A Single Arm Phase II Study Investigating the Efficacy and Safety of the Addition of Ivosidenib to Oral Azacitidine (Onureg®) in Patients Over 55 With Acute Myeloid Leukemia (AML) and IDH1 Mutation, in Complete Remission After Intensive Chemotherapy. A Study of the French AML Intergroup.

After remission post-induction and consolidation, maintenance therapy by an ivosidenib and oral azacitidine combination is susceptible to improve the prevention of AML relapse, which remains a major issue in the study population. We assume that the combination of ivosidenib with oral azacitidine will not be less well tolerated than in combination with the subcutaneous form, therapeutic regimen authorized until progression or toxicity. Ivosidenib and Onureg®, being already authorized treatments, it has been decided to use the classic administration schedules and dosages in combination.
The primary objective of the study is to evaluate relapse free survival (RFS) at 24 months in patients receiving oral azacitidine with ivosidenib.

开始日期2026-09-01

申办/合作机构

Servier Affaires Medicales SARL

ChiCTR2600122486

/ Not yet recruiting临床2期

Neoadjuvant Therapy With Ivonescimab Combined With Chemotherapy for Triple-Negative Breast Cancer

开始日期2026-04-30

申办/合作机构

复旦大学附属肿瘤医院

[+1]

NCT07507760

/ Not yet recruiting临床2期IIT

A Phase II, Multicentre, Open Label Clinical Trial Evaluating the Efficacy and Safety of Oral Decitabine Plus Ivosidenib in Adult Patients With Newly Diagnosed Acute Myeloid Leukemia Older Than 60 Years Old and/or Who Are Ineligible for Standard Induction Chemotherapy

The goal of this clinical trial is to learn if the combination of oral decitabine plus ivosidenib works to treat naïve adult patients with acute myeloid leukemia (AML) with IDH1 R132 mutation older than 60 years old or those who are older than 18 years old with defined comorbidities that make them not suitable for standard induction therapy. The main objectives of this clinical trial are:
* Asses the Complete Remission (CR) and Complete Remission with incomplete marrow recovery (CRi) rates of this treatment.
* Determine the incidence and severity of all adverse events (AEs).
All participants will receive oral ivosidenib and oral decitabine in treatment cycles of 28 days until disease progression, lack of clinical benefit or the end of the study. Patients who achieve CR/CRi will be elegible to receive allogeneic stem cell transplantation.

开始日期2026-04-01

申办/合作机构-

100 项与艾伏尼布相关的临床结果

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100 项与艾伏尼布相关的转化医学

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100 项与艾伏尼布相关的专利（医药）

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380

项与艾伏尼布相关的文献（医药）

2026-04-01·AMERICAN JOURNAL OF HEMATOLOGY

The Care and Cure of the Leukemias in 2026

Review

作者: Wierda, William ; Kadia, Tapan ; Kantarjian, Hagop ; Haddad, Fadi G. ; Freireich, Emil J. ; Ravandi, Farhad ; Chifotides, Helen T. ; Jabbour, Elias ; Jain, Nitin ; Welch, Mary Alma

ABSTRACT:

It is an exciting era in leukemia owing to the development of novel targeted therapies and advances in genomics, pathophysiology, prognostication, and monitoring (e.g., highly sensitive measurable residual disease assays). Currently, most leukemias are effectively treated with immunotherapies (highly effective monoclonal antibodies targeting CD19 [blinatumomab], or CD22 [inotuzumab ozogamicin]), BCR::ABL1 tyrosine kinase inhibitors (TKIs; e.g., dasatinib, ponatinib), Bruton TKIs (e.g., ibrutinib, acalabrutinib), BCL‐2 inhibitors (venetoclax), IDH1/2 inhibitors (ivosidenib, olutasidenib, and enasidenib), FLT3 inhibitors (e.g., midostaurin, quizartinib, and gilteritinib), menin inhibitors (revumenib, ziftomenib), and chimeric antigen receptor T‐cell therapies. These novel agents and their judicious use in combination strategies have transformed the treatment landscape across all leukemias, significantly increased survival and quality of life for patients, and attenuated the need for intensive chemotherapy and hematopoietic stem cell transplantation. Leukemia subtypes, such as Philadelphia‐positive acute lymphoblastic leukemia (incurable before 2000) and chronic lymphocytic leukemia (previously considered incurable) with historically dire prognoses were recently transformed to favorable leukemias with 5‐ and 10‐year survival rates of 80+% and 90+%, respectively. The BCR::ABL1 TKIs resulted in normal life expectancy in chronic myeloid leukemia. Notable advances have also been made in AML with targeted therapies, although some subsets (older/unfit patients for intensive chemotherapy, complex karyotype, TP53 ‐mutated, KMT2A ‐rearranged, and treated secondary AML) still have unfavorable outcomes. Herein, we provide a high‐level overview of prominent clinical developments across all leukemias. In contemporary times, harnessing the benefits of novel targeted therapies and the evolving treatment landscape bolster the optimistic view that most, if not all, leukemias are curable.

