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更新于：2025-10-07

Venetoclax

维奈克拉

更新于：2025-10-07

概要

基本信息

药物类型

小分子化药

别名

VENCLYXTO、Venetoclax (JAN/USAN/INN)、维奈妥拉

+ [15]

靶点

Bcl-2

作用方式

抑制剂

作用机制

Bcl-2抑制剂(细胞凋亡调控因子Bcl-2抑制剂)

治疗领域

肿瘤免疫系统疾病血液及淋巴系统疾病+ [7]

在研适应症

复发性套细胞淋巴瘤难治性套细胞淋巴瘤难治性慢性淋巴细胞白血病+ [141]

非在研适应症

侵袭性非霍奇金淋巴瘤ER阳性/HER2阴性乳腺癌广泛期小细胞肺癌+ [18]

原研机构

在研机构

City of Hope National Medical Center

+ [32]

非在研机构

Janssen Research & Development LLCJanssen Scientific Affairs LLC

Janssen Pharmaceuticals, Inc.

权益机构

Tolero Pharmaceuticals, Inc.

天境生物技术（天津）有限公司

The University of Texas MD Anderson Cancer Center

+ [2]

最高研发阶段批准上市

首次获批日期

美国 (2016-04-11),

慢性淋巴细胞白血病

最高研发阶段(中国)批准上市

特殊审评突破性疗法 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、特殊审批 (中国)、孤儿药 (澳大利亚)、附条件批准 (中国)、孤儿药 (日本)

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结构/序列

分子式C45H50ClN7O7S

InChIKeyLQBVNQSMGBZMKD-UHFFFAOYSA-N

CAS号1257044-40-8

关联

785

项与维奈克拉相关的临床试验

NCT07175415

/ Not yet recruiting临床1/2期IIT

ITCC-104: HEM-iSMART International Proof of Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory HEMatological Malignancies in Children, Sub-Protocol E: Capivasertib + Venetoclax + Dexamethasone in Pediatric Patients With Relapsed or Refractory Hematological Malignancies

HEM-iSMART is a master protocol which investigates multiple investigational medicinal products in children, adolescents and young adults (AYA) with relapsed/refractory (R/R) ALL and LBL. Sub-protocol E is a phase I/II trial evaluating the safety and efficacy of capivasertib + venetocolax in combination with dexamethasone in children and AYA with R/R ped ALL/LBL whose tumor present with alterations of the PAM pathway, or lacking any mutations.

开始日期2026-10-01

申办/合作机构

Princess Maxima Centre For Pediatric Oncology

[+2]

NCT06802523

/ Recruiting临床1期IIT

A Phase I Study of Lintuzumab-Ac-225 in Combination With Venetoclax and ASTX-727 in Adults With Newly Diagnosed AML

This phase I trial tests the safety, side effects, and best dose of lintuzumab-Ac225 in combination with venetoclax and ASTX-727, and how well they work in treating patients with newly diagnosed acute myeloid leukemia (AML). Lintuzumab-Ac225 is a monoclonal antibody, called lintuzumab, linked to a radioactive agent called actinium Ac 225. Lintuzumab attaches to CD33 positive cancer cells in a targeted way and delivers actinium Ac 225 to kill them. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. ASTX-727 is a combination of two drugs, cedazuridine and decitabine. Cedazuridine is in a class of medications called cytidine deaminase inhibitors. It prevents the breakdown of decitabine, making it more available in the body so that decitabine will have a greater effect. Decitabine is in a class of medications called hypomethylation agents. It works by helping the bone marrow produce normal blood cells and by killing abnormal cells in the bone marrow. Giving lintuzumab-Ac225 in combination with venetoclax and ASTX-727 may be safe and tolerable in treating patients with newly diagnosed AML and may improve the chance of going into remission and staying in remission for a longer period of time.

开始日期2026-04-21

申办/合作机构

National Cancer Institute

NCT06649812

/ Recruiting临床2期IIT

A Phase 2 Study of Venetoclax, Ibrutinib, Prednisone, Obinutuzumab, and Revlimid (ViPOR) in Relapsed or Refractory CD10-Negative Diffuse-Large B-Cell Lymphoma (DLBCL) and High-Grade B-Cell Lymphoma With MYC and BCL2 Rearrangements (HGBCL-DH-BCL2)

This phase II trial tests how well venetoclax, ibrutinib, prednisone, obinutuzumab, and Revlimid® (ViPOR) works in treating patients with CD10 negative diffuse large B-cell lymphoma (DLBCL) and high-grade lymphoma with MYC and BCL2 rearrangements that has come back after a period of improvement (relapsed) and/or that has not responded to previous treatment (refractory). Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. Ibrutinib is in a class of medications called kinase inhibitors. It blocks a protein called BTK, which is present on B-cell (a type of white blood cells) cancers at abnormal levels. This may help keep cancer cells from growing and spreading. Anti-inflammatory drugs, such as prednisone lower the body's immune response and are used with other drugs in the treatment of some types of cancer. Obinutuzumab, a monoclonal antibody, binds to a protein called CD20, which is found on B cells and some types of leukemia and lymphoma cells. Obinutuzumab may block CD20 and help the immune system kill cancer cells. Revlimid, a type of anti-angiogenesis agent and a type of immunomodulating agent, may help the immune system kill abnormal blood cells or cancer cells. It may also prevent the growth of new blood vessels that cancers need to grow. ViPOR may be an effective treatment option for patients with relapsed and/or refractory CD10 negative DLBCL and high-grade B-cell lymphoma with MYC and BCL2 rearrangements.

开始日期2026-03-21

申办/合作机构

National Cancer Institute

100 项与维奈克拉相关的临床结果

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100 项与维奈克拉相关的转化医学

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100 项与维奈克拉相关的专利（医药）

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5,033

项与维奈克拉相关的文献（医药）

2025-12-31·ANNALS OF MEDICINE

Significant prognostic improvement in elderly patients with acute myeloid leukemia treated with hypomethylating agents and venetoclax: outcomes from a retrospective real-world analysis

Article

作者: Wu, Yong ; Zheng, Jing ; Wu, Lanlan ; Chen, Yi ; Zhou, Jiayi ; Wu, Zhengjun ; Cai, Ruyu ; Wang, Zhengyang

OBJECTIVE:

This investigation aim to analyze the clinical features and therapeutic outcomes of elderly patients with acute myeloid leukemia (AML).

