, Ya-Qin ; Hall, Matthew D ; DuBois, Steven G ; Aguilar-Quintero, Alejandra ; Gloege, Helen F ; Tanhaemami, Mohammad ; Heaslip, Caleb O ; De Los Santos, Maria Ana Isabel C ; Chadha, Madhav

Ewing sarcoma is a highly aggressive solid malignancy affecting children and young adults. Ewing sarcoma is driven primarily by EWSR1::FLI1, a fusion oncoprotein that has been notoriously difficult to target with traditional pharmacologic agents. There are numerous examples of promising preclinical combinations of small molecules that are never tested in pediatric clinical trials because agents fail to reach the market due to limited efficacy for common adult cancers. Moreover, the effectiveness of single-agent therapies for cancer treatment is often limited. To address these limitations, we selected 28 compounds that were FDA approved at the time of the study or in late stages of clinical development and known to regulate important pathways in Ewing sarcoma. We performed a drug screen in Ewing sarcoma cell lines with 180 combinations of tyrosine kinase inhibitors, cell cycle inhibitors, and conventional chemotherapy. The results of the screen revealed that a PI3K inhibitor, copanlisib, combined with a CDK4/6 inhibitor, ribociclib, exhibited strong synergistic anti-Ewing sarcoma activity. Using proteomic methods such as a reverse-phase protein array and western immunoblotting, we demonstrated that this combination induced a downregulation of the PI3K/AKT pathway as well as proteins involved in cell cycle regulation. We further confirmed these in vitro data using bulk RNA-sequencing. To evaluate the phenotypic effect of the PI3K/CDK4/6 inhibition in Ewing sarcoma lines, we performed apoptosis and cell cycle analyses using flow cytometry and demonstrated that ribociclib primarily induced a G0/G1 arrest with minimal effect on Ewing cell viability but significantly enhanced the apoptotic effect of copanlisib treatment. In two xenograft models of Ewing sarcoma, we demonstrated that the combination significantly prolonged survival compared to treatment with either vehicle or single-agent therapy alone. Our findings identify a new candidate therapy combination for Ewing sarcoma and provide a resource of additional potential synergistic combinations for future validation.

2026-08-01·Clinical Lymphoma Myeloma & Leukemia

A Phase I Study of Copanlisib and Venetoclax in Patients With Relapsed or Refractory Diffuse Large B-Cell Lymphoma

Article

作者: Shipp, Margaret ; Herrera, Alex ; Crombie, Jennifer L ; Bartlett, Nancy ; Parry, Erin ; LaCasce, Ann ; Davids, Matthew S ; Jacobsen, Eric ; Jacobson, Caron A ; Fisher, David ; Odejide, Oreofe ; Redd, Robert ; Patterson, Victoria ; Kim, Austin I ; Carey, Celeste ; Balasubramanian, Sobana ; Shouse, Geoffrey ; Merryman, Reid W ; Armand, Philippe

BACKGROUND:

Preclinical data support the combination of venetoclax and copanlisib in specific genomic subgroups of diffuse large B-cell lymphoma (DLBCL).

PATIENTS AND METHODS:

In this investigator-initiated, phase I, multicenter trial we aimed to determine the maximum tolerated dose (MTD) and recommended phase 2 dose (RP2D) of copanlisib and venetoclax in patients with relapsed/refractory (R/R) DLBCL. Key eligibility criteria included relapse after or noncandidate for autologous stem cell transplantation or chimeric antigen receptor T-cell therapy and adequate hematologic and organ function. Key exclusion criteria were poorly controlled hypertension or diabetes.

RESULTS:

A total of 12 patients enrolled using a 3 + 3 design. The median age was 62 years (range 24-87 years) and 83% were male. The median number of prior treatments was 6 (range 1-11) and 10 patients had received prior CAR T-cell therapy. There were no dose limiting toxicities (DLT)s in dose level (DL)+2. Half of patients (2/4) in DL+3 were not able to escalate to 800 mg of venetoclax due to neutropenia and nonadherence. Key hematologic toxicities included neutropenia (50%, all grade (G) 3/4) and thrombocytopenia (42%, 17% ≥ G3), and the most common nonhematologic toxicities included nausea (33%, 8% ≥ G3), diarrhea (25%, all G1/2), elevated alkaline phosphatase (25%, 8% ≥ G3), fatigue (25%, all G1/2), and headache (25%, all G1/2). One patient had a complete response lasting 3 months. The median overall survival and progression-free survival were 4.1 and 1.6 months, respectively.

CONCLUSION:

Although the combination was tolerable, efficacy was poor in this unselected, heavily pretreated population.

2026-07-03·Expert Opinion On Drug Safety

Infectious complications associated with immune and targeted anti-cancer therapies: a retrospective study of the FDA adverse events reporting system (FAERS)

Article

作者: Alsowaida, Yazed S. ; Alsolami, Ahmed ; Abraham, Ivo ; Almangour, Thamer A.

BACKGROUND:

Immune and targeted anti-cancer therapies are associated with an increased risk of infectious complications. The objectives of the present study were to evaluate the infectious complications associated with immune and targeted anti-cancer drugs.

RESEARCH DESIGN AND METHODS:

This was a retrospective study for immune and targeted anti-cancer drugs submitted to the FDA Adverse Event Reporting System (FAERS) from 1996 to 20 March 2024. The primary outcome was the rate of infectious disease events, and the secondary outcomes were the incidence of febrile neutropenia (FN), all-cause mortality, and the top 10 infections in each class.

RESULTS:

Our study included 14 drug classes comprising 44 drugs. The incidence of infectious complications was 14.31% (110,671/773,130). The highest incidence rate was reported with IL-6 inhibitors (30.89%), the highest incidence of FN was reported with Histone deacetylase inhibitors (8.43%), and the highest all-cause mortality was reported with BCR-ABL tyrosine kinase inhibitors (17.17%).

CONCLUSION:

Immune and targeted anti-cancer therapies vary in the incidence of infectious complications. Pirtobrutinib, copanlisib, sirolimus, vorinostat, and tocilizumab were associated with high infectious complications (>30%) that warrant emphasis in the clinical guidelines. Thus, clinicians should vigilantly monitor patients undergoing immune and targeted therapies for infectious complications and use antimicrobial prophylaxes when indicated.