2026-03-26·JOURNAL OF MEDICINAL CHEMISTRY

Discovery of a Hydroxamic Acid-Based HDAC11 Isoform-Selective Inhibitor with Oral Anti-AML Potency

Article

作者: Wang, Wenjing ; Xue, Xintong ; Liu, Lanlan ; Zhang, Yingjie ; Zhu, Xiaolan ; Zhao, Wei ; Chai, Qipeng ; Liu, Lina ; Yang, Maoshuo ; Zhang, Jinwei ; You, Xiaona ; Liu, Chunxi ; Liu, Fabao

Our previous study not only demonstrated that HDAC11 is a potential therapeutic target for AML but also discovered a specific HDAC11 inhibitor A9 as an anti-AML lead compound. The purpose of the present study was to discover novel specific HDAC11 inhibitors with improved drug-like properties through structural modification and optimization of A9. Among the newly synthesized A9 derivatives, compound 25 stood out as a potent and specific HDAC11 inhibitor with desirable liver microsomal stability. Notably, compared with the well-known HDAC11 inhibitor FT895, compound 25 exhibited much stronger multiple anti-AML effects including proliferation inhibition, apoptosis induction, cell cycle arrest, differentiation promotion, and ferroptosis induction. Moreover, combination of 25 and ivosidenib, an approved targeted therapeutic drug for AML, showed strong synergistic anti-AML potency. Satisfyingly, compound 25 exhibited acceptable oral pharmacokinetic parameters in mouse, which supported its robust oral anti-AML potency in an MLL-AF9-induced mouse AML model, both alone and in combination with ivosidenib.

2026-03-02·CLINICAL CANCER RESEARCH

MAPK Pathway Mutations Emerge in Mutant IDH1 Inhibitor–Resistant Cholangiocarcinoma and Attenuate the IFN Response

Article

作者: Abou-Alfa, Ghassan K. ; Saatcioglu, Hatice Duygu ; Aguado-Fraile, Elia ; Corcoran, Ryan B. ; Choe, Sung ; Wan, Jinkai ; Norden, Bryanna L. ; Xu, Qin ; Kondo, Hiroshi ; Gliser, Camelia ; Lubner, Sam J. ; Pandya, Susan ; Manguso, Robert T. ; Javle, Milind ; Daigle, Scott ; Cleary, James M. ; Oh, Do Youn ; Borad, Mitesh J. ; Tron, Adriana E. ; Gritti, Ilaria ; Bardeesy, Nabeel ; Ellis, Haley ; Macarulla, Teresa ; Kelley, Robin K. ; Noble, Carolina

Abstract:

Purpose::

Mutant IDH1 (mIDH1) defines a therapeutically targetable subtype of intrahepatic cholangiocarcinoma (ICC), with the mIDH1 inhibitor ivosidenib approved for advanced disease. A subset of patients experiences prolonged disease stabilization; however, the molecular basis for eventual progression remains poorly defined.

Experimental Design::

We performed molecular profiling of matched baseline and postprogression circulating tumor DNA (ctDNA) samples from patients with mIDH1 ICC enrolled in the ClarIDHy phase III trial. Functional studies were conducted to characterize candidate resistance mechanisms.

Results::

Longitudinal ctDNA analysis of 18 patients treated with ivosidenib for >6 months revealed emergent genomic alterations in multiple cases. Acquired mutations in mitogen-activated protein kinase (MAPK) pathway genes (KRAS, NRAS, MAP2K1, NF1) were identified in five cases, with instances of concurrent alterations and/or high variant allele fractions (VAF). Additional candidate resistance events included a secondary IDH1 mutation and a hotspot IDH2 mutation, detected at low VAF in the same patient. Functional studies showed that these IDH mutations conferred sustained 2-hydroxyglutarate production and ivosidenib resistance, whereas MAPK activation blunted gene expression induced by ivosidenib plus IFNγ, a key therapeutic output of mIDH1 inhibition. In parallel, baseline ctDNA profiling of 81 patients revealed that ARID1A mutations and elevated mIDH1 VAF were associated with reduced clinical benefit.

Conclusions::

MAPK pathway alterations represent a recurrent mechanism of resistance to mIDH1 inhibition in ICC, whereas emergent IDH1/IDH2 mutations appear infrequent. Functional data suggest that MAPK-mediated resistance may involve impaired IFN signaling. These results support MAPK-directed combination strategies and highlight the utility of ctDNA profiling to identify predictive and resistance biomarkers in mIDH1-driven ICC.