METHOD:

We conducted a retrospective analysis of the clinical and cytogenetic profiles of patients aged 60 years and older diagnosed with AML at the Fujian Medical University Union Hospital from 2016 to 2024.

RESULTS:

Our study cohort included 846 patients, with a median age of 67 years. The median duration of response (DOR) was 15.8 months, with 1-year, 3-year, and 5-year DOR rates of 55.3%, 23.4%, and 13.1%, respectively. The median overall survival (OS) was 21.8 months, with corresponding 1-year, 3-year, and 5-year OS rates of 58.7%, 41.2%, and 30.0%. Patients who received the azacitidine and venetoclax treatment protocol exhibited a complete remission (CR) rate of 57.1% and a minimal residual disease (MRD) - negative rate of 34.1%. These rates were comparable to the 59.2% CR rate and 39.4% MRD-negative rate observed in patients treated with intensive chemotherapy, and were superior to those with other low-intensity regimens. Compared to the treatment outcomes achieved at our center prior to 2016, when chemotherapy was the predominant treatment modality, which were characterized by a CR rate of 42.7%, a median OS of 9.2 months, and a mere 5-year OS rate of 13.5%, the remission rate and long-term survival of elderly patients with AML have been remarkable improved.

CONCLUSION:

The integration of hypomethylating agents and venetoclax into the treatment paradigm for elderly patients with AML has significantly enhanced survival rates.

2025-12-31·Hematology

Identification of t(X;1)(q28;q21) generating a novel GATAD2B::MTCP1 gene fusion in CMML and its persistence during progression to AML

Article

作者: Chen, Yu ; Zhu, Yi-yan ; Liu, Yi-zi ; Hou, Chun-xiao ; Zhang, Zhi-yu ; Chen, Su-ning ; Wang, Qian ; Zhang, Feng-hong

OBJECTIVE:

Hematological malignancies often involve chromosomal translocations and fusion genes that drive disease progression. While MTCP1 is well-known in T-cell prolymphocytic leukemia (T-PLL), its role in myeloid neoplasms is less understood. This report presents the first identification of the t(X;1)(q28;q21) translocation leading to the GATAD2B::MTCP1 fusion in acute myeloid leukemia (AML) transformed from chronic myelomonocytic leukemia (CMML).

METHODS:

The karyotypes were described according to the International System for Human Cytogenetic Nomenclature 2009. We performed targeted next-generation sequencing (NGS) on a panel of 172 genes commonly mutated in hematological malignancies (Supplemental Table 1), using an Illumina platform. RNA sequencing was conducted on total RNA extracted from bone marrow, also using the Illumina platform. The GATAD2B::MTCP1 fusion gene was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and Sanger sequencing, with specific primers for the fusion transcript (GATAD2B-F: CCTCTTTTTTTCGACGCC; MTCP1-R: ACTGAGCACAACACTTACGC).

RESULTS:

The GATAD2B::MTCP1 fusion results from a breakpoint on 1q21 within GATAD2B exon 1 and Xq28 within MTCP1 exon 2. The patient with the GATAD2B::MTCP1 fusion exhibited disease progression from CMML to AML. Despite achieving initial remission with venetoclax-based therapy and allo-HSCT, the patient relapsed and died.

CONCLUSIONS:

We propose that the GATAD2B::MTCP1 fusion upregulates MTCP1 expression rather than generating a fusion protein, thereby contributing to transformation and relapse in AML. Further investigations are needed to elucidate the precise role of this fusion event in myeloid malignancies.

2025-12-31·Hematology

First case report: near early T-cell precursor acute lymphoblastic leukemia with plasmacytoid dendritic cell proliferation effectively treated with Venetoclax plus HAG regimen

Article

作者: Feng, Yi ; Li, Dan ; Chen, Zhe ; Wang, Liping ; Luo, Hongqiang ; Liu, Fang ; Huang, Xin ; Han, Jiongping ; Feng, Weiying

BACKGROUND:

Near early T-cell precursor acute lymphoblastic leukemia represents a distinct subtype of T-cell acute lymphoblastic leukemia characterized by specific immunophenotypic and molecular biological characteristics. Currently, no standardized treatment protocol exists.

METHODS:

This study presents a case of near early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) characterized by plasmacytoid dendritic cell proliferation, which manifested clinically through pancytopenia and generalized multiple rashes.

RESULTS:

The patient underwent successful treatment with chemotherapy consisting of Venetoclax combined with HAG regimen administered for one cycle.

DISCUSSION:

This case report provides preliminary evidence suggesting that the combination of Venetoclax with HAG (homoharringtonine, cytarabine, and granulocyte colony-stimulating factor) regimen may constitute an effective and tolerable therapeutic approach for patients with near ETP-ALL. However, these initial observations necessitate further validation through comprehensive clinical studies with larger sample sizes to definitively establish the treatment's efficacy and safety profile.