110

项与盐酸可泮利塞相关的新闻（医药）

2026-08-31

·BioMed科技

IF：81.2‌！李兰娟院士团队，最新国产顶刊STTT！

系统阐述PI3K/AKT信号通路：肿瘤发生的关键十字路口与治疗创新作为全球范围内肿瘤研究领域持续关注的核心科学问题，磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）信号通路的异常激活究竟如何驱动恶性肿瘤的发生与发展，长期以来是基础研究与临床转化面临的重大挑战。近日，浙江大学医学院附属第一医院李兰娟院士、朱丹华博士团队发表的重磅综述，系统性地整合了该通路在肿瘤生物学中的复杂调控网络、广泛的交互作用以及当前靶向治疗的最新进展，深刻揭示了这一信号枢纽在从实验室走向临床应用过程中所面临的机遇与困境。相关研究成果以“PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation”为题，发表于Signal Transduction and Targeted Therapy。该综述指出，PI3K/AKT信号通路作为一个复杂的调控网络，在细胞生长、增殖、代谢、存活及迁移等核心生命过程中发挥着枢纽作用。在肿瘤背景下，该通路的异常激活是驱动恶性转化、增强侵袭转移能力以及导致治疗耐药的关键因素，最终造成肿瘤进展和不良临床结局。然而，鉴于该通路在正常生理过程中的广泛参与，如何在提升靶向治疗效果的同时最大限度减少系统性毒副作用，仍是当前亟待突破的临床瓶颈。因此，系统而精确地理解该通路在肿瘤生物学中的角色，对于推动基础研究和指导未来临床开发具有决定性意义。研究团队在综述中全面解析了PI3K/AKT通路的核心构成及其相互作用网络。PI3K家族根据结构和底物特异性分为三类，其中Class I PI3K与肿瘤发生的关联最为密切，包含p110α、p110β、p110γ和p110δ四种催化亚型，分别由PIK3CA、PIK3CB、PIK3CG和PIK3CD基因编码。其中p110α在多种人类肿瘤中频繁发生突变，是关键的致癌驱动因子，而p110β在PTEN缺失的肿瘤中发挥关键作用，p110δ和p110γ则主要表达于免疫系统。作为通路核心枢纽的AKT激酶包含三个亚型——AKT1和AKT2在全身广泛表达，其中AKT2在胰岛素反应性代谢组织中发挥关键作用，而AKT3主要表达于脑组织；这三个亚型在肿瘤中展现出甚至相反的功能，例如在乳腺癌中AKT1抑制迁移而AKT2促进侵袭，这一亚型特异性差异为精准干预提出了更高要求。此外，抑癌基因PTEN作为该通路最重要的负调控因子，其功能缺失可导致PI3K/AKT信号的持续激活，在胶质母细胞瘤、前列腺癌、乳腺癌等多种恶性肿瘤中普遍存在，并与不良预后密切相关。mTOR作为下游关键效应分子，其两个复合物mTORC1和mTORC2分别调控细胞生长代谢与AKT活性放大（mTORC2磷酸化AKT Ser473），构成了复杂的前馈与反馈调节回路。尤为值得关注的是，该通路并非孤立运作，而是与其他经典信号通路形成密集的交互网络（crosstalk），从而在肿瘤发生中发挥协同效应（图1）。综述以详细的机制图解展示了PI3K/AKT与Wnt、NF-κB、MAPK/ERK、JAK/STAT、TGF-β、Notch及Hedgehog等通路的深度交叉对话。例如，在Wnt通路中，PI3K/AKT通过磷酸化GSK3β解除其对β-catenin的抑制，促进肿瘤细胞增殖；在NF-κB通路中，乙型肝炎病毒X蛋白通过NF-κB p65/己糖激酶2轴促进有氧糖酵解，进而激活PI3K/AKT信号，驱动肝癌发生；在MAPK通路中，抑制AKT反而可能触发p-ERK的代偿性上调，这一适应性应答为联合用药策略提供了理论依据。这些复杂的交互关系深刻影响了肿瘤细胞的命运决定、可塑性调控以及耐药性的形成。图1 PI3K/AKT信号通路的交叉对话。 PI3K/AKT信号通路与经典信号级联（包括NF-κB、MAPK、JAK/STAT、TGF-β、Wnt、Notch和Hedgehog通路）存在广泛的交互作用，在多种生物学过程中发挥关键作用。NADPH：烟酰胺腺嘌呤二核苷酸磷酸；PTEN：磷酸酶与张力蛋白同源物；PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；EMT：上皮-间质转化；INPP4B：肌醇多磷酸4-磷酸酶II型；HK2：己糖激酶2；STAT：信号转导与转录激活因子；TGF-β：转化生长因子β；GSK3：糖原合成酶激酶3。在肿瘤类型方面，综述系统梳理了该通路在消化、生殖、泌尿、呼吸、神经等多个系统肿瘤中的异常激活模式及其临床意义（图2）。在肝细胞癌中，PIK3CA突变率为4%~6%，且其与YAP1、RasV12等致癌因子协同作用可诱发肝肿瘤形成；长链非编码RNA AWPPH和LINC00152分别通过增强PIK3CA转录和负调控miR-139激活该通路。在结直肠癌中，约30%的病例携带PIK3CA突变，而PTEN蛋白表达缺失则是侵袭性增强和预后不良的可靠标志物。在胃癌中，PIK3CA在转移灶中的表达显著高于原发灶，且AKT1的高磷酸化水平与更短的总生存期密切相关。在食管鳞状细胞癌中，PIK3CA突变与良好预后相关，提示其可作为预测有利临床结局的生物标志物，而PIK3CB高表达则通过PI3K/AKT/mTOR轴促进肿瘤进展并与不良预后相关；PTEN恢复表达可增强顺铂敏感性。在胰腺癌中，PIK3CA基因突变在约3%~5%的病例中发生，PTEN抑制则导致VEGF分泌增加从而促进肿瘤血管生成。在乳腺癌中，PIK3CA突变在激素受体阳性肿瘤中尤为常见，并与曲妥珠单抗耐药相关；在卵巢癌中，AKT2的扩增和过表达促进侵袭复发；在前列腺癌中，PTEN缺失是最常见的突变事件，与生化复发和较短的复发无进展生存期显著相关。在肾细胞癌中，PTEN表达显著低于正常肾组织而磷酸化AKT水平明显升高，circ-AKT3的降低则促进癌细胞迁移和侵袭。这些发现强调了针对不同肿瘤类型和不同亚型患者的个体化靶向策略的必要性。图2 各系统肿瘤中PI3K/AKT通路相关分子的改变、表达特征、临床特征及预后意义。该通路在消化系统、生殖系统、泌尿系统、呼吸系统、神经系统等多种人类肿瘤中均存在显著异常激活，不同肿瘤类型涉及的关键分子改变及其临床相关性各不相同。在机制层面，该综述深入探讨了PI3K/AKT通路介导肿瘤发生和进展的多种生物学过程。