The goal of this clinical trial is to determine how well people tolerate treatment with alisertib at different doses when it is used together with paclitaxel to treat people with SCLC. The main question it aims to answer is:
* What percentage of side effects, both mild and serious, do participants experience when being treated with alisertib and paclitaxel based on the National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0 (NCI CTCAE v.5.0)?
The study will consist of different groups, called cohorts, in which alisertib will be studied at increasing doses. Participants in the first group, Cohort 1, will take 30 mg of alisertib by mouth 2 times a day. The dose will increase by 10 mg 2 times a day for each new cohort of participants joining the study. Side effects will be checked during the study, and the decision to increase the dose of alisertib will be based on the specific side effects experienced during the first 21 days of treatment for each cohort.
Participants will:
* take alisertib by mouth on their own 2 times a day from Day 1 through Day 7 of each 21-day cycle and will be given paclitaxel intravenously at a dose of 60 mg/m2 on Day 1 and Day 8 of each 21-day cycle.
* be given a preventive treatment to increase their body defenses, called granulocyte-colony stimulating factor (G-CSF). Study staff will give G-CSF after the last dose of alisertib or paclitaxel of each 21-day cycle in which alisertib was given.
* provide blood samples to evaluate the different levels of alisertib in the blood at different times. Blood samples will be collected on Days 1 and 7 of the first and second 21-day cycles of treatment.
* be treated with alisertib and paclitaxel until death, worsening of the disease, unacceptable toxicity, unwillingness to continue participating in the trial, or other criteria that requires participants to stop treatment and participation in the study.
* be contacted every 8 weeks after stopping alisertib and paclitaxel treatment as part of a specific study phase called the long-term follow-up period. This will last until death, unwillingness to continue participating in the trial, or until the end of the study.

开始日期2026-09-30

申办/合作机构

Puma Biotechnology, Inc.

NCT06369285

/ Recruiting临床2期

A Phase 2 Study of Alisertib in Combination With Endocrine Therapy in Patients With HR+, HER2-negative Recurrent or Metastatic Breast Cancer

PUMA-ALI-1201 is a randomized, dose optimization, multicenter, Phase 2 study of alisertib administered in combination with endocrine therapy in participants with pathology-confirmed HR-positive/HER2-negative metastatic breast cancer (MBC) following progression on or after at least two prior lines of endocrine therapy in the recurrent or metastatic setting. This study is intended to evaluate the optimal alisertib dose administered in combination with the selected endocrine therapy. The study is also planned to evaluate the efficacy, safety, and pharmacokinetics of alisertib in combination with endocrine and to identify the biomarker-defined subgroup(s) that may benefit most from combined alisertib and endocrine therapy.

开始日期2024-11-19

申办/合作机构

Puma Biotechnology, Inc.

NCT06095505

/ Recruiting临床2期

A Phase 2 Study of Alisertib in Patients With Extensive Stage Small Cell Lung Cancer

PUMA-ALI-4201 is a Phase 2 study evaluating alisertib monotherapy in patients with pathologically-confirmed small cell lung cancer (SCLC) following progression on or after treatment with one platinum-based chemotherapy and anti-PD-L1/PD-1 immunotherapy agent. Up to one additional systemic anti-cancer therapy for SCLC is allowed, for a total of up to two prior treatment regimens. This study is intended to identify the biomarker-defined subgroup(s) that may benefit most from alisertib treatment and to evaluate the efficacy, safety, and pharmacokinetics of alisertib.

开始日期2024-02-08

申办/合作机构

Puma Biotechnology, Inc.

100 项与 Alisertib 相关的临床结果

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100 项与 Alisertib 相关的转化医学

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100 项与 Alisertib 相关的专利（医药）

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603

项与 Alisertib 相关的文献（医药）

2026-07-01·PHYTOMEDICINE

Tongguanteng injection induces cell cycle arrest and drives ferroptosis through AURKA/KEAP1/NRF2 axis in breast cancer

Article

作者: Liang, Hanlu ; Guo, Cheng ; Chen, Junjun ; Shi, Meizhi ; Ding, Qixuan ; Hu, Yujie ; Zhou, Yangyun ; Zhang, Xiangqi ; Han, Yonglong ; Zhao, Shuai ; Chen, Jiayi ; Zhang, Jingxian ; Xu, Lingyan ; Yang, Jiao

BACKGROUND:

Tongguanteng Injection (TGT), derived from the stems of Marsdenia tenacissima, has been demonstrated to exert anti-tumor effects. Aurora Kinase A (AURKA) is a key regulator of cell cycle progression and has become a promising target for breast cancer treatment. However, the role of AURKA in ferroptosis is unclear, particularly regarding its contribution to the therapeutic effect of TGT in breast cancer.

METHODS:

The chemical components of TGT were analyzed by Ultra-high performance liquid chromatography coupled with hybrid quadrupole-orbitrap high resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS). The anti-breast cancer effect of TGT were detected in vitro and in vivo. RNA-seq analysis were used to identify the targets of TGT treatment. Subsequently, flow cytometry, RT-PCR, western blot, Co-IP, immunofluorescence and immunohistochemistry were employed to elucidate the regulatory mechanisms of TGT on ferroptosis and cell cycle. Concurrently, ferroptosis and cell cycle associated pathways were investigated in the plasmids and siRNAs transfected cells. Furthermore, tumor bearing mouse model was established by 4T1 cells stably transduced with lentivirus for further validating the findings.

RESULTS:

A total of 136 compounds were identified from TGT. The study demonstrates that TGT exerts an anti-breast cancer effect by inducing G2/M phase arrest and ferroptosis, evidenced by downregulation of CDK1 and Cyclin B, as well as increased Fe²⁺ accumulation, glutathione (GSH) depletion, and elevated lipid peroxidation. RNA-seq analysis revealed that AURKA was significantly downregulated and identified as a key target of TGT treatment. Mechanistically, TGT disrupts the AURKA-Kelch-like ECH-associated protein 1 (KEAP1) interaction, leading to nuclear factor E2-related factor 2 (NRF2) nuclear translocation and subsequent heme oxygenase 1 (HO-1)-mediated ferroptosis in vitro. Knockdown of AURKA or treatment with its inhibitor alisertib both induce G2/M phase arrest and ferroptosis, while AURKA overexpression reverses the effects of TGT and accelerates tumor progression. Combining TGT with docetaxel enhances ferroptosis sensitivity and amplifies the regulatory effect of AURKA on cell cycle and ferroptosis. Consistent with in vitro results, TGT significantly inhibited tumor growth, arrested cell cycle and promoted ferroptosis in 4T1-AURKA^LV cell bearing mice.