1,635

项与维奈克拉相关的新闻（医药）

2025-10-03

·药明康德

致敬时代 | 五年生存率跃升6倍，多款新型抗癌药为这类患者点亮希望

编者按：2025年，药明康德迎来创立25周年的重要里程碑。值此契机，我们向所有与我们共同书写产业变革篇章的科学家、医药人和投资者致以衷心感谢与诚挚敬意，也特别推出“致敬时代”系列，回顾全球同仁如何借助科学与合作的力量，不断拓展治疗边界、改善患者命运。四分之一个世纪的坚守，只为加速每一款新药的诞生。下一个25年，我们将继续心怀感恩与敬畏，依托独特的CRDMO模式，与全球伙伴携手同行，共赴健康未来。急性髓系白血病（AML）是成年人中最常见的白血病类型之一，多发于60岁及以上的人群，但也可能累及年轻人和儿童。据流行病学统计，2021年全球新发AML病例数超14万例。AML病情发展迅猛，如果不及时接受治疗，患者可能在几周到几个月内就发展为重症并死亡。面对这一高危疾病，AML的治疗策略近年来取得显著进展。除传统化疗、放疗及造血干细胞移植外，靶向药物、免疫疗法、细胞治疗及抗体偶联药物（ADC）等新型治疗方式逐步应用于临床，推动疗效不断提升。数据显示，过去几十年间，AML患者的5年生存率已从1975年的5.4%提升至2017年的33.7%，增长近6倍。在推动AML治疗革新的进程中，药明康德依托25年的行业深耕，不仅见证了AML治疗药物从实验室走向临床转化应用的突破历程，同时凭借其独特的CRDMO业务模式，助力全球合作伙伴加速包括AML在内的多种疾病创新疗法的研发进程，为全球患者带来更多治愈希望。从“脓血”疑云到解密白血病细胞的200年之路 AML的认知经历了两个世纪的探索。19世纪初，医学文献中已零星记载了一类血液异常病例：患者常伴发热、虚弱、肝脾肿大，血液外观呈乳糜状或脓血样。当时虽未精准归类，但这些现象已提示存在一种独特血液疾病。 1845年，显微镜技术带来了关键突破。英国医生约翰·休斯·贝内特（John Hughes Bennett）报道了首例白血病病例：一名28岁男性患者脾肝显著肿大，血管内充斥乳白色脓液样物质。显微镜下，他观察到患者血液中布满无色球体（白细胞），与凝固的纤维蛋白丝交织，并由此提出“白血球增多症（leucocythemia）”的概念，首次明确该病为原发性全身性血液疾病，而非感染引发的继发表现。 ▲贝内特所绘制的白血病患者血液中的无色球体（图片来源：参考资料[7]）贝内特的研究迅速引发学界关注。同年，德国病理学家鲁道夫·菲尔绍（Rudolf Virchow）也报道了类似病例。他通过系统分析发现，患者体内白细胞异常增殖会抑制红细胞生成，进而指出：白细胞增多是疾病的本质特征，而非脓液形成所致。1847年，菲尔绍正式将这类疾病命名为“白血病（leukämie）”，并尝试将其分为脾源性和淋巴性两大类——虽然这一分类尚不精确，却为现代白血病分型奠定了基础。 19世纪下半叶，随着病例积累，白血病逐渐被确认为独立疾病实体，临床与病理学研究的深入，也为探索其本质创造了条件。 1870年代，德国医学家保罗·埃利希（Paul Ehrlich）改进了血细胞染色技术，使血细胞结构清晰可见，进而首次识别出“原始细胞”——即未成熟的血细胞前体（现代医学中的造血干细胞）。埃利希还提出根据病程快慢和细胞成熟度，将白血病分为急性、慢性两大类：急性白血病以未成熟原始细胞大量增殖、病情进展迅速为特征；慢性白血病则由相对成熟但功能异常的细胞增殖主导，进展缓慢。这一分类框架逐步演化为现代白血病四大亚型：AML、急性淋巴细胞白血病（ALL）、慢性髓系白血病（CML）和慢性淋巴细胞白血病（CLL）。从19世纪对“脓血”现象的误解，到埃利希时代对白血病细胞分化特征的精准界定，人类对AML的认识已从宏观深入微观。这些历史积累不仅奠定了现代血液学的基础，更为后续AML分子机制研究与靶向治疗的开发提供了不可或缺的科学前提。化疗筑基，靶向疗法为特殊患者群体破局数十年来，AML的治疗策略经历了从传统化疗到精准靶向治疗的演进。以阿糖胞苷联合蒽环类药物（如柔红霉素或去甲氧柔红霉素、伊达比星）的“7+3方案”为代表的强化诱导化疗，曾长期作为年轻、体健且携带良好风险特征AML患者的基础治疗方案，使部分患者获得长期缓解。然而，AML多发于老年人群，多数患者年龄超过65岁，常因合并症、高危遗传学异常及对强化化疗耐受差等因素，临床预后不佳。针对不适合强化化疗的患者，去甲基化药物如阿扎胞苷的应用显著改善了患者的生存结局。时至今日，传统化疗药物仍构成AML治疗的重要支撑，除“7+3”方案常用药物外，还包括克拉屈滨、氟达拉滨、米托蒽醌、依托泊苷、羟基脲、皮质类固醇（如泼尼松或地塞米松）、甲氨蝶呤、6-巯基嘌呤（6-MP）、地西他滨。随着脂质体递送系统的进步，复方制剂如Vyxeos（柔红霉素/阿糖胞苷脂质体）也进一步优化了传统AML治疗药物的治疗指数。图片来源：123RF 近年来，针对癌细胞特定分子组分的靶向药物迅速发展，显著改变了AML的治疗格局。靶向药物通过特异性抑制白血病细胞的异常信号通路或分子标志，不仅为复发/难治性AML提供了新选择，也逐渐进入一线治疗，为老年及不耐受化疗的脆弱患者群体带来了希望。从4000个化合物中筛出的希望，开启AML靶向治疗新篇在众多分子靶点中，FLT3基因突变尤为关键。FLT3是一种受体酪氨酸激酶，调控造血干细胞的增殖、分化与存活。其突变可促进白血病细胞无限增殖并抑制凋亡，特别是FLT3-ITD突变，与AML预后不良密切相关。随着机制研究的深入，FLT3被确立为AML治疗的重要靶点。 FLT3抑制剂的研发起步于约翰斯·霍普金斯大学唐纳德·斯莫尔（Donald Small）博士团队。上世纪90年代，斯莫尔博士克隆出了首个人类FLT3基因并揭示了其在AML中的致病作用。由于当时缺乏高通量筛选工具，研究团队利用96孔板手动筛选了4000余种化合物，最终发现CEP-701（lestaurtinib）为潜在FLT3抑制剂。随后，通过实验室和动物模型验证，并构建FLT3活性检测方法，研究人员进一步明确了其作用机制。临床研究显示，CEP-701可清除AML患者外周血中的白血病细胞，在部分患者体内甚至还能清除白血病细胞的发源地——骨髓中的白血病细胞。但这种疗效是暂时的，且存在药物与血浆蛋白结合过强等缺陷，最终限制了其应用。基于斯莫尔博士团队的发现以及其他研究成果，新一代的FLT3抑制剂逐步克服了这些局限性。数年后，研究者意外发现多激酶抑制剂Rydapt（midostaurin，米哚妥林）竟是一种强效FLT3抑制剂。该药物最初作为PKC抑制剂开发，在实体瘤模型中展现出抗增殖活性。体外实验表明，米哚妥林可在极低浓度下抑制FLT3-ITD阳性小鼠原B细胞株增殖，并通过诱导凋亡和阻滞细胞周期发挥作用。在动物模型中，其口服治疗显著改善了移植FLT3-ITD骨髓小鼠（模拟AML模型）的生存。由于该药物的安全剂量已在其他疾病患者中确立，研究人员迅速将其应用于AML临床试验。