411

项与艾伏尼布相关的新闻（医药）

2026-04-19

·搜狐新闻

150亿苏州药厂，再度募集10个亿

来源：@21世纪商业评论微博撰文丨韩璐编辑丨谭璐一家苏州药厂，决定再募一笔弹药。4月中旬，基石药业董事会决定，拟通过配售新股方式，净筹10.53亿港元。董事会中，CEO杨建新是唯一的执董。基石药业专注于抗肿瘤药物研发，这家生物医药公司无实控人，第一大股东是一家医药投资基金，由药明康德牵头成立。2022年8月，创始人江宁军离开后，高管杨建新接任CEO，兼任研发总监及执行董事。公司计划将新募资的9 成，用于管线资产的进一步研发，尤其是全球首个进入临床阶段的同靶点三抗药物CS2009、潜在ADC药物CS5001等。过去10年，基石药业公开完成的募资额，折合约86亿港元。其持续依赖资本输血，反映了打造一家创新药企的不可测性。粮草先行配股消息发布前一个月，基石药业的股价从6.5港元/股，一路上涨至10.4港元/股，涨幅接近50%，市值接近150亿港元。上涨的原因，来自其创新管线的出色表现。3月下旬，杨建新团队披露了一款三特异性抗体CS2009的最新进展。该药是全球首个进入临床阶段的同靶点三抗药物，被视为新一代基础免疫疗法，既能增效又能控制毒性，比传统联合用药的副作用可能更小。2025年10月，团队首次披露该药的I期临床研究数据，在72例晚期实体瘤患者中，未发生剂量限制性毒性，相关不良事件发生率，远低于同类双抗产品。到今年3月中旬，CS2009 I期临床试验已入组113例晚期实体瘤患者，安全性得到进一步验证。其在肺癌治疗上有着不错的疗效，对于肾癌、软组织肉瘤等，也体现出广谱抗肿瘤潜力。“期待在今年美国临床肿瘤学会（ASCO）年会和欧洲肿瘤内科学会（ESMO）年会上，公布更多临床数据，目前正与多家跨国公司深入洽谈合作。”杨建新寄予厚望。公司方面透露，2026年底前，会启动CS2009首批III期全球多中心临床试验，重点布局肺癌、结直肠癌等适应症。“三期临床规模大、随访时间久、数据庞杂，还要有多中心，是最昂贵的。”一位创新药企负责人对记者解释，新药临床试验中，每个阶段有不同的目标和规模，对应的成本也不一样。CS2009进展到二期开发阶段，杨建新团队的成本激增。2025年，基石药业投入的研发费用达到3.12亿元，相比2024年的1.35亿元，增长了2.3倍。这次配股，主要目的也是为CS2009等管线，准备资金。断臂求生杨建新率领的基石药业，业绩表现不算太好。2025年收入2.7亿元，同比下降超三成，亏损扩大至4.37亿元，成为上市以来亏损额最高的一年。杨建新接手基石药业时，面对外部资本寒冬和内部经营压力。为求生存，他启动了“断臂求生”战略，从原本的重资产、广铺管线，转向“聚焦核心研发、轻资产商业化”模式。过去几年，他裁撤了七成人员、转让商业化权益、砍掉七成研发费用，终于在2024年上半年，实现净利润1570万元，全年减亏至9100万元。节流的路，在2025年行不通了。杨建新手里一共有四款已上市的创新药，它们的销售及授权费用，为公司贡献了超过七成的收入。由于治疗白血病的艾伏尼布，已售出销售权，杨建新团队的实际销售额，主要来自舒格利单抗、阿伐替尼和普拉替尼。舒格利单抗是首个成功出海的国产PD-L1单抗，已在欧盟和英国获批用于非小细胞肺癌一线治疗。来源：图虫2024年，杨建新通过分区域授权，获得了一次性授权收入，抬高了整体营收。而在2025年，授权费用下滑近两成。2025年，这三款产品的总收入大幅下滑，仅有7830万元。而前一年，阿伐替尼及普拉替尼两款产品，就卖出1.751亿元。其中，普拉替尼作为国内首款获批上市的RET抑制剂，用于治疗肺癌和甲状腺癌。为利于医保谈判，去年杨的团队调整了产品价格，并支付了渠道补偿，销售收入严重滑坡。今年1月起，普拉替尼被纳入国家医保目录，管理层预计，2026年开始以价换量，有望冲抵此前的降价影响。静待收获杨建新现年62岁，是美国德州西南医学中心博士、哈佛大学博士后。2016年加入基石药业前，他担任百济神州临床开发部负责人及高级副总裁。他拥有多年海外从业背景，曾是辉瑞肿瘤生物标记物资深首席科学家。杨氏任过基石药业的CMO（首席医学官），全面负责产品的临床开发策略和执行。基石药业创立于2016年，最初靠引进模式，高效完成了产品商业化，一度是创新药里的明星企业，吸引到新加坡政府投资公司（GIC）、红杉、高瓴等知名机构的融资。2019年基石在港股上市后，市值一度超过200亿港元。之后，投建工厂，组建商业化团队，公司陷入巨额亏损，仅2021年就亏损19亿元，加上遭遇资本寒冬，面临生死关头。杨建新临危受命，一边节流回血，一边想办法开源，推出了“管线2.0”战略。他对新管线的规划是，定位全球前三，即使是非常热门的靶点，也要努力跻身全球前五。目前基石药业的在研管线里，配置了ADC、多特异性抗体、免疫疗法及精准治疗等12款候选药物，覆盖实体瘤、血液瘤、免疫与炎症等多个适应症。核心管线资产里，除了CS2009，还有国内首款靶向ROR1的抗体偶联药物CS5001，适应证覆盖血液瘤和实体瘤。该药是2020年从LegoChem Biosciences引入，交易总额3.63亿美元。目前是全球研发进展最快的靶向ROR1的ADC之一，具有全球同类药物最佳潜力，其一期临床正在澳大利亚和中国同步推进。截至2025年末，基石药业的账上现金及存款约9亿元，加上此次配股筹得10.5亿港元。短期内，杨建新可以带着团队，继续推进研发。图片来源：基石药业，除标注外返回搜狐，查看更多