CONCLUSION:

These findings propose that TGT targets AURKA/KEAP1/NRF2 axis to exert anti-breast cancer effect, and AURKA inhibition represents a potential strategy for breast cancer treatment through inducing cell cycle arrest and driving ferroptosis.

2026-06-23·ACS Nano

NIR-II Imaging-Guided Phototherapy-Induced Senescence Reprograms Immunosuppressive Tumor Microenvironment for Potent Cancer Immunotherapy

Article

作者: Meng, Zixiang ; Deng, Shiquan ; Lu, Xiuxin ; Yang, Zifan ; Zhang, Tianfu ; Ning, Shipeng ; Shangguan, Ping ; Ou, Xinwen ; Suo, Meng ; Tang, Ben Zhong ; Tang, Zhuomin ; Nong, Zhongwen ; Zhang, Xinglong

Cellular senescence, characterized by irreversible cell-cycle arrest, is increasingly recognized as a pivotal mechanism in tumor suppression through regulating the tumor microenvironment (TME). Nevertheless, strategies that exploit senescence inducers to promote senescence-associated secretory phenotypes (SASPs) expression and thereby enhance immune infiltration remain underexplored. In this work, we present a phototherapy-based senescence induction approach to overcome the immunosuppressive TME in triple-negative breast cancer. We developed a reactive oxygen species-responsive nanoplatform that co-delivers a second near-infrared emissive phototheranostic molecule with aggregation-induced emission characteristics and the Aurora kinase inhibitor alisertib. Upon exposure to an 808 nm laser, the appropriate phototherapy induces alisertib release and oxidative stress, resulting in irreversible growth arrest and senescence. This process augments the secretion of immunostimulatory SASPs while suppressing tumor-promoting factors. The nanodrug remodels the TME by activating cytotoxic T lymphocytes and depleting both myeloid-derived suppressor cells and regulatory T cells, producing efficient tumor regression. Importantly, it establishes durable immunological memory, preventing postoperative recurrence without systemic toxicity. By integrating phototherapy-enhanced drug delivery with SASP-driven immunosurveillance, our study introduces senescence induction as a promising paradigm for next-generation photoimmunotherapy.

2026-06-01·JOURNAL OF DAIRY SCIENCE

Dynamics of mammary cell division during pregnancy and lactation in dairy cows

Article

作者: Corl, Benjamin A ; Trott, Josephine F ; Quinn, Mackenzie J ; Hovey, Russell C ; Perez-Hernandez, Gabriela ; Myer, Rachel G ; Webster, Haylee H ; Machiela, Maia N

Binucleated mammary epithelial cells (MEC) contribute to milk production in mice, yet their prevalence and function in species including dairy cattle remain unclear. The objective of this study was to determine the incidence and contribution of binucleated MEC in the bovine mammary gland during lactation. In a first study, we induced lactation in nulliparous Holstein heifers while concurrently labeling dividing MEC with intramammary nucleotide analogs (EdU and BrdU) and/or co-delivering the aurora kinase inhibitor, alisertib, to block binucleation. In a second study, we determined the abundance of binucleated MEC in the udder of multiparous Holstein cows that had increased milk production in response to unilateral frequent milking of one udder half. Contrary to data for mice, binucleated MEC comprise only 1-3% of the total MEC population in the bovine udder. Interestingly, the rear quarters of the udder contained a higher proportion of binucleated MEC (1.1%) versus front quarters (0.7%). Intramammary alisertib during mammogenesis tended to reduce milk yield and was associated with increased abundance of somatic cells and MEC in milk at the start of lactation. Cellular proliferation during hormone-induced lactation was consistently low during both the growth phase and lactation, where EdU or BrdU labeled-MEC were retained in the lactating udder up to 39 d post-labeling. In response to increased milking frequency, the incidence of binucleated MEC tended to increase from 2% to 3.2% of the epithelium, while the incidence of Ki-67-positive MEC decreased from 1% to 0.5%. Taken together, these data indicate that binucleated MEC constitute a small but potentially significant population in the bovine mammary gland.