在EMT过程中（图3），该通路通过调控Snail等关键转录因子，促进E-钙黏蛋白向N-钙黏蛋白的转换，增强肿瘤细胞的迁移和侵袭能力。在代谢重编程方面（图4），AKT激活可显著促进有氧糖酵解（Warburg效应），通过激活mTORC1、磷酸化GSK3及上调HIF-1α等机制，使肿瘤细胞高度依赖葡萄糖进行生存和增殖。在药物耐药方面（图5），该通路通过调节自噬、凋亡、DNA损伤应答等多种机制介导对化疗药物和靶向药物的抵抗——例如在胰腺癌中，circACTR2通过海绵吸附miR-221-3p上调PTEN表达从而抑制PI3K/AKT信号并降低吉西他滨耐药；FTO敲低则通过调节NEDD4影响PTEN表达，进而影响该通路及耐药性。在肿瘤血管生成方面（图6），PI3K/AKT通过调控VEGF和HIF-1α的表达，促进内皮细胞增殖和管腔形成。在免疫逃逸方面（图7），PTEN失活导致PD-L1上调，从而抑制T细胞功能；COX-2来源的PGE2则通过该通路诱导PD-1表达，促进免疫耐受；此外，甲状腺癌中CD133-AKT轴可增强PD-L1表达，HCC中FGF19/FGFR4通过IGF2BP1上调PD-L1并抑制PI3K/AKT信号，NSCLC中MUC3A则通过稳定EGFR减少PD-L1表达。这些机制的阐明为多维度干预肿瘤恶性进程提供了丰富的靶点选择。图3 PI3K/AKT信号通路在EMT中的作用。 EMT是伤口愈合、组织再生、器官纤维化和癌症进展等生物学过程的重要环节，PI3K/AKT信号通路在多种肿瘤的EMT调控中发挥核心作用。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；EMT：上皮-间质转化；HPIP：造血PBX相互作用蛋白；PCSK9：前蛋白转化酶枯草溶菌素/kexin 9型；MMP-9：基质金属蛋白酶9。图4 PI3K/AKT信号通路在肿瘤代谢重编程中的作用。代谢重编程是一个涉及信号通路激活、转录因子调控和酶活性调节的多因素复杂过程，PI3K/AKT级联反应是肿瘤细胞内驱动该过程的关键因素。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；PDK1：磷酸肌醇依赖性蛋白激酶-1；mTORC1：哺乳动物雷帕霉素靶蛋白复合物1；HIF-1α：缺氧诱导因子1α；Zeb1：锌指E-box结合同源盒1；ROS：活性氧；POU2F2：POU同源盒2类；CD36：分化簇36；Rheb：脑中富集的Ras同源蛋白。图5 PI3K/AKT信号通路在药物耐药中的作用。 PI3K/AKT通路在抗肿瘤药物耐药性的发展中发挥着根本性作用，探究其分子机制对于提高肿瘤治疗疗效至关重要。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；EGFR：表皮生长因子受体；PTEN：磷酸酶与张力蛋白同源物；FAK：黏着斑激酶；ITGA10：整合素α10；ANXA1：膜联蛋白A1；ANXA3：膜联蛋白A3；HIF：缺氧诱导因子；FTO：脂肪量与肥胖相关蛋白；NEDD4：神经前体细胞表达发育下调4。图6 PI3K/AKT信号通路在肿瘤血管生成中的作用。 PI3K/AKT级联反应是调控血管生成的关键因素，影响内皮细胞的增殖、迁移和管腔形成。全面理解该通路在肿瘤血管生成中的作用对于制定有效抑制肿瘤血管生成的策略至关重要。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；VEGF：血管内皮生长因子；PTEN：磷酸酶与张力蛋白同源物；HIF-1α：缺氧诱导因子1α；CPT：隐丹参酮；VRAP：VEGFR相关蛋白。图7 PI3K/AKT级联反应在肿瘤免疫逃逸中的作用。肿瘤免疫逃逸机制包括抗原丢失、免疫抑制、漏逸介导的逃逸、共刺激信号缺陷及抗凋亡效应等，这些机制常源于影响PI3K/AKT通路的突变。此类干扰改变了肿瘤生物学特性和免疫原性，促进免疫逃逸。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；COX-2：环氧合酶2；PGE2：前列腺素E2；PD-1：程序性细胞死亡蛋白1；PD-L1：程序性死亡配体1；EGFR：表皮生长因子受体；M-CSF：巨噬细胞集落刺激因子；HER2：人表皮生长因子受体2；ICAM-1：细胞间黏附分子1；MMP-9：基质金属蛋白酶9；NF-κB：核因子κB。针对该通路的治疗干预，综述全面总结了目前处于临床或试验阶段的各类抑制剂（图8），包括泛PI3K抑制剂、PI3K亚型选择性抑制剂、PI3K-mTOR双重抑制剂以及AKT抑制剂。Copanlisib和Buparlisib作为泛PI3K抑制剂，在非霍奇金淋巴瘤和乳腺癌中展现出临床疗效，但高血糖、高血压等副作用限制了其广泛应用。PI3Kα选择性抑制剂Alpelisib已获批用于携带PIK3CA突变的乳腺癌，而新型变构抑制剂STX-478则显示出不诱发高血糖的优势。PI3Kδ抑制剂Idelalisib和Leniolisib在血液系统恶性肿瘤和原发性免疫缺陷病中表现活跃；PI3Kγ抑制剂Eganelisib在实体瘤免疫联合治疗中展现出潜力。AKT抑制剂Capivasertib联合氟维司群已在激素受体阳性晚期乳腺癌的III期试验中显著延长无进展生存期。尽管如此，耐药机制、代偿性信号通路激活以及系统毒性仍然是制约临床获益的关键障碍。图8 PI3K/AKT信号通路及其抑制剂。 PI3K/AKT通路在关键生物学过程的调控中至关重要，是抗肿瘤药物研发的重要靶点。本图概述了靶向PI3K/AKT通路的抑制剂，重点标注了目前已在临床使用或处于临床研究阶段的代表性药物。PI3K：磷脂酰肌醇3-激酶；AKT：蛋白激酶B；mTOR：哺乳动物雷帕霉素靶蛋白。综述最后强调，未来研究应重点关注通路上下游功能依赖性的深入解析、耐药机制的攻克（尤其是联合抑制PI3K/AKT与MEK/ERK等代偿通路）、亚型特异性抑制剂的开发以及新型递送系统（如纳米制剂和抗体药物偶联物）的应用。尽管在阐明PI3K/AKT通路在癌症中的作用方面已取得长足进展，但要实现持久的临床获益，仍需多学科协作和持续的创新突破。这一系统性的总结不仅为肿瘤学家和药物研发者提供了宝贵的理论资源，也为最终将这一关键通路转化为切实有效的抗癌治疗策略指明了前进方向。「BioMed科技」关注生物医药×化学材料交叉前沿研究进展！交流、合作，请添加杨主编微信！来源：BioMed科技声明：仅代表作者个人观点，作者水平有限，如有不科学之处，请在下方留言指正！