在早期单药研究中，米哚妥林虽能降低外周血原始细胞计数，但完全缓解率有限，引发了对其疗效的质疑。然而，联合治疗方案改变了这一局面：米哚妥林与标准化疗联合使用，显著提高了AML患者的治疗结局。最终，2017年，美国FDA批准米哚妥林联合标准阿糖胞苷+柔红霉素诱导治疗及阿糖胞苷巩固治疗，用于FLT3突变阳性的成人AML患者。图片来源：123RF 米哚妥林的成功标志着AML靶向治疗的开端，也推动了更多高效、选择性更强的FLT3抑制剂相继问世。其中，Xospata（gilteritinib，吉瑞替尼）于2018年获FDA批准，用于复发/难治性FLT3突变AML；2023年，Vanflyta（quizartinib）也获得FDA批准，可联合化疗用于新确诊FLT3-ITD阳性AML成人患者，并在巩固化疗后可作为维持治疗单药使用。不杀死癌细胞也能治病的抗癌药在AML研究的另一条路径上，科学家的目光逐渐转向了癌细胞代谢。2009年，基因测序揭示了一个意外的发现：异柠檬酸脱氢酶（IDH）基因在部分AML患者中发生突变。最初，这一结果让研究者颇感困惑，毕竟，IDH是糖代谢和三羧酸循环中的关键酶，长期以来并未被视为典型的癌基因。然而，深入研究揭示了谜底。IDH突变改变了细胞代谢的走向：原本应生成α-酮戊二酸（a-KG）的反应被打断，反而触发了其“逆向反应”，产生异常代谢物2-羟基戊二酸（2-HG）。2-HG的大量积累抑制了a-KG依赖性酶的活性，导致DNA甲基化紊乱和基因表达失调，由此使癌基因被激活、抑癌基因沉默。更为重要的是，这一代谢异常阻碍了造血细胞的正常分化，迫使其停留在“幼稚”的状态，从而推动白血病的发生与进展。研究者同时发现，在星形细胞瘤、胶质母细胞瘤等多种肿瘤中也存在IDH1/2突变，凸显了其在肿瘤发生中的普遍性作用，高水平的2-HG更是与AML的不良预后相关。由此，一个全新的治疗设想浮现：如果能够抑制突变IDH的功能，让分化阻滞解除，使白血病细胞重新分化为成熟血细胞，疾病或许就能被逆转。这一理念不同于“直接杀死癌细胞”的传统模式，而是采用了“诱导分化”的全新思路。带着这一希望，医药界纷纷针对IDH靶点开展研发工作。经过多年探索，IDH2抑制剂Idhifa（enasidenib）率先问世，并于2017年获得FDA批准，用于治疗IDH2突变的复发/难治性AML。随后，IDH1抑制剂Tibsovo（ivosidenib，艾伏尼布）在2018年被FDA批准用于IDH1突变的复发/难治性AML；2019年，其适应症扩展至一线治疗——适用于≥75岁或因合并症无法耐受强化化疗的AML患者。2022年，FDA进一步批准艾伏尼布联合阿扎胞苷用于高龄（≥75岁）或其他不适合强化治疗的新确诊AML患者，显著拓宽了受益人群。同年，Rezlidhia（olutasidenib）也获FDA批准用于治疗IDH1突变的复发/难治性AML，为患者提供了更多选择。与依赖强烈细胞毒性的传统化疗不同，IDH抑制剂的作用机理别具一格：它们并不是直接摧毁癌细胞，而是通过解除分化阻滞，让“迷途”的白血病细胞回归正常发育轨迹，重新成为成熟的血细胞。这种“以分化代替杀伤”的新理念，为更多AML患者带来了与癌症长期共存甚至逆转疾病的希望。多靶点突破，AML治疗百花齐放随着靶向治疗的不断进展，AML治疗领域中多个关键靶点逐渐被开发，CD33、BCL-2、Hedgehog信号通路以及menin等靶点相继迎来突破性药物，持续推动AML治疗模式的革新。在CD33靶向药物方面，目前已获批的药物包括Mylotarg（gemtuzumab ozogamicin），其于2017年获美国FDA批准，用于新确诊的CD33阳性AML成人患者，以及2岁及以上的复发/难治性CD33阳性AML儿童和成人患者。 BCL-2抑制剂中，已有Venclexta（venetoclax，维奈克拉）获批上市。该药物于2018年获美国FDA加速批准，与阿扎胞苷/地西他滨或低剂量阿糖胞苷联合，用于≥75岁或因合并症无法接受强化化疗的AML患者一线治疗。在Hedgehog信号通路抑制剂方面，Daurismo（glasdegib）于2018年获FDA批准，可联合低剂量阿糖胞苷用于≥75岁或因合并症不适合强化化疗的新确诊AML成人患者，进一步拓宽了化疗不耐受人群的治疗选择。图片来源：123RF Menin抑制剂及DNA去甲基化药物组合也取得重要进展：2024年11月，美国FDA批准menin抑制剂Revuforj（revumenib）上市，用于治疗成人及≥1岁儿童中携带KMT2A易位的复发/难治性急性白血病患者；2023年，欧盟委员会批准Inaqovi（地西他滨 + cedazuridine），用于新确诊且不适合标准诱导化疗的AML成人患者，目前美国FDA已受理该药物与维奈克拉联合治疗同类患者的申请，预计将于2026年2月做出决定。在生物制品领域，已有多款药物用于AML辅助治疗：重组人粒细胞集落刺激因子Neutrogin（lenograstim）、Neupogen（filgrastim）在日本获批，用于缩短AML患者化疗后中性粒细胞恢复时间及发热持续时间；氨肽酶N（APN）抑制剂Bestatin（ubenimex，乌苯美司）上世纪80年代在日本获批用于AML维持治疗；硫鸟嘌呤（tabloid/tioguanine）早在上世纪60年代就获美国FDA批准，用于AML缓解诱导及巩固治疗；Ceplene（histamine dihydrochloride）在2008年获EMA批准，与IL-2联合用于首次缓解期AML成人患者的维持治疗。一体化CRDMO为AML患者带来曙光过去25年间，靶向疗法、免疫疗法和细胞疗法等创新治疗模式的不断涌现，持续重塑着血液癌症的治疗格局，让越来越多患者在延长生命的同时获得更好的生活质量。而这些疗法突破的背后，离不开科研人员对医学前沿的执着探索，以及产业伙伴间高效协同的支撑。长期以来，药明康德始终凭借“一体化、端到端”的CRDMO平台，持续赋能合作伙伴在血液癌症新药研发中不断突破，加速创新成果落地，惠及全球患者。在AML治疗领域，过去25年间，全球监管机构已先后批准了数十款AML创新疗法，为长期面临治疗困境的AML患者带来了新的治疗希望。作为创新的赋能者，药明康德很高兴能为其中多款疗法提供赋能，助力合作伙伴将这些创新疗法带到全球患者身边。在25年发展历程中，药明康德始终致力于支持全球合作伙伴从药物研究发现（R）、开发（D）到商业化生产（M）各个阶段的需求，助力突破性疗法加速研发进程。以血液肿瘤的小分子药物为例，药明康德化学服务平台能支持各种化学药物的分子形式及类别，满足从药物发现到商业化生产各个阶段、各个规模的各种物料需求。药明康德生物学业务平台作为综合性的早期发现和转化生物学赋能平台，能为包括血液肿瘤在内的多个疾病领域的新药研发提供从早期发现到临床研究阶段的生物学解决方案。药明康德测试业务平台可为包括血液肿瘤在内多个疾病领域的药物提供全生命周期的一体化研发测试服务及全方位的临床研究服务，助力合作伙伴的药物成功申报IND、NDA以及通过核查上市。