105

项与 Alisertib 相关的新闻（医药）

2026-07-14

·衡道病理

【衡道丨干货】2026 CSCO小细胞肺癌诊断指南共识

《2026 CSCO小细胞肺癌诊疗指南》已正式颁布，旨在为临床诊疗提供更多依据。文末另附《2025 中国肿瘤整合诊治指南（CACA) ——肺癌》作为参考。一、小细胞肺癌的MDT诊疗模式小细胞肺癌的MDT诊疗模式 1.小细胞肺癌（small cell lung cancer，SCLC）异质性、侵袭性强，诊治过程中更应重视多学科团队（multidisciplinary team，MDT）的作用，推荐有条件的单位尽可能进行SCLC的MDT，对患者进行全程管理。 2.MDT的实施过程中需由多个学科的专家共同分析患者的病史、临床表现、影像学、病理学和分子生物学资料，并对患者的一般状况、疾病的诊断、分期、发展趋势和预后做出全面的评估，并根据当前国内外的治疗指南/规范和高级别的循证医学证据，结合目前可及的治疗手段和患者的治疗意愿，制订个体化的整体治疗策略。 3.MDT团队可根据治疗过程中患者体能状态的变化和治疗效果适时调整治疗方案，目的是最大化地延长患者的生存期、提高治愈率和改善生活质量。二、影像和分期诊断影像和分期诊断 1.筛查肺癌是中国和全球范围内发病率和病死率较高的恶性肿瘤，其中SCLC占肺癌的13%~17%。由于SCLC恶性程度高，早期极易发生远处转移，确诊时多为晚期，预后极差。而早期发现是延长SCLC患者生存期的有效方法，但目前尚无专门针对SCLC筛查的临床试验，多为肺癌高危人群的筛查研究。美国国家肺癌筛查试验（national lung screening trial，NLST）纳入了53454例重度吸烟患者进行随机对照研究，评估采用低剂量螺旋CT筛查肺癌的获益和风险，结果提示与胸片相比，低剂量螺旋CT筛查的高危人群，肺癌相关病死率降低了20%（95%CI 6.8%~26.7%，P=0.004），其中SCLC占8%；其他较大的肺癌筛查试验诊断的肺癌患者中，SCLC占4%~9%。 2.诊断与分期胸部增强CT、腹部、盆腔增强CT、头部增强MRI或增强CT及全身骨显像是SCLC分期和诊断的主要方法。对于下列情况，有条件者推荐使用PET/CT：①肺癌治疗前分期，PET对于淋巴结转移和胸腔外转移（脑转移除外）有更好的诊断效能；②辅助鉴别常规CT无法判断的肿瘤术后瘢痕与肿瘤复发，如PET/CT摄取增高，需活检证实；③辅助鉴别常规CT无法判断的肿瘤放疗后纤维化与肿瘤残存/复发，如PET/CT摄取，需活检证实。FDG-PET/CT对分期诊断有较好的效能，近期研究显示PET/CT可以改善SCLC患者的分期和治疗计划；另外有临床试验和随机对照研究发现，肺癌患者通过FDG-PET/CT扫描可以降低17%~20%的开胸率。但由于PET/CT价格昂贵，故仅作为Ⅱ级推荐；SCLC诊断时脑转移的发生率为10%~18%，其中，近30%的患者无脑转移相关症状，PET/CT在发现脑转移方面不如MRI或者CT。Seute等对比了不同时期481例SCLC患者脑转移发生的流行病学数据，发现在CT时期SCLC脑转移的发生率为10%，而核磁时期发生率高达24%，其中11%的患者为无症状脑转移，并且多发脑转移的检出率也明显增高。当纵隔淋巴结或浆膜腔积液影响治疗决策，而现有手段又难以确认时，推荐EBUS、浆膜腔积液穿刺等有创手段明确纵隔淋巴结或浆膜腔积液性质；痰细胞学由于容易产生诊断错误，在组织学检查可行的情况下，应减少痰细胞学的应用。 3.分期方法 SCLC的分期一直沿袭美国退伍军人肺癌协会（VALG）的二期分期法，主要基于放疗在SCLC治疗中的重要地位。AJCC TNM分期系统可以选出适合外科手术的T1~2N0M0的局限期患者，能更准确地了解患者所处的疾病阶段、判断患者的预后及制订合适的治疗方案。建议临床使用VALG分期法和TNM分期系统两者相结合的方法对SCLC进行分期，因其更能准确地指导治疗和评估预后。（1）VALG二期分期法局限期：病变限于一侧胸腔，且能被纳入一个放射治疗野内。广泛期：病变超过一侧胸腔，且包括恶性胸腔和心包积液或血行转移。（2）NCCN治疗小组建议SCLC分期采取AJCC TNM分期方法与VALG二期分期法相结合局限期：AJCC（第8版）Ⅰ～Ⅲ期（任何T，任何N，M0），可以安全使用根治性的放疗剂量。排除T3-4由于肺部多发结节或者肿瘤/结节体积过大而不能被包含在一个可耐受的放疗计划中。广泛期：AJCC（第8版）Ⅳ期（任何T，任何N，M1a/b/c），或者T3-4由于肺部多发结节或者肿瘤/结节体积过大而不能被包含在一个可耐受的放疗计划中。三、病理学诊断病理学诊断上述证据类别全部为2A类。不同类型肺神经内分泌肿瘤特点相当于胃肠道的NET G3，形态学同不典型类癌，但伴有较高的核分裂象（>10个/2mm2）或Ki67增殖指数（>30%）小细胞肺癌病理诊断报告原则（一）细胞学标本诊断原则 1.细胞学的标本来源主要包括气管镜刷检、浆膜腔积液、细针穿刺、痰及支气管灌洗等。 2.根据肿瘤细胞的大小及形态，小细胞癌细胞学镜下可分为燕麦细胞型和中间细胞型。（1）燕麦细胞型通常体积较小，可呈圆形、卵圆形、短梭形及长形，胞质少或无，大小为静止期淋巴细胞的1.5~3倍，在同一张涂片中肿瘤细胞大小较一致，也可见紧密巢状聚集，两种形态可同时出现于一张涂片中；核染色质呈均匀细颗粒状，可见染色质集结点，也可由于细胞退化而导致染色质呈固缩状，通常较少见到明显核仁；相邻肿瘤细胞贴边镶嵌状排列，制片过程中易出现核拉丝现象，但这种现象一般不在液基制片中出现。（2）中间细胞型的肿瘤细胞排列及核特征与燕麦细胞型相似，肿瘤细胞可呈圆形、卵圆形、短梭形或多角形等；核染色质也可呈粗颗粒状，胞质可相对较丰富，同一张涂片中肿瘤细胞胞质可多可少甚至裸核，形态不规则，核分裂较多。 3.