临床1期

2026-08-24

·PRNewswire

BRC Therapeutics Appoints Biopharma Veteran Chandra Ramanathan as Executive Vice President of Commercialization and Strategy

Seasoned Executive Brings Track Record of Drug Launches, External Innovation, and Portfolio Growth at Bristol Myers Squibb, Wyeth, Bayer, and Danaher to BRC's Next Phase of Growth MONTEREY, Calif., Aug. 24, 2026 /PRNewswire/ -- BRC Therapeutics (BRC), a clinical-stage pharmaceutical company developing multimodal cannabinoid therapeutics for neurological and inflammatory conditions, today announced the appointment of Chandra Ramanathan, Ph.D., M.B.A., as Executive Vice President of Commercialization and Strategy. Ramanathan brings more than 30 years of biopharmaceutical leadership spanning drug development, global product launches, commercialization, and external innovation to BRC as the company advances its pipeline and prepares for its next phase of growth. Ramanathan joins BRC from Danaher Corporation, where he served as Vice President and Global Head of Innovation Hubs and Head of External Innovation, Life Sciences Innovation Group (LSIG) building a funnel of product-oriented partnerships across genomic medicine, diagnostics, LSIG, and biomanufacturing. Prior to Danaher, he spent more than 12 years at Bayer, most recently as Global Head of Pharma R&D Open Innovation, where he chaired the Open Innovation Committee overseeing an annual investment budget of more than $90 million across more than 50 academic and biotech partnerships. While leading Bayer's East Coast Innovation Center in Cambridge, MA, Ramanathan built major partnerships with the Broad Institute, MassGeneral Brigham, and Johns Hopkins University. Earlier in his career, Ramanathan led global launch teams behind two approved therapies (Bosulif®, Aliqopa®) and contributed to the launches of Orencia®, and Sprycel® across roles at Wyeth (now Pfizer), Bristol Myers Squibb, and Bayer. As the Head of oncology strategic marketing, he grew Bayer's oncology clinical portfolio from two assets to fifteen over five years. His experience spans the full spectrum of drug development and commercialization: external innovation, product development, companion diagnostics strategy, portfolio and launch planning, and building cross-functional global teams across the U.S., Europe, and Asia. "Chandra has spent his career doing precisely what BRC needs next: progressing promising science into the next phase of clinical development and ultimately into approved medicines that reach patients, based on proven growth strategies and commercial infrastructure to get there," said George Hodgin, Founder and CEO of BRC Therapeutics. "He has led launches at some of the most respected companies in our industry, built innovation engines from the ground up, and has a rare ability to move fluidly between science, innovation strategy, and commercial strategy. As we advance our pipeline in CRPS, AIIA, RLS and additional indications and prepare for our next phase of growth, Chandra's judgment, expertise and experience will be invaluable." "BRC is pursuing something genuinely novel: FDA-regulated cannabinoid medicines for patients with too few good options. The company's foundation is innovative science, a strong intellectual property estate, unique and evolving regulatory approach, and an unwavering drive to make a difference for patients," said Chandra Ramanathan. "I've spent my entire career helping companies bridge early science and commercial reality, and I see that same opportunity here. I'm excited to work alongside George and the BRC team as the company moves toward pivotal trials, new opportunities, and ultimately helping patients." Ramanathan currently serves as Chairperson of the Board of Directors of Nucleate, a nonprofit developing the next generation of biotech entrepreneurs, and holds board and advisory roles with the McLean Hospital, the Johns Hopkins University Innovation, Development & Entrepreneurial Advisory Board and Harvard Business School Blavatnik Fellowship Council. He was also a board member with MassBIO and Chair of the Innovation Committee where he recently finished his 9-year term. He is also an Adjunct Assistant Professor at Tufts University School of Medicine. Ramanathan holds an M.B.A. from Columbia Business School and a Ph.D. in Genomics and Bioinformatics from the University of Georgia. BRC Therapeutics (BRC) is a pharmaceutical company focused on developing innovative therapeutics to deliver relief from pain and other symptoms in chronic conditions. BRC's medicines are multimodal and contain cannabinoids at defined ratios. BRC has developed a pipeline of investigational prescription medicines addressing neurological and inflammatory conditions. Investigational products are currently being tested in clinical trials for Complex Regional Pain Syndrome (CRPS), Restless Legs Syndrome (RLS), and Aromatase Inhibitor-Induced Arthralgia (AIIA) and an additional confidential indication. BRC is registered with the Drug Enforcement Administration and is based in Monterey, CA. To learn more about BRC, visit . Forward-Looking Statements This news release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934 that involve risks, uncertainties and assumptions, including without limitation statements about the development, use, benefits and effects of BRC Therapeutics' (BRC) therapeutic product candidates and related technology, future plans for BRC's business and growth, and expected plans with respect to clinical trials, including the number of patients enrolled and timing of patient enrollment. In some cases, you can identify forward-looking statements by terms such as "may," "will," "should," "expect," "design," "plan," "anticipate," "could," "intend," "target," "project," "contemplates," "believes," "estimates," "predicts," "potential" or "continue" or the negative of these terms or other similar expressions. Such statements and other statements in this press release that are not descriptions of historical facts are forward-looking statements that are based on management's current expectations and assumptions and are subject to risks and uncertainties. If such risks or uncertainties materialize or such assumptions prove incorrect, our business, operating results, financial condition, and stock price could be materially negatively affected. Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements. The forward-looking statements made herein speak only as of the date of this press release and, unless otherwise required by law, BRC does not undertake any obligation to publicly update such forward-looking statements to reflect subsequent events or circumstances. SOURCE BRC Therapeutics 21% more press release views with Request a Demo