2026-04-16

·allsci.com

Partner Therapeutics seeking third indication for Bizengri in NRG1 fusion-positive cholangiocarcinoma

Partner Therapeutics submitted a supplemental Biologics License Application (sBLA) to the US FDA on April 14, 2026 for Bizengri (zenocutuzumab-zbco), seeking approval for adults with advanced unresectable or metastatic cholangiocarcinoma harboring an NRG1 gene fusion. The filing marks the first regulatory submission for Bizengri in this bile duct malignancy with the aim of adding a third indication to the molecule’s existing accelerated approvals in NRG1 fusion-positive non-small cell lung cancer and pancreatic adenocarcinoma. The sBLA seeks approval without restriction to a specific line of therapy, the company said. The filing is supported by data from the eNRGy study, a basket trial evaluating zenocutuzumab-zbco across NRG1 fusion-positive solid tumors. No priority review or accelerated pathway designation was disclosed in the announcement, and the company did not provide a projected PDUFA date. Bizengri’s cholangiocarcinoma data The cholangiocarcinoma cohort of the eNRGy study generated an overall response rate of 36.8% (95% CI: 16.3, 61.6%) and a median duration of response of 12.9 months, as assessed by blinded independent central review. No patients in that cohort discontinued therapy due to adverse events, the company said. The mechanism underlying the filing differs from all currently approved CCA therapies: zenocutuzumab-zbco is a bispecific antibody that simultaneously blocks HER2/HER3 heterodimerization and NRG1 fusion interactions with HER3, disrupting downstream signaling driven by NRG1 chimeric ligands rather than the chimeric receptors targeted by FGFR inhibitors such as pemigatinib and futibatinib. NRG1 fusions are estimated to occur in fewer than 2% of cholangiocarcinoma cases, and the source material states that no approved therapies currently target this molecular subgroup in the disease. The rarity of the alteration creates a diagnostic challenge: unlike NTRK, RET, or FGFR fusions, NRG1 fusions produce chimeric ligands that are frequently missed by DNA-only next-generation sequencing panels and require tissue-based RNA testing for reliable detection. Partner Therapeutics noted this in its announcement, with Chief Development Officer Pritesh Gandhi stating that RNA testing is essential to ensure patients with NRG1-driven tumors are identified. NCCN guidelines The filing arrives alongside a notable guideline development. The National Comprehensive Cancer Network added zenocutuzumab-zbco to its oncology clinical practice guidelines for biliary tract cancers as a Category 2A subsequent-line therapy and as a Category 2B recommendation for front-line treatment of NRG1 fusion-positive cholangiocarcinoma — the latter positioning preceding any formal regulatory approval for the indication. Dr. James Cleary of Dana-Farber Cancer Institute, commenting in the release, described NRG1 gene fusions as an actionable biomarker in this disease and said the eNRGy data suggest targeted inhibition with zenocutuzumab may represent a meaningful treatment approach. The cholangiocarcinoma treatment landscape has undergone substantial change since 2020, when pemigatinib became the first targeted therapy approved in the disease. Ivosidenib followed in 2021 for IDH1-mutant CCA, futibatinib in 2022 for FGFR2 fusion-positive intrahepatic disease, and durvalumab in combination with gemcitabine and cisplatin was approved the same year for first-line biliary tract cancer regardless of biomarker status. Pembrolizumab combined with gemcitabine and cisplatin received approval in 2023 for the same unselected population. Despite this expansion, the molecular subgroup defined by NRG1 fusions has remained without a specifically labeled therapy, and the eNRGy data represent the primary clinical evidence base for this population in CCA. The sBLA adds to a field where accelerated approval pathways have played a central role, and where the durability of those approvals has varied. Infigratinib, an FGFR1–3 inhibitor that received accelerated approval in 2021 for FGFR2 fusion-positive CCA, was voluntarily withdrawn in 2024 after a confirmatory trial failed to verify clinical benefit — a precedent that underscores the regulatory risk associated with response-rate-based submissions in this disease. The eNRGy cholangiocarcinoma cohort was small, as is typical for trials enrolling rare fusion-defined populations, and the 95% confidence interval for the reported ORR is correspondingly wide. Bizengri’s existing accelerated approvals in NSCLC and pancreatic adenocarcinoma were also granted based on overall response rate and duration of response, with continued approval in those indications contingent on confirmatory trial data. The cholangiocarcinoma sBLA follows the same evidentiary model. Partner Therapeutics holds exclusive US rights to develop and commercialize zenocutuzumab-zbco under an agreement with Merus B.V., a wholly owned subsidiary of Genmab. Leave a Reply Cancel reply Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