对于浆膜腔积液和细针吸取标本，细胞学蜡块切片中肿瘤细胞的镜下形态与组织学相似，可见由小的圆形、卵圆形或梭形的裸核样细胞聚集成巢或弥散分布，也可出现“人工挤压”现象。免疫细胞化学抗体选择与组织学基本相同，常用的抗体包括TTF1、CD56、Syn、CgA、Ki-67、CK等。（二）组织标本诊断原则 1.肺肿瘤分类将神经内分泌肿瘤分为小细胞癌、大细胞神经内分泌癌、典型类癌、不典型类癌。小细胞癌与大细胞神经内分泌癌属于高级别肿瘤，典型类癌与不典型类癌属于低-中级别肿瘤。因此鉴别小细胞癌与其他神经内分泌肿瘤，特别是典型和不典型类癌在流行病学、遗传学、治疗及预后等方面具有重要意义。2022年WHO神经内分泌肿瘤分类提出了一个新的亚型：类癌伴有高核分裂象或高Ki-67增殖指数，此型分化较好，形态学与不典型类癌相同，但生长快，生物学行为与高级别神经内分泌癌重叠。 2.神经内分泌肿瘤标志物包括CD56、Syn、CgA，在具有神经内分泌肿瘤形态学特征的基础上至少有一种神经内分泌免疫组化标志物明确阳性，且神经内分泌标记阳性的细胞数应大于10%肿瘤细胞数才可诊断神经内分泌肿瘤。当不具有神经内分泌肿瘤的组织学形态时，不推荐进行神经内分泌标志物染色。明确的鳞状细胞癌或腺癌伴神经内分泌分化并不影响治疗决策或预后。TTF-1在85%~90%的小细胞肺癌中呈阳性表达（但此时TTF-1阳性表达不能区分肺小细胞癌或肺外小细胞癌，因为20%~80%肺外部位，如胃肠道、膀胱、子宫颈、前列腺等处发生的小细胞癌亦可表达TTF-1）。当少数小细胞肺癌病例中不表达神经内分泌标志物时，结合形态、TTF-1弥漫阳性、CK核旁点状阳性颗粒特点及高Ki-67指数（一般为50%~100%）也有助于小细胞癌的诊断。此外，有报道INSM1是一个较“CD56+Syn+CgA组合”效用性更强的神经内分泌分化标记，尤其在小细胞肺癌中。应尽量减少诊断辅助检查项目，以节约标本用于后续治疗指导性检查。 3.依据2021版WHO分类标准，肺神经内分泌肿瘤基于形态学，根据核分裂象和是否存在坏死进行分类，Ki-67阳性指数目前还无法用来鉴别典型类癌及不典型类癌，但在小活检标本中建议增加Ki-67检测，有助于肿瘤科医生进行治疗决策，同时有助于区分不典型类癌和高级别神经内分泌癌，并可避免将伴有机械性损伤的类癌、不典型类癌诊断为小细胞肺癌。 4.进行核分裂象计数时，应选取核分裂象最多的区域进行计数（个/2mm2），应是明确的核分裂象。如果数值位于阈值附近，应选取3个2mm2区域进行计数，最后报告平均值。 5.复合型小细胞肺癌为小细胞肺癌同时伴有其他任何非小细胞肺癌成分，如腺癌、鳞状细胞癌、大细胞神经内分泌癌等。除大细胞癌和大细胞神经内分泌癌需满足至少10%的比例外，其他非小细胞肺癌类型可以是任何比例。 6.如果同时有细胞学标本及活检标本时，应将两者结合进行考量，综合做出更恰当的诊断。 7.手术标本怀疑肿瘤累及胸膜时，应进行弹力纤维特殊染色辅助诊断。 8.同一患者治疗后不同时间小标本活检病理诊断应尽量避免使用组织类型之间转化的诊断。此种情况不能除外小活检标本取材受限，未能全面反映原肿瘤组织学类型，有可能原肿瘤是复合型小细胞肺癌，化疗后可致其中非小细胞癌成分残留。 9.近年研究表明，小细胞肺癌具有明显的分子水平异质性。如TP53和RB1双等位基因失活、Notch信号通路改变及体细胞基因拷贝数变异等。另外基于谱系转录因子（lineage-definingtranscription factors）定义的分子分型概念，按照ASCL1、NEUROD1、YAP1和POU2F3的相对高表达将小细胞肺癌分为4个分子亚型（SCLC-A、-N、-P、-Y）。SCLC-A和SCLC-N为神经内分泌表型，伴有神经内分泌分化驱动基因INSM1及TTF-1等高表达；SCLC-P和SCLC-Y亚型为非神经内分泌表型，伴有上皮间质转化、Notch、HIPPO信号通路等激活。体外实验研究及部分小样本临床试验观察到不同分子亚型的治疗敏感性不同。在免疫治疗方面，各亚型的不同免疫环境状态提示其对免疫治疗有不同敏感性。SCLC-P、SCLC-Y亚型的肿瘤间质浸润淋巴细胞较多，坏死也较明显，谓之“免疫绿洲”；而SCLC-A、SCLC-N亚型肿瘤间质浸润淋巴细胞较少，谓之“免疫沙漠”。这种免疫微环境异质性特征为解释化疗联合免疫治疗方案的敏感性/耐药性机制及药物研发提供了新的思路。然而，某一SCLC患者的分子亚型并非一成不变，遗传学、起源细胞和肿瘤细胞的可塑性共同影响着SCLC分子亚型，例如，Notch通路的激活或可导致亚型转化。有学者探索了基于循环肿瘤细胞进行分子分型，为亚型转化的动态监测带来希望。随着对SCLC异质性的深入认识，未来可能会践行出以分子生物学为指导的临床新兴疗法。 10.近年来大细胞神经内分泌癌的分子基因组研究也有进展。根据基因组特征，LCNEC（大细胞神经内分泌癌）可分为SCLC-like（小细胞肺癌样）、NSCLC-like（非小细胞肺癌样）或类癌样。SCLC样LCNEC表现为RB1、TP53、CREBBP、EP300和MLL基因的突变。此外，具有STK11和KEAP1突变的I型LCNEC表现出ASCL1和DLL3的高表达，这两者是NOTCH的负调控因子。相比之下，具有RB1突变的Ⅱ型LCNEC会上调NOTCH信号通路。NSCLC样LCNEC则表现为PI3K-AKT-mTOR通路的突变以及其他可靶向基因的突变，如EGFR、ERBB2和FGFR1。最后，类癌样LCNEC与MEN1基因突变相关。四、分子标志物分子标志物注：proGRP.胃泌素释放肽前体（pro-gastrin-releasing peptide，proGRP）；NSE.神经元特异性烯醇化酶（neuronspecific enolase，NSE）。 1.胃泌素释放肽前体（pro-gastrin-releasing peptide，proGRP）和神经元特异性烯醇化酶（neuronspecific enolase，NSE）是SCLC诊断以及治疗效果监测的重要肿瘤标志物。