高管变更

2026-07-31

·拓派生命

2026年第31周：生物医药学术圈

本期中文导读 01前期治疗定义儿童癌症复发时的突变谱 02工程菌诱发的肿瘤特异性抗体促进膀胱癌免疫治疗 03Izalontamab Brengitecan（Iza-Bren），一种首创EGFR-HER3双特异性抗体偶联药物治疗广泛期小细胞肺癌：I期临床研究结果 04Copanlisib联合Nivolumab治疗微卫星稳定型结直肠癌：一项1/2期试验 05粪便微生物移植联合免疫检查点抑制剂治疗中的微生物植入与免疫调控 06抗体偶联药物与cmLumiOpto联合治疗三阴性乳腺癌 07尼洛替尼诱导免疫原性铜死亡以增强癌症免疫治疗 08空间蛋白质组学揭示癌症免疫治疗相关性胃炎的四阶段分子演化 #cancer immunotherapy#single-cell cancer#spatial transcriptomics cancer#cancer genomics#artificial intelligence drug discovery#antibody-drug conjugate NO. 01热度 38前期治疗定义儿童癌症复发时的突变谱核心内容本研究探讨化疗所致DNA损伤的程度。采用突变特征分析方法，基于多机构队列的全基因组测序肿瘤样本（统一收集治疗剂量与总暴露量），测量化疗与放疗的致突变效应。结果显示，复发儿童肿瘤中化疗与放疗是唯一的外源诱变剂，且常为DNA改变的主要来源；治疗后癌症携带的私有突变特征数量约为未治疗肿瘤的三倍，体细胞突变总负荷约为两倍。铂类化疗相关突变特征数量翻倍，且在多数患者中导致最高变异数。通过治疗时间追踪，发现铂类相关突变可在一年内检测到，超过三分之一接受铂类治疗的肿瘤存在可检测的铂类特征。该研究提供了化疗在儿童癌症中关键致突变效应的基因组证据，并提示降阶梯治疗及追踪耐药克隆的可能性。应用前景该研究为儿童癌症治疗策略优化提供了基因组学依据，特别是通过突变特征监测治疗相关损伤。未来可能用于早期识别铂类耐药克隆，指导治疗降阶梯或替代方案。结合治疗时间数据，可建立个性化突变监测窗口，减少远期副作用。行业影响这项研究首次系统量化了化疗对儿童癌症基因组的致突变效应，挑战了传统上认为化疗主要杀伤肿瘤细胞而较少诱发突变的观点。其发现直接支持儿童肿瘤治疗降阶梯策略，并提示可在治疗早期进行耐药克隆追踪，具有重要的临床转化价值。来源信息 · 学术论文期刊：Nature 发表/更新日期：2026年7月22日 DOI：10.1038/s41586-026-10803-1 作者：Layeghifard M、Díaz-Gay M、Bergstrom EN、Mahendralingam MJ、Light N、Blay S、Nash JO、Anderson ND 等阅读原文 → 论文标题：Prior therapy defines mutation profiles in childhood cancer at relapse. NO. 02热度 35工程菌诱发的肿瘤特异性抗体促进膀胱癌免疫治疗核心内容瘤内微生物群被认为是癌症的新标志，可能影响治疗反应。本研究利用合成生物学技术，将益生菌大肠杆菌Nissle 1917（EcN）改造为表达人趋化因子CXCL13，该因子是生发中心形成的关键组分。在膀胱癌原位小鼠模型中，膀胱内递送的工程化EcN成功定植于肿瘤，并在肿瘤引流淋巴结中诱发生发中心反应。当与程序性死亡受体1（PD-1）阻断联合时，工程化EcN在两种侵袭性、快速生长且免疫冷性的原位膀胱癌模型中增强了抗肿瘤活性。机制上，该抗肿瘤效应依赖于CD8+T细胞和CD4+T滤泡辅助细胞，联合治疗增加了肿瘤特异性抗体应答，并促进了长期生存和保护性免疫。该研究表明，合成生物学改造的CXCL13表达EcN可通过扩增肿瘤特异性体液免疫增强PD-1检查点阻断疗效。应用前景该研究展示了工程菌作为免疫治疗增效剂的潜力，通过激活体液免疫克服免疫冷肿瘤的耐药性。未来可探索将CXCL13或其他免疫调节因子整合到益生菌中，并结合膀胱内给药途径实现局部免疫激活，减少全身毒性。行业影响这项工作开创性地将细菌载体与体液免疫调控相结合，揭示了肿瘤特异性抗体在检查点阻断中的重要作用。为膀胱癌及其他免疫冷肿瘤的治疗提供了新策略，并拓展了合成生物学在肿瘤免疫治疗中的应用边界。来源信息 · 学术论文期刊：Science translational medicine 发表/更新日期：2026年7月22日 DOI：10.1126/scitranslmed.adv7600 作者：Rouanne M、Chen N、Mariuzza DL、Yang Z、Li F、de Los Santos-Alexis K、Savage TM、Vincent RL 等阅读原文 → 论文标题：Tumor-specific antibodies elicited by engineered bacteria promote bladder cancer immunotherapy in preclinical mouse models. NO. 03热度 33Izalontamab Brengitecan（Iza-Bren），一种首创EGFR-HER3双特异性抗体偶联药物治疗广泛期小细胞肺癌：I期临床研究结果核心内容小细胞肺癌（SCLC）是一种侵袭性强的恶性肿瘤，一线化疗免疫治疗后的选择有限。Izalontamab brengitecan（iza-bren，BL-B01D1）是一种靶向EGFR和HER3的首创双特异性抗体偶联药物。该I期剂量扩展研究（NCT05194982）纳入既往系统治疗进展的广泛期SCLC患者，接受iza-bren 2.5 mg/kg（每3周周期第1、8天给药）。截至2024年12月5日，共52例患者入组，客观缓解率（ORR）为48.1%，中位无进展生存期（PFS）4.1个月，中位总生存期（OS）12.2个月。二线治疗亚组（22例）ORR达72.7%，中位PFS 6.2个月，中位OS 15.0个月。常见治疗相关不良事件为血液学毒性。探索性生物标志物分析提示HER3阳性表达可能与更好治疗反应相关。结论：Iza-bren在复发ES-SCLC中显示令人鼓舞的抗肿瘤活性，尤其在二线治疗中；一项对比托泊替康的III期随机对照试验（NCT06500026）正在进行。应用前景 Iza-bren作为双靶点ADC，在ES-SCLC中显示了高效低毒潜力，特别是二线治疗数据令人期待。未来III期结果若证实其优于标准治疗，将改变SCLC治疗格局。同时，HER3表达作为预测标志物需前瞻性验证。行业影响该研究为SCLC患者提供了新的治疗选项，尤其是对化疗免疫治疗后进展的患者。双靶点设计可能克服单一EGFR或HER3靶向的耐药，其初步疗效数据优于现有二线方案，具有重要临床意义。来源信息 · 学术论文期刊：Journal of clinical oncology : official journal of the American Society of Clinical Oncology 发表/更新日期：2026年7月24日 DOI：10.1200/jco-26-00243 作者：Zhao Y、Zhao H、Wang Q、Yang K、Li Y、Fu Z、Yang W、He Z 等阅读原文 → 论文标题：Izalontamab Brengitecan (Iza-Bren), a First-in-Class EGFR-HER3 Bispecific Antibody-Drug Conjugate in Extensive-Stage Small Cell Lung Cancer: Results From a Phase Ib Study. NO. 04热度 30Copanlisib联合Nivolumab治疗微卫星稳定型结直肠癌：一项1/2期试验核心内容约15%的结直肠癌（CRC）存在PIK3CA突变。PI3K调控免疫力，抑制可能增强抗肿瘤免疫。研究者启动了一项copanlisib（PIK3CA抑制剂）联合nivolumab（抗PD-1）治疗转移性微卫星稳定型CRC的1/2期试验（NCT03711058）：队列A（PIK3CA野生型，n=17）和队列B（PIK3CA突变型，n=22）。推荐2期剂量为nivolumab 480 mg第1天，copanlisib 60 mg第1/8/15天（28天周期）。主要终点6个月客观缓解率未达到：队列A为0/17，队列B为2/22。次要终点包括中位无进展生存期（队列A: 1.7个月；队列B: 1.6个月）、中位总生存期（队列A: 8.5个月；队列B: 6.7个月）、缓解持续时间（队列A: 13.1个月；队列B: 17个月）和6个月疾病控制率（队列A: 2/17；队列B: 3/22）。