更新于：2024-04-26

Alisertib

更新于：2024-04-26

概要

研发状态

概要

基本信息

药物类型

小分子化药

别名

Alisertib (USAN)、Alsertib、MLN-8237

靶点

Aurora A

作用机制

Aurora A抑制剂(丝氨酸/苏氨酸蛋白激酶Aurora-A抑制剂)

治疗领域

肿瘤呼吸系统疾病皮肤和肌肉骨骼疾病+ [3]

在研适应症

复发性乳腺癌HR阳性/HER2阴性乳腺癌复发性HER2阴性乳腺癌+ [15]

非在研适应症

复发性急性淋巴细胞白血病急性髓性白血病前列腺腺癌+ [92]

原研机构

Takeda Pharmaceutical Co., Ltd.

在研机构

Puma Biotechnology, Inc.

National Cancer InstituteUS Oncology Research LLC

+ [2]

非在研机构

Washington University School of Medicine

University of Colorado Denver

Millennium Biotechnologies, Inc.

+ [2]

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评孤儿药 (美国)

结构

分子式C27H20ClFN4O4

InChIKeyZLHFILGSQDJULK-UHFFFAOYSA-N

CAS号1028486-01-2

关联

项与 Alisertib 相关的临床试验

NCT06369285 / Not yet 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2024-12-31

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 in patients with pathologically-confirmed extensive-stage small cell lung cancer (ES-SCLC) following progression on or after first-line treatment with platinum-based chemotherapy along with an anti-PDL-1 immunotherapy agent. This study is intended to evaluate the efficacy, safety, and pharmacokinetics of alisertib and to identify the biomarker-defined subgroup(s) that may benefit most from alisertib treatment.

开始日期2024-02-08

申办/合作机构

Puma Biotechnology, Inc.

NCT04555837 / Active, not recruiting临床1/2期IIT

A Phase I-II, Open Label Study Evaluating the Safety and Efficacy of Alisertib and Pembrolizumab in Patients With Rb-Deficient Head and Neck Squamous Cell Carcinomas

This phase I/II trial investigates the best dose and effect of alisertib in combination with pembrolizumab in treating patients with Rb-deficient head and neck squamous cell cancer. Alisertib may help block the growth of cancer.. Immunotherapy with monoclonal antibodies, such as pembrolizumab, may help the body's immune system attack the tumor, and may interfere with the ability of tumor cells to grow and spread. Giving alisertib in combination with pembrolizumab may help control Rb-deficient head and neck squamous cell cancer. HPV positive head and neck cancers are Rb-deficient.

开始日期2020-09-15

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+1]

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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311

项与 Alisertib 相关的文献（医药）

2024-02-01·Hepatology

Multiomics identifies metabolic subtypes based on fatty acid degradation allocating personalized treatment in hepatocellular carcinoma

Article

作者: Wang, Ye ; Yu, Decai ; Liu, Qi ; Li, Huan ; Li, Binghua ; Xu, Yanchao ; Mehal, Wajahat Z ; Qian, Liyuan ; Zhou, Huajun ; Lu, Jiaming ; Cao, Yajuan ; Zhang, Yuchen ; Xu, Zhu ; Xie, Yuanyuan ; Su, Ke ; Guo, Sheng ; Li, Yunzheng ; Zhang, Laizhu ; Peng, Jin ; Lu, Yijun ; Hu, Yue ; Cheng, Chunxiao

Background and Aims::

Molecular classification is a promising tool for prognosis prediction and optimizing precision therapy for HCC. Here, we aimed to develop a molecular classification of HCC based on the fatty acid degradation (FAD) pathway, fully characterize it, and evaluate its ability in guiding personalized therapy.

Approach and Results::

We performed RNA sequencing (RNA-seq), PCR-array, lipidomics, metabolomics, and proteomics analysis of 41 patients with HCC, in which 17 patients received anti-programmed cell death-1 (PD-1) therapy. Single-cell RNA sequencing (scRNA-seq) was performed to explore the tumor microenvironment. Nearly, 60 publicly available multiomics data sets were analyzed. The associations between FAD subtypes and response to sorafenib, transarterial chemoembolization (TACE), immune checkpoint inhibitor (ICI) were assessed in patient cohorts, patient-derived xenograft (PDX), and spontaneous mouse model ls. A novel molecular classification named F subtype (F1, F2, and F3) was identified based on the FAD pathway, distinguished by clinical, mutational, epigenetic, metabolic, and immunological characteristics. F1 subtypes exhibited high infiltration with immunosuppressive microenvironment. Subtype-specific therapeutic strategies were identified, in which F1 subtypes with the lowest FAD activities represent responders to compounds YM-155 and Alisertib, sorafenib, anti-PD1, anti-PD-L1, and atezolizumab plus bevacizumab (T + A) treatment, while F3 subtypes with the highest FAD activities are responders to TACE. F2 subtypes, the intermediate status between F1 and F3, are potential responders to T + A combinations. We provide preliminary evidence that the FAD subtypes can be diagnosed based on liquid biopsies.