研究证实，胃泌素释放肽是SCLC组织的重要产物，其在血清里的前体可被稳定检测。SCLC可表现为神经内分泌细胞的特性，因此NSE往往会有过量表达。联合检测proGPR和NSE可以提高SCLC的诊断率，在局限期SCLC治疗有效的情况下，这两个值会随之下降。 2.肿瘤突变负荷（tumor mutation burden，TMB）可能预测免疫检查点抑制剂疗效，利用NGS多基因组合估测TMB是临床可行的方法。免疫治疗在SCLC中已取得一定疗效。Ⅰ/Ⅱ期CheckMate032研究证实，纳武利尤单抗+伊匹木单抗治疗高TMB患者有效率可达46.2%，1年PFS率为30.0%，显著优于低、中TMB亚组。在组织标本不足时，利用NGS检测循环血肿瘤细胞DNA（ctDNA）进行TMB估测是潜在可行的技术手段之一。 3.目前针对SCLC尚无批准的靶向药物或指导治疗的标志物。替莫唑胺（temozolomide）在复发性SCLC中有一定的疗效，脑转移、MGMT（O-6-甲基鸟嘌呤-DNA-甲基转移酶）基因甲基化阳性患者可能疗效更好。国家药品监督管理局（National Medical Products Administration，NMPA）已于2019年批准人类MGMT基因甲基化检测试剂盒（荧光PCR法）用于定性检测石蜡切片样本中MGMT的甲基化状态。 4.在SCLC中，DNA损伤修复相关基因（如BRCA1/2）突变并不常见，不能用来预测PARP抑制剂疗效。研究表明，PARP依赖的碱基剪切修复是替莫唑胺耐药重要机制之一，替莫唑胺联合PARP抑制剂veliparib与替莫唑胺联合安慰剂相比，虽然未能明显延长PFS和OS，但显著提高了SCLC患者ORR（39%vs.14%，P=0.016）。Schlafen-11（SLFN11）调控DNA损伤应答和复制应激，可在多种癌症中预测DNA损伤机制，化疗药物和PARP抑制剂敏感性。SLFN11蛋白表达与替莫唑胺联合veliparib治疗患者的PFS和OS显著相关，有望成为PARP抑制剂治疗SCLC疗效的预测标志物。 5.循环肿瘤细胞（circulating tumor cells，CTC）是指在循环血液中存在的具有肿瘤特征的细胞，作为一种代表原发肿瘤的“液态活检标本”，CTCs可实时、动态、无创性地对SCLC患者病情进行监测。研究证实SCLC细胞分裂周期短、增殖快，易进入血液循环继而发生远处转移，CTCs在SCLC人群中检出率为67%~86%，检测CTCs有助于正确判断疾病临床分期，以便选择合适的治疗方案、指导SCLC患者的个体化治疗、监测肿瘤复发与转移、判定治疗效果及预测预后生存，同时也是分析耐药分子机制及解决肿瘤异质性的一种手段。研究证实，与单纯化疗患者相比，接受免疫治疗联合化疗、基线血液中非整倍体CTC评分（ACS）水平较高（>1.115）的SCLC患者具有更长PFS（7.7个月vs.4.9个月，P=0.007）和OS（16.3个月vs.13.6个月，P=0.033）。 6.对于混有NSCLC成分的复合型SCLC，推荐不吸烟的广泛期患者进行分子检测，以协助明确诊断和评估潜在的靶向治疗方案。 7.低钠血症（血Na+<135mmol/L）是SCLC常见并发症之一。回顾性研究发现，伴有低钠血症的SCLC患者OS显著低于血钠正常的患者；纠正低钠血症可能增大SCLC患者生存获益。 8.自2019年起，多个研究团队利用多组学技术，基于患者标本、PDX、CDX模型及细胞系数据提出了多种小细胞肺癌的分子分型学说，一致性观点为不同分子分型对不同作用机制药物的敏感性不同，但目前均无可适用于临床指导药物治疗的分子分型标志物。以中国学者研究为例，利用进行转录组学、蛋白质组学以及磷酸化组学的研究发现，高神经内分泌评分的nmfl亚型对ATR、TOP1抑制剂和依托泊苷联合顺铂（EP）敏感。高受体酪氨酸激酶（receptor tyrosine kinase，RTK）信号活性、高EMT评分的nmf3亚型对安罗替尼敏感。MYC高表达且与AURKA扩增相关的nmf4亚型对极光激酶抑制剂（alisertib、barasertib和AMG-900）更敏感。不同亚型转换可能是导致SCLC获得性耐药的机制。同时，利用纵向液体活检（cfDNA）可监测SCLC肿瘤表型在疾病进展和治疗过程中存在动态变化，尤其是鉴定出SCLC-A向炎症型SCLC-I亚型转换，进而有望推动未来SCLC个性化、精准化治疗。 9、大部分具有神经内分泌表型SCLC属于“免疫冷肿瘤”，而少数“热肿瘤”则表现出干扰素-γ通路激活、抗原提呈能力增强等特征。“免疫热肿瘤”在一线纳武利尤单抗单药治疗中比“免疫冷肿瘤”具有生存获益趋势。ZFHX3突变与“热肿瘤”特征及更好的免疫治疗应答相关联，提示其或可作为预测免疫获益的潜在生物标志物。 10.EXTENTORCH探索性研究患者肿瘤活检组织全外显子组测序结果证实，特瑞普利单抗组中具有野生型KMT2D或COL4A4的患者比基因序列发生变异的患者具有更好的PFS（5.85个月vs.5.45个月，P=0.0004）和OS（16.23个月vs.13.09个月，P=0.004）；CTNNA2和SCN4A基因序列发生变化的患者相比野生型患者具有显著延长的PFS（14.98个月vs.5.65个月，P=0.009）和OS（22.23个月vs.14.59个月，P=0.006）；COL1A1、COL4A4、ITGA8、KIT和PRKCG基因组成的黏着斑/整合素途径突变患者相比野生型患者具有更短的PFS（4.14个月vs.6.24个月，P<0.0001）和OS（10.81个月vs.16.56个月，P<0.0001）；肿瘤内异质性较低（突变-等位肿瘤基因异质性评分小于29）的患者具有显著改善的PFS（6.90个月vs.5.59个月，P=0.05）和OS（18.86个月vs.13.16个月，P=0.01）；HLA-A11+HLA-B62-单倍型患者表现出延长的PFS（7.03个月vs.5.55个月，P=0.05）和OS获益（18.43个月vs.12.94个月，P=0.04）。 