次要终点在队列间无统计学差异。应用前景尽管主要终点未达到，但突变队列中少数患者的持久缓解提示需寻找预测性生物标志物。未来可探索更高剂量或联合其他靶向药物。行业影响该试验明确了copanlisib联合nivolumab的安全性，并提供了在PIK3CA突变型CRC中潜在疗效的初步临床证据。来源信息 · 学术论文期刊：Nature communications 发表/更新日期：2026年7月23日 DOI：10.1038/s41467-026-72985-6 作者：Christenson ES、Wala JA、Parkinson R、Collins NB、Jakubowski C、Lin JR、Qian K、Lu J 等阅读原文 → 论文标题：Copanlisib in combination with nivolumab formicrosatellite stable colorectal cancer: a phase 1/2 trial. NO. 05热度 30粪便微生物移植联合免疫检查点抑制剂治疗中的微生物植入与免疫调控核心内容肠道微生物是免疫检查点抑制剂（ICIs）癌症免疫治疗中疗效和免疫相关毒性的关键决定因素。粪便微生物移植（FMT）作为引入有益微生物功能的策略已出现，但临床结果仍存在差异。本综述整合了近期将FMT与ICIs联合的临床试验证据，建立了一个基于机制的框架来理解这种变异性并指导更安全的临床应用。作者讨论了特定微生物功能程序如何缓冲或降低免疫失调阈值，并概述了在肿瘤学中供体选择、纵向监测和试验设计的意义。来源摘要未说明具体数值结果或结论。应用前景未来研究需要精确界定微生物功能程序与免疫应答的关系，并通过前瞻性试验验证基于机制的供体筛选策略。纵向监测手段和生物标志物的开发将有助于识别FMT与ICIs联合治疗中的应答者和非应答者。行业影响该综述为个体化微生物组调控策略提供了理论框架，有望推动FMT与免疫治疗联合方案的优化，提高疗效并降低毒性。来源信息 · 学术论文期刊：Nature communications 发表/更新日期：2026年7月23日 DOI：10.1038/s41467-026-76051-z 作者：Ninkov M、Maleki Vareki S. 阅读原文 → 论文标题：Microbial engraftment and immune regulation during fecal microbiota transplantation and immune checkpoint inhibitor therapy. NO. 06热度 30抗体偶联药物与cmLumiOpto联合治疗三阴性乳腺癌核心内容三阴性乳腺癌（TNBC）是一种侵袭性强、化疗耐药且易转移的亚型，单一疗法效果有限。本研究评估了CD276（B7-H3）靶向抗体偶联药物（ADC）与线粒体靶向基因治疗（cmLumiOpto平台）的联合策略。抗CD276单克隆抗体-美登素偶联物在低剂量下显著减少肿瘤负荷，并与cmLumiOpto在三种TNBC细胞系中表现出强协同作用，损害线粒体功能并增强免疫反应。在小鼠模型中，ADC/cmLumiOpto联合抑制TNBC转移，并在患者来源异种移植模型中抑制肿瘤生长95%-100%。机制研究发现转移信号下调、肿瘤微环境重塑、凋亡增加及免疫上调。组织学和体重分析显示最小全身毒性。该结果表明CD276靶向ADC联合线粒体基因治疗具有治疗侵袭性TNBC的转化潜力。应用前景该联合策略通过同时靶向肿瘤表面抗原和线粒体功能，可能克服TNBC的化疗耐药和免疫逃逸。未来需在临床前模型中进一步优化剂量和给药方案，并评估长期安全性。若成功转化，将为TNBC提供新的联合治疗模式。行业影响本研究首次将CD276靶向ADC与线粒体基因治疗结合，实现了高抗肿瘤活性与低系统毒性，为TNBC治疗提供了新思路。其机制涉及免疫调节和代谢干预，具有创新性。来源信息 · 学术论文期刊：Cell reports. Medicine 发表/更新日期：2026年7月24日 DOI：10.1016/j.xcrm.2026.102934 作者：Varadkar T、Zhou ZZ、Si Y、Zhang J、Du Z、Khanal AG、Chowdhury S、Tsaliki C 等阅读原文 → 论文标题：Combine antibody-drug conjugate with cmLumiOpto for triple-negative breast cancer treatment. NO. 07热度 29尼洛替尼诱导免疫原性铜死亡以增强癌症免疫治疗核心内容免疫治疗疗效受限于肿瘤免疫原性低和免疫浸润不足。铜死亡（cuproptosis）具有治疗潜力，但其是否具有免疫原性尚不明确。研究通过筛选240种FDA批准的抗肿瘤药物，发现尼洛替尼（nilotinib）是一种强效的铜死亡诱导剂，尤其在生理相关铜浓度下。机制上，尼洛替尼-铜通过ETV1抑制铜输出蛋白ATP7A，驱动线粒体铜积累，并通过ERK2磷酸化激活MAPK通路。临床前研究显示，尼洛替尼-铜诱导免疫原性铜死亡，并在多种黑色素瘤模型（如B16F10荷瘤小鼠、Braf/Pten自发黑色素瘤小鼠和PBMC人源化小鼠）中增强抗PD-1疗效。临床上，ATP7A低/MAPK高信号与改善的免疫治疗应答和更长总生存期相关。本研究确立尼洛替尼为一种临床可行的、非离子载体的免疫原性铜死亡诱导剂，能够激活抗肿瘤免疫以增强免疫治疗。应用前景未来可进一步探索尼洛替尼-铜联合免疫检查点抑制剂的临床转化，并验证ATP7A和MAPK信号作为预测性生物标志物的价值。行业影响该发现为铜死亡在免疫治疗中的应用提供了新机制，并鉴定出一种FDA批准的药物可作为免疫原性铜死亡诱导剂，具有快速临床转化的潜力。来源信息 · 学术论文期刊：Cell reports. Medicine 发表/更新日期：2026年7月22日 DOI：10.1016/j.xcrm.2026.102928 作者：Yao L、Zhao D、Meng Y、Liu Y、Su H、Chen D、Guo Z、Li D 等阅读原文 → 论文标题：Nilotinib induces immunogenic cuproptosis to potentiate cancer immunotherapy. NO. 08热度 28空间蛋白质组学揭示癌症免疫治疗相关性胃炎的四阶段分子演化核心内容免疫检查点抑制剂（ICIs）显著改善癌症治疗，但免疫相关不良事件（irAEs）如免疫治疗相关性胃炎（IRAEG）常导致治疗中断，影响抗肿瘤疗效。IRAEG症状不典型，缺乏特异性生物标志物，且与其他胃炎组织病理学重叠，诊断与管理困难。本研究利用空间蛋白质组学分析7例患者（4例非免疫治疗相关性胃炎对照，3例实体瘤ICI治疗后发生IRAEG的癌症患者）在四个疾病阶段（基线G1、急性严重炎症G2、早期恢复G3、完全恢复G4）的胃组织样本，通过激光捕获显微切割联合数据非依赖性采集质谱分析177个空间解析区域。结果显示IRAEG以广泛HLA分子激活和抗原加工增强为特征，类似器官移植排斥免疫表型；急性G2阶段出现过度中性粒细胞胞外陷阱形成、代谢抑制和免疫稳态崩溃；早期恢复G3阶段炎症损伤转向修复，脂肪酸代谢和PPAR信号激活；即使在完全临床恢复G4阶段，仍有超过1000种蛋白差异表达，形成持续增强的代谢和免疫“记忆”状态。作者结论认为，这些发现定义了IRAEG进展和恢复的四个分子学阶段，阶段特异性标志物可作为诊断、分期和治疗反应评估的候选生物标志物，并指导irAE管理、治疗调整及安全ICI再挑战决策。应用前景该研究的四阶段分子图谱为IRAEG的精准诊断提供了潜在生物标志物，可能帮助临床医生在irAE发生早期识别并干预，减少ICI治疗中断。未来可基于这些分子特征开发血液或组织检测面板，指导ICI再挑战的安全性评估，从而最大化免疫治疗的持续性获益。行业影响本研究首次系统描绘了IRAEG从急性炎症到完全恢复的分子演化全景，揭示代谢和免疫记忆状态，挑战了irAE完全可逆的传统认知。这为癌症免疫治疗中irAE的管理提供了新框架，可能改变临床实践，促使医生在完全恢复后仍警惕长期分子改变，并探索阶段特异性干预策略。来源信息 · 学术论文期刊：Molecular cancer 发表/更新日期：2026年7月21日 DOI：10.1186/s12943-026-02737-z 作者：Shi L、Lin Z、Zhang H、Lu Y、Sun Z、Lan B、Xia H、Luo S 等阅读原文 → 论文标题：Spatial proteomics reveals four-stage molecular evolution in cancer immunotherapy-related gastritis.