2026-04-15

·商业新知

亏额升、股价涨基石药业收获季还远么

深度客观穿透生生不息，不期而遇！点击上方蓝字关注利空出尽了？作者：行者编辑：张戈风品：俊逸来源：首财——首条财经研究院伴随百济神州、信达生物等多家企业宣布盈利，2025年创新药业集体回暖、行业春天来啦。意外的是，凭借三抗管线打出名头的基石药业却走出一波逆行：营收下降、亏额更创下2019年上市以来新高。好在资本信心依然强劲、甚至还迎来一波拉升：3月24日以来，基石药业股价震荡上涨，其中3月27日单日涨幅达20.72%、收盘报8.33港元/股。截至4月15日，公司股价进一步上涨2.14%，收报9.90港元/股，总市值攀至146.13亿港元，较3月23日的6.22港元累涨近6成。业绩股价面背离的原因是什么？这波拉升热度能持续多久、业绩何以下滑后续能否改善？1销售收入、授权费双滑 3月26日，公司2025年报亮相：营收2.70亿元，同比下降33.80%；归母净利亏损4.37亿元，较上年同期的0.91亿元亏额同比扩大379.13%。回望2025年创新药业，集体从侧重规模研发过渡至效益挂帅阶段，盈利成首要任务。本文开头提到的百济神州、信达生物、睿智医药均一举扭亏：前两者分别营收382.05亿元、130.42亿元，归母净利14.22亿元、8.14亿元；睿智医药也预计净利1230.00万元至1845.00万元，对比之下基石药业着实有些掉队，需要知耻后勇了。要知道，2024年公司刚迎一波亏损收窄，亏额从2023年的3.67亿元大幅缩至0.91亿元，正当外界期许基石要否极泰来时，一个大亏又泼了一盆冷水。不过细究会发现，上述减亏根基并不多牢固。首先，压缩成本和削减费用贡献良多，难具有持续性。如研发开支从2023年的5.28亿元骤降至2024年的1.35亿元，降幅高达74.48%；行政开支从1.83亿元削减至0.78亿元，降幅57.42%；销售及市场推广开支从1.99亿元压缩至1.34亿元，降幅32.87%；员工量从2022年末的476人减至2024年6月末的164人，一年半时间减员超65%。其次，业务收入承压。2025年，基石药业药品销售、授权费双双下滑，成业绩恶化的一个核心原因。其中，阿伐替尼、普拉替尼及舒格利单抗三产品合计贡献7830万元，而2024年仅前两款产品销售额就达1.751亿元。再看授权费，2025年收入1.68亿元，同比下滑17.81%，占总收入62.19%；特许权使用费收入2357.7万元，同比下滑16.15%，占比8.75%。主因2024年收取了大额一次性首付款及里程碑付款，高基数高波动导致业绩起伏较大。说到底，业绩面最终取决于业务面，后者改善不扎实前者波动也就不足奇。2BD交易、创新管线各有烦恼打深一度看，公司收入较依赖BD交易，重点管线也面临竞品挑战。回顾近几年业绩，盈利表现与BD交易密切相关。早在2023年底，基石药业就一口气敲定了三项合作：将PD-1单抗CS1003部分商业化权益转让给三生制药，将普拉替尼胶囊中国大陆地区独家商业化推广权移交至上海艾力斯，将艾伏尼布片相关权益出售给施维雅。由此大幅改观了财务数据，2024上半年更首次实现净利1570万元，为2015年末公司成立后首次半年度盈利。这也是中国创新药企普遍做法，国家药监局数据显示，2025年中国全年批准创新药76个，对外授权157件，首付款70亿美元，总金额约1357亿美元，均创新高。上文提及的信达生物扭亏，同样少不了BD交易助力。只是，该模式有利有弊，短期看能快速改善盈利，长远则被质疑“卖血求生”，持续性是个考量。据华夏时报，基石药业曾于2021年底启动试运营的苏州工厂生产基地，总投资达10亿元，一度承载着公司的产业化雄心，却在大约一年后的2022年11月宣布暂停试运营，一度曾引发外界不少猜测。好在，基石药业已在改变经营战略，从被动“收缩过冬”转向主动“研发聚焦”，从“资产出售求生”转向“核心管线押注”，比如将回笼资金集中投向最具差异化竞争优势的下一代管线，尤其是PD-1/VEGF/CTLA-4三特异性抗体CS2009。只是挑战同样不算小，眼下三抗领域堪称热门赛道，可市场争夺也日益加剧。比如2026年3月，华东医药公告控股子公司浙江道尔生物申报的注射用DR30206获批进入临床试验，联合标准化疗用于局部晚期或转移性非小细胞肺癌患者。而且，创新药开发长周期、高投入、不确定性强，具有一定失败风险。聚焦基石药业，据环球网、投资者网，公司就曾发生过PD-1抑制剂在晚期肝细胞癌等疾病治疗上临床失败的案例。财报显示,2016年至2019上半年公司累亏超36亿元。虽然过去不代表现在，然警钟犹在耳畔，提示公司要高效高质，毕竟竞品不等人、资本有耐心限度。2025年，基石药业现金及现金等价物增加额-6.038亿元，期末现金及现金等价物仅3.879亿元，现金流有吃紧迹象。说千道万，创新药研发是一场马拉松，持续考验企业创新力、造血能力，如何平衡好研发投入与现金流安全是一严肃课题。3临床硬实力+商业化先手渐入卡位收获季当然，作为三抗管线先行者，基石药业同样不不缺乏价值看点、实力亮点。就在年报公布期间，公司同步披露了PD-1/VEGF/CTLA-4三特异性抗体CS2009最新开发进展及I/II期关键临床数据。首席执行官、研发总裁及执行董事杨建新表示，预计今年ASCO和（或）ESMO大会上公布更多I期和II期数据，目前正与多家全球跨国公司（MNC）深入洽谈合作，并计划2026年底前启动多项III期MRCT（国际多中心临床试验）研究。