11.Delta样配体3（delta-like ligand 3，DLL3）是Notch受体的抑制性配体，在正常组织的胞内极低表达，在胞内通过顺式结合Notch受体，阻止其转运到细胞膜进而阻断Notch信号激活，由此解除Notch通路对细胞增殖的抑制作用，间接激活P13K/Akt、Wnt，从而促进肿瘤生长。DLL3在85%~97%的SCLC肿瘤细胞膜特异性过表达，其表达稳定性及可通过液体活检监测的特性，使其成为兼具诊断和治疗价值的靶点。DeLLphi-301研究显示无论DLL3表达水平，均观察到对DLL3-TCE药物（tarlatamab）的响应，在未检测DLL3表达和DLL3阴性患者中，也观察到临床获益。但也有学者对5项tarlatamab系列研究共计1078例患者进行回顾性系统分析，提出DLL3的表达水平与tarlatamab更好的客观缓解率（ORR）和延长的生存期呈正相关。因此DLL3的表达水平能否作为tarlatamab疗效预测标志物尚待检测技术的标准化和大样本前瞻性临床研究验证。 12.人源癫痫相关同源物6（seizure related 6 homolog，SEZ6）作为神经树突形成和信号传递的关键调控因子，在神经内分泌肿瘤（neuroendocrine tumor，NET）尤其是SCLC中发挥重要作用，目前已是成药的靶点之一。ABBV-706是一种靶向SEZ6的药物抗体偶联物（antibody-drug conjugate，ADC），在Ⅰ期研究中表现出有希望的抗肿瘤活性和可控安全性。 13.B7-H3属于B7免疫调节家族，参与肿瘤免疫逃逸，还直接促进肿瘤细胞增殖、转移、耐药及血管生成；在约65%的SCLC样本中呈阳性表达，与患者的不良预后相关，且B7-H3在SCLC的四种主要分子亚型中均呈现高且一致的表达，异质性较低，这使其具有更广泛的潜在治疗人群基础。靶向B7-H3有望同时解除免疫抑制并直接攻击肿瘤细胞。目前已有多款以B7-H3为靶点的ADC药物已进入广泛期小细胞肺癌（extensive-stage small cell lung cancer，ES-SCLC）的Ⅲ期研究阶段。 14.SCLC对免疫治疗不敏感的一个关键机制在于MHCⅠ类分子的显著下调，导致肿瘤细胞难以被T细胞识别和清除。MHCⅠ类分子相关特征与免疫治疗获益显著相关，CheckMate 032研究的探索性分析发现，直接检测到MHCⅠ类分子高表达的SCLC患者，接受免疫治疗后显示出更长的OS获益趋势。另外，近期研究还揭示了干扰素诱导跨膜蛋白3（IFITM3）可上调NLRC5（MHCⅠ基因的关键转录激活因子）的表达并促进其核转位，进而直接提升MHCⅠ类分子的水平。因此，IFITM3的表达与MHCⅠ类分子水平及抗程序性死亡受体1/程序性死亡受体配体1（programmed death-1/programmed death-ligand 1；PD-L1,PD-1/PD-L1）疗法的疗效相关，其本身或可作为预测免疫治疗反应的潜在生物标志物。 15.ASTRUM-005探索性研究证实，ENPP2、GAL、CCDC50、WASF3、PLCB1、SMC3、PRKAG3、PAPPA、SH3BGRL2、TSPAN1、VCAN、PRC1、CEACAM20、ACTN2及MMP3蛋白组成的15个蛋白特征评分与疗效相关，接受斯鲁利单抗联合化疗、血清中15个蛋白特征评分高的SCLC患者，相比评分低的患者，具有显著更长的PFS（7.9个月vs.4.4个月）和OS（17.2个月vs.9.1个月）。同时，一项最新的研究者发起的临床研究（investigator-initiated trial，IIT）整合了外周血蛋白组学（CSF-1、CCL4、CCL3、CD83、IL-12及CD244）及临床特征[乳酸脱氢酶（lactate dehydrogenase，LDH）水平、骨转移状态及肝转移状态]等指标，建立并验证了一种无创的多模态模型，该模型可以精准地预测接受免疫治疗的ES-SCLC患者的获益[（high risk）vs.（low risk），PFS：5.4个月vs.10.0个月，P<0.001；（high risk）vs.（low risk），OS：15.7个月vs.未达到，P=0.010]。 16.多组学联合分析也有了进一步突破。最新研究通过整合空间多组学（CODEX、CosMx）和传统组学技术，对165例SCLC患者（930万细胞）进行空间图谱解析，不仅揭示肿瘤内部高度分子异质性，且在SCLC-A亚型中发现高表达SLFN11的“多阳性肿瘤细胞邻域”，与预后差相关。研究同时提出肿瘤细胞与免疫细胞的空间互作规律，开发新型细胞群落检测算法ColonyMap，鉴定出由抗肿瘤巨噬细胞、CD8+ T细胞及自然杀伤T细胞（MT2）组成的空间聚集免疫微环境，可精准预测免疫疗效及患者预后。附录 2021版WHO肺神经内分泌肿瘤分类肺神经内分泌肿瘤病理诊断流程参考文献及书籍： 1.中国临床肿瘤学会指南工作委员会. 中国临床肿瘤学会(CSCO)小细胞肺癌诊疗指南 2026[M]. 北京 :人民卫生出版社, 2026. 扩展阅读：【衡道丨干货】2025 中国肿瘤整合诊治指南（CACA) ——肺癌的诊断设计：鹏飞编辑：小约翰本公众号发布所有原创内容，版权均属衡道医学病理诊断中心及相关版权方所有，内容仅供学术交流，如有侵权请联系删除。未经授权的转载是侵权行为，版权方保留追究法律责任的权利。投稿、转载或版权疑议，请联系：tougao@histo.cn；商务合作请联系：info@histo.cn。衡道病理官网：www.histo.cn 喜欢就奖励小衡一个“看一看”和“👍”吧~