100 项与盐酸可泮利塞相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10797 D10867	盐酸可泮利塞	L01XX61	DB12483

研发状态

批准上市

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适应症	国家/地区	公司	日期
滤泡性淋巴瘤	美国	Bayer HealthCare Pharmaceuticals, Inc.	2017-09-14

未上市

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适应症	最高研发状态	国家/地区	公司	日期
惰性B细胞非霍奇金淋巴瘤	申请上市	加拿大	Bayer, Inc.	2021-12-01
小淋巴细胞淋巴瘤	申请上市	加拿大	Bayer, Inc.	2021-12-01
巨球蛋白血症	申请上市	加拿大	Bayer, Inc.	2021-12-01
边缘区B细胞淋巴瘤	申请上市	欧盟	Bayer AG	2021-06-12
非霍奇金淋巴瘤	申请上市	中国	Bayer AG	2021-03-10
惰性非霍奇金淋巴瘤	临床3期	美国	Bayer Pharma AG	2016-01-06
惰性非霍奇金淋巴瘤	临床3期	美国	拜耳医药保健有限公司	2016-01-06
惰性非霍奇金淋巴瘤	临床3期	阿根廷	拜耳医药保健有限公司	2016-01-06
惰性非霍奇金淋巴瘤	临床3期	阿根廷	Bayer Pharma AG	2016-01-06
惰性非霍奇金淋巴瘤	临床3期	澳大利亚	Bayer Pharma AG	2016-01-06

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临床结果

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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