随着对血液肿瘤发病机制理解的持续深化和治疗技术的不断创新，全球血液肿瘤药物研发正迈向更加精准、高效的新阶段。展望未来，药明康德将继续秉承“让天下没有难做的药，难治的病”的愿景，助力合作伙伴加速更多好药新药问世。参考资料： [1] Acute myelogenous leukemia，Retrieved september 9, 2025 from https://www.mayoclinic.org/diseases-conditions/acute-myelogenous-leukemia/symptoms-causes/syc-20369109 [2] Acute Myeloid Leukemia Treatment (PDQ®)–Patient Version，Retrieved september 9, 2025 from https://www.cancer.gov/types/leukemia/patient/adult-aml-treatment-pdq [3] Acute myeloid leukaemia，Retrieved september 9, 2025 from https://www.nhsinform.scot/illnesses-and-conditions/cancer/cancer-types-in-adults/acute-myeloid-leukaemia [4] Acute Myeloid Leukemia (AML)，Retrieved september 9, 2025 from https://my.clevelandclinic.org/health/diseases/6212-acute-myeloid-leukemia-aml [5] Key Statistics for Acute Myeloid Leukemia (AML). Retrieved september 9, 2025 from https://www.cancer.org/cancer/types/acute-myeloid-leukemia/about/key-statistics.html#:~:text=About%2022%2C010%20people%20will%20be,is%20about%20%C2%BD%20of%201%25. [6] Thomas X. First contributors in the history of leukemia. World J Hematol 2013; 2(3): 62-70 [DOI: 10.5315/wjh.v2.i3.62] [7] Kampen, Kim R. “The discovery and early understanding of leukemia.” Leukemia research vol. 36,1 (2012): 6-13. doi:10.1016/j.leukres.2011.09.028 [8] Strebhardt, K., Ullrich, A. Paul Ehrlich's magic bullet concept: 100 years of progress. Nat Rev Cancer 8, 473–480 (2008). https://doi.org/10.1038/nrc2394 [9] The History of Leukemia. Retrieved september 9, 2025 from https://bloodcancerunited.org/resources/blog/history-leukemia#early-leukemia-discoveries [10] Blum S, Bacher U, Pabst T. The Evolving Treatment Landscape of AML. healthbook TIMES Onco Hema. 2022;11(1):32-41. doi:10.36000//hbT.OH.2022.11.065 [11] Targeted Therapy Drugs for Acute Myeloid Leukemia (AML)，Retrieved september 9, 2025 from https://www.cancer.org/cancer/types/acute-myeloid-leukemia/treating/targeted-therapy.html [12] FLT3 Inhibitors. Retrieved september 9, 2025 from https://www.hopkinsmedicine.org/news/articles/2018/05/flt3-inhibitors#:~:text=Pediatric%20Oncology%20Director%20and%20leukemia,laborious%2C%20time%2Dconsuming%20process. 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In Encyclopedia of Cancer, 3rd ed.; Boffetta, P., Hainaut, P., Eds.; Academic Press: Cambridge, MA, USA, 2019; pp. 528–537. [18] Mardis, Elaine R et al. “Recurring mutations found by sequencing an acute myeloid leukemia genome.” The New England journal of medicine vol. 361,11 (2009): 1058-66. doi:10.1056/NEJMoa0903840 [19] Issa, Ghayas C, and Courtney D DiNardo. “Acute myeloid leukemia with IDH1 and IDH2 mutations: 2021 treatment algorithm.” Blood cancer journal vol. 11,6 107. 3 Jun. 2021, doi:10.1038/s41408-021-00497-1 [20] Yun, Zhangjun, et al. "Global, Regional and National Burden of Leukemia, 1990-2021: Analysis of Data from the Global Burden of Disease Study 2021." Blood 144 (2024): 7907. 免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