2026-07-02

·BioSpace

Puma Biotechnology Reports Inducement Awards Under Nasdaq Listing Rule 5635(c)(4) - July 2, 2026

LOS ANGELES--(BUSINESS WIRE)--Puma Biotechnology, Inc. (NASDAQ: PBYI), a biopharmaceutical company, announced that on July 1, 2026, the Compensation Committee of Puma’s Board of Directors approved the grant of inducement restricted stock unit awards covering 31,625 shares of Puma common stock to four new non-executive employees. The awards were granted under Puma’s 2017 Employment Inducement Incentive Award Plan, which was adopted on April 27, 2017 and provides for the granting of equity awards to new employees of Puma. The restricted stock unit awards vest over a three-year period, with one-third of the shares underlying the award vesting on the first anniversary of the award’s vesting commencement date, July 1, 2026, and one-sixth of the shares underlying the award vesting on each six-month anniversary of the vesting commencement date thereafter, subject to continued service. The awards were granted as an inducement material to the new employees entering into employment with Puma, in accordance with Nasdaq Listing Rule 5635(c)(4). About Puma Biotechnology Puma Biotechnology, Inc. is a biopharmaceutical company with a focus on the development and commercialization of innovative products to enhance cancer care. Puma in-licensed the global development and commercialization rights to PB272 (neratinib, oral) in 2011. Neratinib, oral was approved by the U.S. Food and Drug Administration in 2017 for the extended adjuvant treatment of adult patients with early stage HER2-overexpressed/amplified breast cancer, following adjuvant trastuzumab-based therapy, and is marketed in the United States as NERLYNX® (neratinib) tablets. In February 2020, NERLYNX was also approved by the FDA in combination with capecitabine for the treatment of adult patients with advanced or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. NERLYNX was granted marketing authorization by the European Commission in 2018 for the extended adjuvant treatment of adult patients with early stage hormone receptor-positive HER2-overexpressed/amplified breast cancer and who are less than one year from completion of prior adjuvant trastuzumab-based therapy. NERLYNX® is a registered trademark of Puma Biotechnology, Inc. In September 2022, Puma entered into an exclusive license agreement for the development and commercialization of the anti-cancer drug alisertib, a selective, small molecule, orally administered inhibitor of aurora kinase A. Initially, Puma intends to focus the development of alisertib on the treatment of small cell lung cancer and breast cancer. In February 2024, Puma initiated ALISCA®-Lung1, a Phase II clinical trial of alisertib monotherapy for the treatment of patients with extensive-stage small cell lung cancer. In November 2024, Puma initiated ALISCA®-Breast1, a Phase II clinical trial of alisertib in combination with endocrine therapy for the treatment of patients with HER2-negative, HR-positive metastatic breast cancer. Contacts Alan H. Auerbach or Mariann Ohanesian, Puma Biotechnology, Inc., +1 424 248 6500 info@pumabiotechnology.com ir@pumabiotechnology.com

上市批准引进/卖出临床2期

2026-06-04

·BioSpace

Puma Biotechnology Reports Inducement Awards Under Nasdaq Listing Rule 5635(c)(4) - June 3, 2026

LOS ANGELES--(BUSINESS WIRE)--Puma Biotechnology, Inc. (NASDAQ: PBYI), a biopharmaceutical company, announced that on June 1, 2026, the Compensation Committee of Puma’s Board of Directors approved the grant of inducement restricted stock unit awards covering 7,000 shares of Puma common stock to two new non-executive employees. The awards were granted under Puma’s 2017 Employment Inducement Incentive Award Plan, which was adopted on April 27, 2017 and provides for the granting of equity awards to new employees of Puma. The restricted stock unit awards vest over a three-year period, with one-third of the shares underlying the award vesting on the first anniversary of the award’s vesting commencement date, June 1, 2026, and one-sixth of the shares underlying the award vesting on each six-month anniversary of the vesting commencement date thereafter, subject to continued service. The awards were granted as an inducement material to the new employees entering into employment with Puma, in accordance with Nasdaq Listing Rule 5635(c)(4). About Puma Biotechnology Puma Biotechnology, Inc. is a biopharmaceutical company with a focus on the development and commercialization of innovative products to enhance cancer care. Puma in-licensed the global development and commercialization rights to PB272 (neratinib, oral) in 2011. Neratinib, oral was approved by the U.S. Food and Drug Administration in 2017 for the extended adjuvant treatment of adult patients with early stage HER2-overexpressed/amplified breast cancer, following adjuvant trastuzumab-based therapy, and is marketed in the United States as NERLYNX® (neratinib) tablets. In February 2020, NERLYNX was also approved by the FDA in combination with capecitabine for the treatment of adult patients with advanced or metastatic HER2-positive breast cancer who have received two or more prior anti-HER2-based regimens in the metastatic setting. NERLYNX was granted marketing authorization by the European Commission in 2018 for the extended adjuvant treatment of adult patients with early stage hormone receptor-positive HER2-overexpressed/amplified breast cancer and who are less than one year from completion of prior adjuvant trastuzumab-based therapy. NERLYNX® is a registered trademark of Puma Biotechnology, Inc. In September 2022, Puma entered into an exclusive license agreement for the development and commercialization of the anti-cancer drug alisertib, a selective, small molecule, orally administered inhibitor of aurora kinase A. Initially, Puma intends to focus the development of alisertib on the treatment of small cell lung cancer and breast cancer. In February 2024, Puma initiated ALISCA™-Lung1, a Phase II clinical trial of alisertib monotherapy for the treatment of patients with extensive-stage small cell lung cancer. In November 2024, Puma initiated ALISCA™-Breast1, a Phase II clinical trial of alisertib in combination with endocrine therapy for the treatment of patients with HER2-negative, HR-positive metastatic breast cancer. Contacts Alan H. Auerbach or Mariann Ohanesian, Puma Biotechnology, Inc., +1 424 248 6500 info@pumabiotechnology.com ir@pumabiotechnology.com

上市批准引进/卖出临床2期

100 项与 Alisertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10085	Alisertib	-	DB05220

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
难治性外周T细胞淋巴瘤	临床3期	美国	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	澳大利亚	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	奥地利	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	白俄罗斯	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	比利时	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	巴西	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	保加利亚	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	加拿大	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	智利	Millennium Pharmaceuticals, Inc.	2012-06-11
难治性外周T细胞淋巴瘤	临床3期	捷克	Millennium Pharmaceuticals, Inc.	2012-06-11

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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