NCT03711058 (Pubmed \| Nat Commun)	临床1/2期	转移性微卫星稳定结直肠癌 microsatellite stable \| PIK3CAwt \| PIK3CAmut	39	Copanlisib/nivolumab (PIK3CAwt)	憲網窪艱糧選遞鑰鹽鹹(廠遞餘範艱遞醖齋衊選) = 衊鏇糧醖鬱遞鏇願觸艱鹹鹽憲網顧鹽鏇繭構遞 (簾艱窪製範鹽襯蓋艱廠 ) 更多	不佳	2026-07-23
				Copanlisib/nivolumab (PIK3CAmut)	憲網窪艱糧選遞鑰鹽鹹(廠遞餘範艱遞醖齋衊選) = 壓願鹹遞窪願構製鑰範鹹鹽憲網顧鹽鏇繭構遞 (簾艱窪製範鹽襯蓋艱廠 ) 更多
NCT03789240 (CTgov)	临床2期	滤泡性淋巴瘤	33	Copanlisib+Rituximab	餘選願蓋範鹽鏇憲廠淵 = 鑰餘鏇糧衊衊淵襯遞顧鬱鹹遞鑰夢鑰鏇淵範範 (願鏇積範餘壓艱衊鑰憲, 獵餘繭繭觸淵壓獵糧範 ~ 襯壓窪蓋憲製膚鏇簾鹹) 更多	-	2026-03-03
NCT03842228 (COD, CTgov)	临床1期	转移性实体瘤 \| 晚期恶性实体瘤 \| 不可切除的实体瘤	39	Copanlisib+Olaparib (Step 1 Dose Level 1)	鏇鬱襯齋顧壓構襯顧醖 = 餘製餘鹽願鹽顧鑰夢鹹艱積夢膚遞鏇鹹鹽襯鹽 (淵積襯獵觸範衊鹹憲網, 廠壓願淵願積觸鹹構獵 ~ 淵顧獵選齋構繭廠繭製) 更多	-	2025-08-03
				Copanlisib+Olaparib (Step 1 Dose Level 2)	鏇鬱襯齋顧壓構襯顧醖 = 膚壓膚壓簾糧糧顧餘網艱積夢膚遞鏇鹹鹽襯鹽 (淵積襯獵觸範衊鹹憲網, 觸積簾構衊遞鬱糧夢淵 ~ 積觸鹹願鹽鏇鏇廠鹹網) 更多
NCT04345913 (CTgov)	临床1/2期	转移性乳腺癌 \| 转移性三阴性乳腺癌	24	Computed Tomography+Copanlisib Hydrochloride+Eribulin Mesylate (Phase I, DL1 (Eribulin, Copanlisib))	淵糧範淵艱憲膚餘鏇願 = 鏇網構簾餘遞鑰鏇壓餘網艱構築觸選淵鹽鬱顧 (遞壓鹽繭廠顧製積憲襯, 製獵膚鑰糧齋構製願醖 ~ 膚衊網鬱淵衊願糧網觸) 更多	-	2025-07-28
				Computed Tomography+Eribulin Mesylate (Group I (Phase II, Eribulin))	衊觸蓋積齋鹽範蓋憲醖(齋夢壓願遞憲壓夢鹹築) = 淵顧觸繭蓋範膚衊積醖憲鹽鹽築衊鹹壓選鏇艱 (顧繭獵願壓艱構製醖遞, 願壓築顧襯鹹醖顧糧醖 ~ 齋積淵醖壓壓願觸顧願) 更多
NCT05082025 (CTgov)	临床2期	卵巢癌 \| 子宫内膜癌	7	Copanlisib+Fulvestrant	襯觸築顧範蓋顧齋築齋 = 繭夢淵製蓋憲獵鹹餘簾築獵醖衊壓繭觸鹽願範 (遞選獵鏇範鏇簾觸獵遞, 壓遞鏇積壓夢鑰鏇壓襯 ~ 獵餘壓窪糧選鏇觸簾糧) 更多	-	2025-07-11
A PROSPECTIVE MULTICENTER PHASE 2 STUDY (EHA2025)	临床2期	Bcl-2/IgH-rearrangement	102	Copanlisib plus Obinutuzumab	鑰襯製積憲膚膚廠衊夢(壓衊齋範範餘製願艱獵) = 範築衊繭積積網鑰蓋衊膚糧淵膚鹽積製繭獵餘 (製憲鑰醖鹹淵構齋鏇願, 93 ~ 100) 更多	积极	2025-05-14
NCT06360588 (CTgov)	临床2期	恶性实体肿瘤	22	Radiologic Examination+Copanlisib	遞範壓網壓願鹹鬱鑰糧 = 網獵鏇遞製鹹蓋範築選製餘繭齋範鹽積鏇窪繭 (艱糧構鏇齋夢糧衊憲艱, 獵衊醖壓遞繭鑰範鏇壓 ~ 膚壓糧壓鹹齋夢窪網廠) 更多	-	2025-04-16
NCT06400238 (CTgov)	临床2期	难治恶性实体肿瘤 \| 晚期恶性实体瘤 \| 晚期淋巴瘤 ... 更多	35	Computed Tomography+Copanlisib	積鏇願鏇鬱構遞廠艱製 = 網簾構壓夢鏇範襯鬱網選製膚網製觸獵醖構網 (餘鹹糧獵窪淵鬱艱艱鹽, 衊齋鬱襯蓋淵鹽襯積糧 ~ 築膚膚艱鏇壓築鹹鹽鹽) 更多	-	2025-04-16
NCT04750941 (CTgov)	临床2期	难治性滤泡性淋巴瘤 \| 子宫内膜癌	1	Copanlisib+Ketogenic Diet (Follicular Lymphoma (FL))	鑰顧鹹簾膚鬱鑰艱獵範 = 憲淵糧膚遞衊艱觸餘鬱鹽齋鏇遞顧餘遞繭艱鹹 (網窪蓋憲繭範鏇遞鏇鹹, 鏇構簾壓廠蓋醖壓鏇願 ~ 鹹壓繭網願鹽積顧壓廠) 更多	-	2025-03-04
				Copanlisib+Ketogenic diet (Endometrial Cancer (EC))	鑰鬱餘鑰選構築夢憲鏇(範鑰憲構餘醖壓糧蓋醖) = 鹹夢壓鑰選鏇廠選遞艱願鏇憲夢顧獵齋願窪夢 (鏇夢夢構淵繭壓糧鏇網, 願製網糧齋築廠齋糧鏇 ~ 願觸齋選鹹醖繭積觸積) 更多
NCT04462471 (CTgov)	临床1期	滤泡型甲状腺癌 \| 乳头状甲状腺癌 \| 难治性甲状腺癌	8	Copanlisib+Vemurafenib (Dose Level 1)	繭製遞衊襯願窪選鑰壓 = 膚網鬱獵鑰廠衊選衊築夢範鹹繭鑰獵淵觸範鬱 (積鏇觸鏇憲選繭廠鑰觸, 繭鑰糧範夢衊製簾積窪 ~ 齋艱選艱積鏇獵壓蓋膚) 更多	-	2025-02-28
				Copanlisib+Vemurafenib (Dose Level 2)	繭製遞衊襯願窪選鑰壓 = 遞蓋齋鹹構鹹蓋繭鹹簾夢範鹹繭鑰獵淵觸範鬱 (積鏇觸鏇憲選繭廠鑰觸, 壓鏇醖顧遞夢鬱艱窪範 ~ 餘鹽範襯製積壓襯糧鏇) 更多