这意味着在，在三抗前沿领域，基石药业有望持续夯实先发优势，继而“引爆市场”。一些直观数据或有更深体会。2025年10月，基石药业首次披露CS2009的I期临床研究数据：在72例晚期实体瘤患者中，未发生剂量限制性毒性，最大耐受剂量未达到，3级以上治疗相关不良事件发生率仅13.9%，远低于同类双抗产品。疗效方面，在暂定的II期推荐剂量及更高剂量下，客观缓解率达25.0%；在驱动基因阴性的非小细胞肺癌亚组中，客观缓解率同样达25%。靓丽质效表现，首先得益于CS2009颇具巧思的分子设计：一方面通过PD-1阻断、CTLA-4阻断、VEGF阻断三重信号阻断，完整覆盖免疫激活与血管调控通路，实现机制协同增效；一方面依托结构创新实现靶向增效与毒性控制平衡。直指当前免疫治疗PD-(L)1单药有效率偏低，传统联合方案又伴随不可忽视的毒性的核心痛点，目标是打造更高效、更安全的下一代基础免疫方案。就在上月，新发布的数据进一步夯实CS2009三大核心优势：一是安全性表现突出。≥3级治疗相关不良事件发生率为23%，与已上市PD-(L)1/VEGF双抗相当甚至更优。即便多纳入一个CTLA-4靶点，并未带来毒性叠加升级，也未出现CTLA-4与PD-(L)1联合方案中常见的严重免疫相关毒性，且≥3级VEGF相关不良反应发生率维持在较低水平。二是单药一线NSCLC ORR 90%为全球顶级水平。在10例一线PD-L1 TPS≥50%的非小细胞肺癌患者中，ORR达90%、DCR达100%，显著优于PD-1单药及PD-(L)1/VEGF双抗的历史数据。虽然受限于早期样本量较小，后续仍需更大队列验证，但单药突破性的疗效数据以及突出的安全性，为后续联合疗法继续精进埋下伏笔。三是具备下一代免疫治疗的核心特质。在免疫经治、驱动基因阴性的后线NSCLC患者这类难治人群中，CS2009抗肿瘤活性同样远超其它双抗；在对PD-(L)1单抗天然不敏感的后线冷肿瘤中同样起效，非透明肾细胞癌患者ORR达40%，软组织肉瘤患者ORR 33.3%，广谱抗肿瘤潜力初步显现。一句话：作为有望定义下一代免疫治疗范式的潜力分子，CS2009临床价值与商业化前景均可期待。基石药业也公告称，在后续首批III期国际多中心临床中，重点布局NSCLC、结直肠癌、小细胞肺癌等大癌种，均存在明确未满足的临床需求。而这只是一个奋进缩影。基石药业还在推进CS5001（ROR1 ADC）、CS5005（SSTR2 ADC）、CS5006（ITGB4 ADC）等多款创新药的研发，研发管线储备了16款候选药物。如能推进顺利，2026年有望成为公司转型全面落地、开始兑现成果的一年。4双轮驱动、2.0管线爆发野望事实上，经过多年深耕，“基石质效”、“基石速度”不止体现在管线创新，商业化落地能力也初具雏形。与弊端类似，BD交易优势同样明显：即通过技术转让能帮助出让方最大程度规避商业风险，这也是大量创新药企热衷该交易的重要出发点。基石药业也不例外，且做出更优的战略取舍，即放弃重资产自建商业化闭环的“重模式”，转而回归研发核心，以“授权合作+里程碑付款+销售分成”的轻资运营，实现管线价值的快速变现。随着本土与海外两板块明确增量，上述模式2026年将进入集中兑现窗口。一是在合作伙伴推动下，本土市场普拉替尼、阿伐替尼等核心产品依托医保准入与渠道下沉，持续放量已是明确事实。二是舒格利单抗全球商业化开始进入真正收获期，继获批用于IV期NSCLC后，舒格利单抗又于2025年11月、2026年2月先后获得欧盟、英国批准。国内国外双轮驱动下，基石药业成长预期清晰可见，甚至盈利拐点可能早日到来。这也是公司股价持续走高，资本市场对其投下信任票的最大底气。再看管线创新能力，不应将CS2009视作单一产品，其重要意义在于验证了基石药业战略正确性，即用实打实的临床推进效率印证了“轻资产商业化+聚焦核心研发”模式的内在潜力。这源于几年前做出的前瞻性抉择：锚定研发与创新为核心根基，以具备泛肿瘤潜力的重磅大单品构筑管线2.0核心矩阵，通过合作变现为外部增长杠杆，层层夯实发展底盘。这才有了如今的CS2009、ROR1 ADC CS5001等创新管线，才有了瞩目的“基石质效”、“基石速度”。更令人振奋的是，2026年基石药业2.0管线有望迎来爆发，承上启下的战略布局逐步成型。公司不仅在多抗领域做到引领，还是新一代ADC赛道领跑者，旗下核心产品CS5001（ROR1 ADC）临床数据超预期，一线联合R-CHOP在一线 DLBCL患者中展现出广泛且深度的抗肿瘤活性，ORR 100%、CR 95.5%。其中，在前沿双靶点ADC、双载荷ADC领域，基石药业饱有先发优势。以EGFR/HER3双抗ADC药物CS5007为例，清晰展现出优质临床潜质，核心逻辑源于分子设计、疗效与安全性的三重差异化优势，且临床前数据已充分支撑这一定位。至此，高效、稳定与可持续性的研发体系与梯度化价值兑现矩阵，共同构筑了公司成长护城河，未来估值空间有望彻底打开。不过，授权费依赖、盈利根基不扎实、外部竞争日烈，仍是稳优前行的绊脚石。面对喜点槽点交织，如何让预期顺利落地，让研投尽快转化为更多商业价值，基石药业还有诸多硬仗要打。都说利空出尽便是利好，经历了上市以来最大亏损，基石药业利空出尽了么？伴随战略收获季渐行渐近，业绩翻身仗还有多远？本文为首财原创如需转载请留言内容微信：suishenlicai商务微信：deerss__本账号系新浪财经／一点资讯／凤凰新闻／网易财经／搜狐财经／腾讯财经／今日头条／蓝鲸财经／百度百家／新浪微博／天天快报／中金在线／东方财富／雪球等22家媒体入驻账号