免疫疗法细胞疗法抗体药物偶联物临床研究

2025-10-03

·Biotech前瞻

艾伯维专利大战落败丨BeOne凭泽布替尼逆袭BTK全球格局

点击蓝字关注我们本期看点 2025 年，全球 BTK 抑制剂市场迎来拐点。美国专利商标局（USPTO）近期宣布，艾伯维公司专利 No. 11,672,803 的全部权利要求无效。随着这一判决，艾伯维与 BeOne（原百济神州）围绕泽布替尼（Brukinsa）的专利大战正式落幕。而就在同一时间，Brukinsa 的全球销量首次超越阿斯利康的 Calquence，进一步甩开艾伯维的 Imbruvica。这一连串事件，不仅意味着一场跨国专利博弈的终结，更宣告着 BTK 靶点全球竞争格局的重塑。本期内容 01 艾伯维与BeOne专利大战落幕 02 泽布替尼商业表现与百济神州战略转型 03 政策风险与关税影响 04 竞争格局变化与新药进展【01 艾伯维与BeOne专利大战落幕】 2023 年，艾伯维在 ’803 专利获批后不久便对 BeOne 提起诉讼，指控 Brukinsa 在 CLL/SLL 的给药方法上侵犯其专利。这一做法因时机敏感而饱受争议：该专利距离 Imbruvica 获 FDA 批准已近 10 年，而诉讼则发生在 Brukinsa III 期头对头试验战胜 Imbruvica 后不久。 ’803 专利的核心内容是：每日口服 BTK 抑制剂，直至 CLL/SLL 疾病进展或不可接受毒性出现，其中“淋巴细胞增多症不视为进展”。艾伯维认为 Brukinsa 的临床设计构成侵权。 BeOne 迅速发起反击。2025 年 4 月，USPTO 裁定该专利过于宽泛，全部权利要求无效。艾伯维上诉遭拒，9 月 30 日双方提交联合协议，自愿撤诉。BeOne 在公告中称该事项已“彻底解决”。这场专利大战的落幕，意味着 Brukinsa 在法律层面扫清了障碍，为其全球扩张打下坚实基础。 02 泽布替尼商业表现与百济神州战略转型 Brukinsa的崛起不仅在于临床数据，更体现在商业化表现： 2025年第二季度，百济神州（BeOne）公布布鲁金萨（zanubrutinib）全球销售数据：美国市场销售额达6.84亿美元（同比增长43%），欧洲市场1.50亿美元（增长85%）。据Fierce Pharma报道，同期布鲁金萨全球销售约9.50亿美元，领先阿斯利康Calquence（acalabrutinib）的8.72亿美元，拉大了领先优势（差额78百万美元，高于一季度的30百万美元差距）。 BeOne首席财务官Aaron Rosenberg指出，由于布鲁金萨被列为医保优先用药（protected class）且覆盖面广，绝大多数患者能够不受阻碍地获得用药；即便竞争对手采取降价策略，布鲁金萨的净价在2025年下半年也将保持稳定。布鲁金萨凭借其差异化优势正在抢占新患者份额，这为其带来强劲的销量增长。今年5月，百济神州正式更名为BeOne，并将注册地从开曼迁至瑞士。公司表示，此举反映出其成熟度提升，瑞士优越的贸易和税收协定环境有助于全球业务拓展。为了应对全球市场变化，BeOne积极构建多元化供应链和生产布局。供应链全球化与在地化的策略已经显现成效：BeOne在美国本土拥有布鲁金萨的生产能力，并计划在新泽西Hopewell建立新的生物制剂生产设施，用于未来产品商业化供应。目前，BeOne与多家第三方代工厂合作完成布鲁金萨在美的制剂生产和包装，但活性药物成分（API）仍需进口：公司已在欧盟和中国各获得两个FDA批准的布鲁金萨API供应商，并正寻求在欧洲新增第三家来源。通过这种全球/区域化布局，BeOne试图降低贸易关税和政策变动带来的风险。这样子的百济神州，还能称之为中国Biotech企业吗？悬在在美药企头上的剑正在逐步落下，那就是药品降价和关税大战。 03 政策风险与关税影响美国新政府频繁提出针对医药进口和定价的改革举措，对BTK抑制剂厂商构成潜在压力。据报道，特朗普政府计划逐步对进口药品征收关税，从最初的数十个百分点，最终或提升至150%-250%。同时，一项“最惠国定价”行政令要求美国药价与其他发达国家持平。为应对这些风险，BeOne强调其全球化供应链已在很大程度上缓解了关税冲击：管理层表示，公司已将生产环节转向美国本土，并已对运营成本进行了相应规划。业内也在探索新的定价模式：例如诺和诺德、礼来、罗氏等药企正试行“直达患者”低价策略（DTC），BeOne方面已在研究此类模式，但指出此举在肿瘤药领域的适用性尚需评估。总体而言，在最惠国定价和关税政策面前，BeOne通过灵活调整供应链和积极铺设美国制造能力，力求保障患者用药和企业利润不受剧烈冲击。 04 竞争格局变化与新药进展 BTK 赛道竞争加剧。礼来的 Jaypirca（pirtobrutinib）在三期试验中已展现出优于伊布替尼的潜力；阿斯利康的固定疗程方案已在欧盟获批并进入美国审评。BeOne 也紧随其后，启动全球三期 Celestial-301 研究，以 Brukinsa + sonrotoclax 对比 Venetoclax 联合方案，积极布局 BTK 与 BCL2 联合治疗。与此同时，BeOne 的 sonrotoclax 已在套细胞淋巴瘤试验中取得积极结果，意图挑战 AbbVie/Roche 的 Venclexta。未来，Brukinsa+sonrotoclax 有望成为 CLL/SLL 的新标准，进一步重塑靶点格局。市场层面，BTKi 行业仍保持高速增长：2025 年预计规模将达 219 亿美元。随着伊布替尼销售下滑，布鲁金萨凭借更优疗效和医保覆盖实现持续放量，正逐步坐稳二代 BTKi 的全球领跑地位。未来竞争将更加依赖差异化疗效、安全性、固定疗程策略，以及药企应对医保与定价政策不确定性的能力。 ★