SABCS2025	临床1/2期	ER阳性/HER2阴性乳腺癌 ER+/HER2-	126	Alisertib monotherapy	繭鏇獵齋獵壓齋襯顧鬱(構築齋夢窪鹹鑰鹽窪膚) = hematologic AEs (neutropenia, leukopenia, and anemia), and fatigue. 鑰鹽壓簾鑰網憲選鬱憲 (鹹糧廠壓積選鹽獵鹽製 )	积极	2025-12-10
				Alisertib ± fulvestrant
NCT06369285 (ALISCA-Breast1, ASCO2025)	临床2期	HR阳性/HER2阴性乳腺癌 RB1 \| MYC \| TP53 ... 更多	-	Alisertib 30 mg + Endocrine Therapy	憲顧願窪膚構窪廠醖醖(襯遞繭製鬱觸醖繭襯襯) = 積夢鬱壓窪糧鑰蓋網觸衊簾構廠鹹淵遞鑰顧製 (膚鑰鏇醖願獵顧醖壓艱 ) 更多	积极	2025-05-30
				Alisertib 40 mg + Endocrine Therapy	憲顧願窪膚構窪廠醖醖(襯遞繭製鬱觸醖繭襯襯) = 顧繭鏇壓觸窪範齋衊簾衊簾構廠鹹淵遞鑰顧製 (膚鑰鏇醖願獵顧醖壓艱 ) 更多
NCT04555837 (CTgov)	临床1/2期	转移性头颈部鳞状细胞癌 \| 头颈部鳞状细胞癌 \| 恶性实体肿瘤	24	Alisertib+Pembrolizumab (Phase I)	夢網獵鏇蓋夢鏇構觸窪 = 願製鬱艱窪衊糧構艱窪製鏇顧鑰淵齋鬱選繭顧 (顧繭壓網遞繭積憲廠窪, 糧簾糧簾壓糧選網廠範 ~ 廠齋糧選廠齋築醖鹽夢) 更多	-	2024-12-16
				Alisertib+Pembrolizumab (Phase II)	憲築獵艱膚遞製齋積鏇 = 鹽構淵觸糧築鹹鹹衊積鬱鏇艱製網艱觸鏇選夢 (繭廠淵簾願窪網顧製憲, 夢糧積範憲膚築築遞淵 ~ 壓壓積簾積鏇範糧壓遞) 更多
NCT02860000 (TBCRC041, CTgov)	临床2期	局部晚期乳腺癌 \| 转移性乳腺癌 \| 激素难治性乳腺癌 ... 更多	96	Laboratory Biomarker Analysis+Alisertib (Arm I (Alisertib))	遞齋鬱築鏇鹹艱鹽鑰淵(夢廠襯齋繭鹹齋衊衊廠) = 獵鹹願壓鑰糧齋積積蓋鏇築鏇憲鏇窪襯鬱衊鹽 (觸簾鏇憲積繭積蓋襯膚, 壓遞鹹襯夢醖齋壓餘遞 ~ 獵憲獵窪鏇構淵積齋鹹) 更多	-	2024-10-18
				Laboratory Biomarker Analysis+Alisertib+fulvestrant (Arm II (Alisertib, Fulvestrant))	遞齋鬱築鏇鹹艱鹽鑰淵(夢廠襯齋繭鹹齋衊衊廠) = 獵鬱鏇構網壓築廠構構鏇築鏇憲鏇窪襯鬱衊鹽 (觸簾鏇憲積繭積蓋襯膚, 構窪廠鹹衊積獵蓋淵鏇 ~ 鏇蓋願獵憲顧衊齋窪艱) 更多
NCT02187991 (CTgov)	临床2期	转移性乳腺癌	169	Paclitaxel (ER+/HER2- Paclitaxel Alone)	艱窪鏇簾繭淵鏇遞艱遞(願膚窪鏇網膚鏇淵餘繭) = 顧鏇糧壓壓獵獵遞餘網艱願製積鬱顧夢餘鬱構 (夢鹽顧淵窪範糧網鑰鹹, 製淵憲築願鏇鑰壓窪膚 ~ 淵艱蓋壓製顧糧鹹觸獵) 更多	-	2024-10-09
				Alisertib+Paclitaxel (ER+/HER2- Paclitaxel Plus Alisertib)	艱窪鏇簾繭淵鏇遞艱遞(願膚窪鏇網膚鏇淵餘繭) = 觸鑰築襯糧淵製糧膚艱艱願製積鬱顧夢餘鬱構 (夢鹽顧淵窪範糧網鑰鹹, 鹹範蓋網願製獵憲構膚 ~ 簾窪鹽鏇鏇襯淵艱遞蓋) 更多
NCT04085315 (phase I/Ib study, ASCO2024) 人工标引	临床1期	EGFR突变肺癌 EGFR	21	alisertib+osimertinib	夢餘餘積願獵築餘遞鏇(鑰淵願鏇齋衊壓製築壓) = neutropenia (42.9%), anemia (42.9%), and diarrhea (38.1%) 繭範膚鏇願夢糧夢淵憲 (選廠構範醖蓋憲網鏇齋 )	积极	2024-05-24
NCT02860000 (TBCRC041, ASCO2024)	临床2期	转移性乳腺癌 ESR1 \| PIK3CAmutation \| AKT1 ... 更多	91	Alisertib + Fulvestrant	範簾齋窪鹽構簾餘範鏇(糧築夢憲觸獵鹽衊觸遞): HR = 1.8 (95% CI, 1.1 ~ 2.9), P-Value = 0.014	积极	2024-05-24
				Alisertib
NCT02187991 (ASCO2023) 人工标引	临床2期	转移性三阴性乳腺癌 \| HR阳性/HER2阴性乳腺癌 HR Positive \| PR Negative \| ER Negative \| ... 更多	96	alisertib (A) combined with paclitaxel (P) or P alone	窪願網膚鹹齋餘齋鏇餘(蓋憲糧繭憲願蓋築憲範) = 衊構糧網齋製壓襯繭鹽獵膚願壓憲窪齋構製憲 (餘淵醖選願願衊廠鹹齋 )	积极	2023-05-31
NCT02860000 (Pubmed)	临床2期	晚期乳腺癌 CDK 4/6i	91	Alisertib	蓋襯鑰壓餘範憲憲壓鬱(遞構簾築觸顧簾簾繭壓) = 鹹淵鏇艱構衊獵艱蓋膚製選鬱蓋壓淵鹹蓋壓鏇 (鹽糧鬱膚簾夢蓋憲餘餘, 29.0% ~ 54.5%) 更多	-	2023-03-09
				Alisertib + Fulvestrant	蓋襯鑰壓餘範憲憲壓鬱(遞構簾築觸顧簾簾繭壓) = 繭襯淵鬱餘製齋觸遞鑰製選鬱蓋壓淵鹹蓋壓鏇 (鹽糧鬱膚簾夢蓋憲餘餘, 18.0% ~ 42.0%) 更多
NCT02293005 (CTgov)	临床2期	不可切除的胸膜恶性间皮瘤 \| 恶性间皮瘤 \| 肺癌	28	Alisertib	糧構積鑰遞顧築願餘膚 = 構醖襯願遞艱壓膚製廠選窪積選淵衊繭觸範網 (網顧簾壓簾願願蓋憲鹽, 築鹹鏇鏇製糧網選齋簾 ~ 蓋網壓繭積鬱願鹹鹹艱) 更多	-	2022-10-04