100 项与艾伏尼布相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11090	艾伏尼布	L01XX62	DB14568

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
骨髓增生异常综合征	美国	Servier Pharmaceuticals LLC	2023-10-24
IDH1突变的胆管癌	澳大利亚	Servier Laboratories (Australia) Pty Ltd.	2023-04-06
IDH1突变急性髓性白血病	中国	Servier Pharmaceuticals LLC	2022-01-30
IDH1突变急性髓性白血病	中国	基石药业（苏州）有限公司	2022-01-30
胆管癌	美国	Servier Pharmaceuticals LLC	2021-08-25
急性髓性白血病	美国	Servier Pharmaceuticals LLC	2018-07-20

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
软骨肉瘤	临床3期	美国	Servier Bio-Innovation LLC	2024-07-09
软骨肉瘤	临床3期	美国	Institut de Recherches Intern Servier	2024-07-09
软骨肉瘤	临床3期	中国	Servier Bio-Innovation LLC	2024-07-09
软骨肉瘤	临床3期	中国	Institut de Recherches Intern Servier	2024-07-09
软骨肉瘤	临床3期	日本	Institut de Recherches Intern Servier	2024-07-09
软骨肉瘤	临床3期	日本	Servier Bio-Innovation LLC	2024-07-09
软骨肉瘤	临床3期	澳大利亚	Servier Bio-Innovation LLC	2024-07-09
软骨肉瘤	临床3期	澳大利亚	Institut de Recherches Intern Servier	2024-07-09
软骨肉瘤	临床3期	比利时	Institut de Recherches Intern Servier	2024-07-09
软骨肉瘤	临床3期	比利时	Servier Bio-Innovation LLC	2024-07-09

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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