专利侵权专利无效

2025-10-02

·FiercePharma

AbbVie, BeOne end BTK blood cancer drug patent fight

The U.S. Patent and Trademark Office recently invalidated all claims of AbbVie’s patent, No. 11,672,803, which underpinned the Illinois pharma’s patent infringement lawsuit filed against BeOne Medicines in 2023. BeOne Medicines and AbbVie’s Pharmacyclics have decided to voluntarily dismiss the patent lawsuit the Big Pharma firm brought against its competitor over their BTK inhibitors.BeOne announced the decision in a securities filing (PDF) to the Hong Kong stock exchange. The move comes after the U.S. Patent and Trademark Office (USPTO) recently invalidated all claims of AbbVie’s patent, No. 11,672,803, which underpinned the Illinois pharma’s patent infringement lawsuit filed in 2023.The patent covers a method of use for a BTK inhibitor developed under a certain chemical structure for treating chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL), the most important indication of the drug class.Filing of the lawsuit was not a good look on AbbVie because it was initiated right after the ’803 patent was issued, nearly 10 years after the FDA approval for the company’s Johnson & Johnson-partnered Imbruvica in CLL/SLL. And it came shortly after BeOne’s Brukinsa beat Imbruvica in a head-to-head phase 3 trial in second-line CLL/SLL. Specifically, the patent describes orally administering a BTK inhibitor with a certain structure daily until CLL/SLL disease progression or unacceptable toxicity, wherein lymphocytosis is not considered progression. AbbVie argued that BeOne—formerly BeiGene—stepped on its patent because Brukinsa describes the same method of use.In response, BeOne challenged the ’803 patent with the USPTO. April 29, the U.S. agency invalidated all claims of the patent, siding with BeOne that the patent was overly broad. AbbVie filed a request for a director review, hoping to overthrow the earlier verdict, but was denied by the USPTO on July 17, according to a recent BeOne securities filing.Sept. 30, the two companies filed a joint stipulation to voluntarily dismiss the related lawsuit, and the matter is considered “fully resolved,” BeOne said in its Oct. 2 filing.Brukinsa has become a major growth engine for BeOne. In the second quarter, the drug hauled in $950 million in sales, ahead of AstraZeneca’s second-generation BTK inhibitor Calquence, which generated $872 million during the period. By comparison, AbbVie reported Imburvica global revenues of $754 million in the second quarter, down by 9.5% year over year. The AbbVie number included profit sharing for Imbruvica internal revenues with J&J.BeOne is also working on a next-generation BCL2 inhibitor for combination with Brukinsa in CLL/SLL. The drug, called sonrotoclax, just turned in a positive pivotal readout in mantle cell lymphoma. Similar to Brukinsa’s proposition as a more efficacious and more tolerable BTK than Imbruvica, BeOne is angling sonrotoclax as a better BCL2 than AbbVie and Roche’s Venclexta. Analysts have predicted that the Brukinsa-sonrotoclax duo has potential to further transform CLL/SLL treatment.

专利侵权上市批准临床3期

100 项与维奈克拉相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10679	维奈克拉	L01XX52	DB11581

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
复发性套细胞淋巴瘤	日本	AbbVie LLC	2025-03-27
难治性套细胞淋巴瘤	日本	AbbVie LLC	2025-03-27
难治性慢性淋巴细胞白血病	日本	AbbVie LLC	2019-09-20
复发性慢性淋巴细胞白血病	日本	AbbVie LLC	2019-09-20
小淋巴细胞淋巴瘤	美国	AbbVie, Inc.	2018-06-08
成人急性髓性白血病	欧盟	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	冰岛	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	列支敦士登	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	挪威	AbbVie Deutschland GmbH & Co. KG	2016-12-04
急性髓性白血病	加拿大	AbbVie AS	2016-10-31
慢性淋巴细胞白血病	美国	AbbVie, Inc.	2016-04-11

未上市

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
复发性急性髓细胞白血病	临床3期	美国	AbbVie, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	美国	Genentech, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	日本	Genentech, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	日本	AbbVie, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	澳大利亚	Genentech, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	澳大利亚	AbbVie, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	奥地利	AbbVie, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	奥地利	Genentech, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	比利时	AbbVie, Inc.	2022-10-01
复发性急性髓细胞白血病	临床3期	比利时	Genentech, Inc.	2022-10-01

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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


NCT05184842 (Phase II, CTgov)	临床2期	急性髓性白血病 \| 慢性粒单核细胞白血病 \| 骨髓增生异常综合征	-	Venetoclax+Decitabine	鬱壓範窪繭願夢簾範簾 = 範廠範觸願餘鬱鹽鏇獵顧襯鏇鹹糧鹽廠窪齋簾 (觸積選鏇衊網簾壓繭憲, 鹹糧顧夢膚範壓選糧選 ~ 窪廠糧廠憲範膚艱齋願) 更多	-	2025-08-26
NCT04102020 (VIALE-M, CTgov)	临床3期	急性髓性白血病	112	Venetoclax+Azacitidine (Part 1: Venetoclax 400 mg + Azacitidine 20 mg/m^2)	糧鏇顧範鏇廠顧鏇遞構 = 遞糧襯簾鏇壓願顧衊遞廠願願獵齋網鹽網積遞 (顧遞範鬱顧網顧衊鏇構, 鏇繭壓鏇蓋鹹鬱鹽鏇顧 ~ 選網糧選鑰壓艱鏇鹹製) 更多	-	2025-08-20
NCT04102020 (VIALE-M, CTgov)	临床3期	急性髓性白血病	112	Venetoclax+Azacitidine (Part 1: Venetoclax 400 mg + Azacitidine 36 mg/m^2)	糧鏇顧範鏇廠顧鏇遞構 = 鬱蓋蓋遞壓膚顧遞齋獵廠願願獵齋網鹽網積遞 (顧遞範鬱顧網顧衊鏇構, 膚獵構顧壓遞製構鹹觸 ~ 簾窪淵繭鏇鹽選壓壓觸) 更多	-	2025-08-20
NCT03580928 (AMPLIFY \| AVO, CTgov)	临床2期	慢性淋巴细胞白血病	72	Acalabrutinib+Venetoclax+Obinutuzumab (Acalabrutinib/Venetoclax/Obinutuzumab (AVO) With Non-high-risk CLL Disease)	襯選觸廠鏇廠觸網鏇夢 = 壓艱繭壓齋蓋顧膚願鑰獵壓壓鬱鹹願築鑰顧鏇 (積觸築鹹選鹹網廠鏇範, 鹽窪壓積築壓齋選鏇餘 ~ 鏇鏇遞築顧衊網醖繭選) 更多	-	2025-08-12
NCT03580928 (AMPLIFY \| AVO, CTgov)	临床2期	慢性淋巴细胞白血病	72	Acalabrutinib+Venetoclax+Obinutuzumab (Acalabrutinib/Venetoclax/Obinutuzumab (AVO) With High-risk CLL Disease)	襯選觸廠鏇廠觸網鏇夢 = 積顧齋築窪簾襯鹹淵獵獵壓壓鬱鹹願築鑰顧鏇 (積觸築鹹選鹹網廠鏇範, 壓範觸觸鹽獵網鑰艱襯 ~ 鏇艱願獵鏇構遞觸廠顧) 更多	-	2025-08-12
NCT03013998 (Pubmed \| J Clin Oncol)	临床1期	难治性急性髓细胞白血病 NPM1m \| KMT2Ar	43	Azacitidine, Venetoclax, and Revumenib	艱網艱衊夢鏇鏇襯範製(衊選艱醖願廠糧遞構簾) = present in 8 (19%) patients 簾廠壓鏇範繭簾艱壓範 (鹽簾醖淵醖觸網鬱鏇築 ) 更多	积极	2025-08-10
NCT03872180 (CTgov)	临床2期	套细胞淋巴瘤	23	bendamustine+Venetoclax+Obinutuzumab	壓顧遞夢願積簾簾窪餘 = 鑰遞築艱鬱衊窪衊衊壓願衊鹽製築憲觸淵觸醖 (糧製窪選齋獵蓋觸糧醖, 淵襯壓衊膚顧鹹範繭艱 ~ 積淵構艱遞窪網襯夢廠) 更多	-	2025-08-06
NCT04797767 (Phase 1 trial of venetoclax with cladribine, cytarabine, G-CSF, and mitoxantrone for AML and high-grade myeloid neoplasm, Pubmed)	临床1期	髓系肿瘤 \| 急性髓性白血病	-	Venetoclax 400 mg	積鹽築鬱簾鏇構築獵繭(醖築醖繭獵遞鑰遞願鏇) = 5% 築製淵願顧簾窪壓餘醖 (顧積膚構廠夢鬱蓋鬱膚 )	积极	2025-08-01
NCT02755597 (BELLINI, Pubmed \| Lancet Haematol)	临床3期	难治性多发性骨髓瘤	291	Venetoclax	窪繭衊範鬱顧糧鑰繭築(膚糧醖製築鑰齋鏇糧選) = 30% of 193 vs 8% of 96 patients 構艱鏇廠鬱鹹醖膚鏇蓋 (衊簾繭鬱鏇襯餘簾窪壓 ) 更多	不佳	2025-08-01
NCT02755597 (BELLINI, Pubmed \| Lancet Haematol)	临床3期	难治性多发性骨髓瘤	291	Placebo		不佳	2025-08-01
NCT03112174 (SYMPATICO, CTgov)	临床3期	套细胞淋巴瘤	366	Ibrutinib+Venetoclax (Randomization Phase: Ibrutinb + Venetoclax)	鬱製築壓遞觸醖鏇廠壓(廠鑰窪鏇築獵廠醖艱繭) = 顧廠壓艱餘餘製鹽構鹹範餘積廠繭憲構鹽鏇糧 (憲顧蓋齋鹹艱鹹遞鏇範, 鏇齋糧醖壓衊築膚繭顧 ~ 製構選鏇淵築齋廠夢衊) 更多	-	2025-07-22
NCT03112174 (SYMPATICO, CTgov)	临床3期	套细胞淋巴瘤	366	Placebo Oral tablet to match Venetoclax+Ibrutinib (Randomization Phase: Ibrutinib + Placebo)	鬱製築壓遞觸醖鏇廠壓(廠鑰窪鏇築獵廠醖艱繭) = 繭選鬱簾壓衊衊憲膚範範餘積廠繭憲構鹽鏇糧 (憲顧蓋齋鹹艱鹹遞鏇範, 範繭願淵選壓繭觸積醖 ~ 憲觸衊襯遞積襯夢廠製) 更多	-	2025-07-22
NCT02966756 (M14-728, NEWS) 人工标引	临床2期	慢性淋巴细胞白血病 Loss of Chromosome 17p	69	Venetoclax	鹹鬱襯蓋製襯蓋淵窪鏇(鹽製範鹽簾淵構蓋膚觸) = 衊築壓蓋構醖製願膚鹽繭繭蓋壓淵蓋獵廠遞鏇 (製衊夢顧蓋繭窪製憲構 ) 更多	积极	2025-07-20
NCT01889186 (M13-982, NEWS) 人工标引	临床2期	慢性淋巴细胞白血病 Loss of Chromosome 17p	153	维奈克拉	淵餘蓋廠獵窪範夢蓋衊(選觸顧獵衊淵積餘獵獵) = 襯築襯鹹鏇鹽衊網構遞鏇觸選繭憲遞簾膚蓋繭 (繭鹹衊鬱構窪範糧餘簾, 22.8 ~ 37.1) 更多	积极	2025-07-20