NCT04195555 (CTgov)	临床2期	难治性软组织肉瘤 \| 室管膜瘤 \| 复发性实体肿瘤 ... 更多	3	Ivosidenib	範壓獵選餘齋糧範衊膚 = 願選範衊蓋廠醖鹽遞淵鬱窪簾鑰簾鬱選簾夢鬱 (鬱鹽獵遞願鏇製願選壓, 餘構構艱鏇淵顧網選構 ~ 繭廠壓廠顧網餘繭繭蓋) 更多	-	2026-03-25
NCT05921760 (CTgov)	临床1/2期	IDH1突变的胆管癌 \| 转移性胆管癌	7	ipilimumab+Nivolumab+Ivosidenib (Safety Lead-In Phase - Ivosidenib 500mg)	築鹹壓簾夢齋鹽鹽蓋獵 = 糧鹹廠膚製襯廠憲構獵餘淵蓋憲願壓醖構淵衊 (醖鏇餘製餘顧醖範願糧, 鹹構願夢遞繭齋衊鑰遞 ~ 廠餘壓壓遞築襯膚鑰襯) 更多	-	2026-02-12
NCT05921760 (CTgov)	临床1/2期	IDH1突变的胆管癌 \| 转移性胆管癌	7	Ipilimumab+Nivolumab+Ivosidenib (Safety Lead-In Phase - Ivosidenib 250mg)	築鹹壓簾夢齋鹽鹽蓋獵 = 衊衊顧膚艱齋艱餘糧鹽餘淵蓋憲願壓醖構淵衊 (醖鏇餘製餘顧醖範願糧, 範鑰鏇鹽醖鹹膚選鑰積 ~ 獵襯鏇積夢鹹淵構鬱餘) 更多	-	2026-02-12
NCT06501625 (ASCO_GI2026)	临床1/2期	IDH1突变的胆管癌一线 IDH1 Mutation	7	Ivosidenib 500 mg + Durvalumab + Gemcitabine/Cisplatin	觸築餘憲製夢鹹壓鬱獵(鹽夢顧範淵積製廠鹽製) = 觸醖壓襯鹹獵醖衊淵選獵築積襯蓋艱窪遞艱築 (遞襯艱簾鹽艱顧獵簾鹽 ) 更多	积极	2026-01-08
NCT06081829 (ClarIDHy, CTgov)	临床2期	转移性胆管癌	12	Ivosidenib	積鹹鹽繭積繭窪選選壓 = 餘衊積選蓋網鏇鏇簾築積鏇鹽簾遞醖襯顧蓋願 (簾廠鹽構遞製壓顧糧網, 齋鏇積鬱觸獵衊製鹽製 ~ 醖築鏇鹽築蓋顧糧顧齋) 更多	-	2025-12-09
NCT05907057 (ALIDHE, ASH2025)	临床3期	IDH1突变急性髓性白血病 mutant isocitrate dehydrogenase 1 (mIDH1)	92	Ivosidenib+Azacitidine	壓鏇願觸積鏇夢繭淵艱(膚鬱構憲築憲壓窪鹽遞) = 醖顧範製願鹹淵積壓遞糧網衊膚膚鹹餘齋顧遞 (獵廠憲膚餘齋艱繭蓋衊 ) 更多	积极	2025-12-06
NCT03173248 (AGILE, ASH2025)	临床3期	IDH1突变急性髓性白血病 mutant isocitrate dehydrogenase 1 (mIDH1)	146	Ivosidenib+AZA	淵繭觸齋鹽憲遞鏇餘網(鹹鹹壓顧願夢積顧範糧) = 襯糧窪蓋廠衊蓋蓋築膚遞鹹糧艱蓋齋夢窪淵獵 (築鏇壓蓋鹹鏇艱網選顧 ) 更多	积极	2025-12-06
NCT03173248 (AGILE, ASH2025)	临床3期	IDH1突变急性髓性白血病 mutant isocitrate dehydrogenase 1 (mIDH1)	146	Placebo+AZA	淵繭觸齋鹽憲遞鏇餘網(鹹鹹壓顧願夢積顧範糧) = 醖衊網艱遞構淵簾襯艱遞鹹糧艱蓋齋夢窪淵獵 (築鏇壓蓋鹹鏇艱網選顧 ) 更多	积极	2025-12-06
NCT02632708 (ASH2025)	临床1期	IDH1突变急性髓性白血病一线 isocitrate dehydrogenase (IDH)1 mutation	60	Ivosidenib + intensive chemotherapy	艱獵膚鏇觸網願構鹽遞(顧膚網膚餘顧範選淵築) = 糧鹹壓壓簾觸齋網鹹築廠構網憲壓膚齋積膚顧 (簾鹹壓遞醖網製顧齋鏇 ) 更多	积极	2025-12-06
ASH2025	临床2期	意义不明的克隆性血细胞减少症 IDH1 mutation	20	Ivosidenib	鹽鹹鏇憲獵醖鏇遞窪鑰(廠選繭壓網夢鏇遞構糧) = 願獵鹹繭壓願鏇簾繭餘鹽淵淵蓋網窪構遞餘膚 (顧觸觸鏇鏇簾範醖壓襯 ) 更多	积极	2025-12-06
NCT05030441 (ASH2025)	临床2期	IDH1突变急性髓性白血病 IDH1/2-mutant	20	Ivosidenib (CCUS)	構醖製製淵壓鏇憲願簾(齋膚製衊構齋顧選鏇鹹) = 築鑰廠繭夢衊範顧築窪糧壓廠鑰鬱壓膚夢衊鹽 (鑰鹽淵淵製餘艱醖願醖 ) 更多	积极	2025-12-06
ASH2025	N/A	急性髓性白血病	387	Ivosidenib monotherapy (FL IDH1-mut AML)	簾夢窪壓製遞鹽製構簾(繭衊襯艱鏇範鏇餘積築) = 醖範簾憲鹹繭築衊醖簾壓襯構鏇淵鹽鹹膚鑰鑰 (範鬱獵艱淵簾積簾積鑰, 46.0 ~ 84.6) 更多	积极	2025-12-06
ASH2025	N/A	急性髓性白血病	387	Ivosidenib+azacitidine (FL IDH1-mut AML)	簾夢窪壓製遞鹽製構簾(繭衊襯艱鏇範鏇餘積築) = 觸鹹窪範觸醖壓衊鏇襯壓襯構鏇淵鹽鹹膚鑰鑰 (範鬱獵艱淵簾積簾積鑰, 21.1 ~ 53.1) 更多	积极	2025-12-06