Conclusions::

We identified 3 FAD subtypes with unique clinical and biological characteristics, which could optimize individual cancer patient therapy and help clinical decision-making.

2024-01-01·Biochemical and Biophysical Research Communications

Aurora-A inhibitor synergistically enhances the inhibitory effect of anlotinib on hepatocellular carcinoma

Article

作者: Wang, Rui ; Wang, Ting ; Lin, Xinrong ; Abudoureyimu, Mubalake ; Pan, Fan ; Hao, Liping

METHODS:

In this study, we used HCC cell lines to investigate whether the combination of the two drugs could enhance their individual strengths and mitigate their weaknesses, thereby providing greater clinical benefits both in vitro and in vivo.

RESULTS:

Our findings confirmed that the Aurora-A inhibitor alisertib and anlotinib exhibited a time-dose-dependent inhibitory effect on HCC cells. In vitro cytological experiments demonstrated that the combination of the two drugs synergistically inhibited cell proliferation, invasion, and metastasis, while promoting cell apoptosis. Furthermore, we identified the underlying molecular mechanism by which the combination of the Aurora-A inhibitor alisertib and anlotinib inhibited HCC through the inhibition of the NF-ĸB signaling pathway.

CONCLUSIONS:

In summary, we have demonstrated the effectiveness of combining anlotinib with an Aurora-A inhibitor, which expands the potential applications of anlotinib in the clinical treatment of HCC in the future.

2023-12-01·International Journal of Radiation Oncology*Biology*Physics

Combined Aurora Kinase A and CHK1 Inhibition Enhances Radiosensitivity of Triple-Negative Breast Cancer Through Induction of Apoptosis and Mitotic Catastrophe Associated With Excessive DNA Damage

Article

作者: Chen, Fei Xavier ; Liao, Jiatao ; Wang, Xuanyi ; Li, Chunyan ; Guo, Xiaomao ; Chen, Xingxing

PURPOSE:

There is an urgent need for biomarkers and new actionable targets to improve radiosensitivity of triple-negative breast cancer (TNBC) tumors. We characterized the radiosensitizing effects and underlying mechanisms of combined Aurora kinase A (AURKA) and CHK1 inhibition in TNBC.

METHODS AND MATERIALS:

Different TNBC cell lines were treated with AURKA inhibitor (AURKAi, MLN8237) and CHK1 inhibitor (CHK1i, MK8776). Cell responses to irradiation (IR) were then evaluated. Cell apoptosis, DNA damage, cell cycle distribution, and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and Phosphoinositide 3-Kinase (PI3K) pathways were evaluated in vitro. Transcriptomic analysis was performed to facilitate the identification of potential biomarkers. Xenograft and immunohistochemistry were carried out to investigate the radiosensitizing effects of dual inhibition in vivo. Finally, the prognostic effect of CHEK1/AURKA in TNBC samples in the The Cancer Genome Atlas (TCGA) database and our center were analyzed.

RESULTS:

AURKAi (MLN8237) induced overexpression of phospho-CHK1 in TNBC cells. The addition of MK8776 (CHK1i) to MLN8237 greatly reduced cell viability and increased radiosensitivity compared with either the control or MLN8237 alone in vitro. Mechanistically, dual inhibition resulted in inducing excessive DNA damage by prompting G2/M transition to cells with defective spindles, leading to mitotic catastrophe and induction of apoptosis after IR. We also observed that dual inhibition suppressed the phosphorylation of ERK, while activation of ERK with its agonist or overexpression of active ERK1/2 allele could attenuate the apoptosis induced by dual inhibition with IR. Additionally, dual inhibition of AURKA and CHK1 synergistically enhanced radiosensitivity in MDA-MB-231 xenografts. Moreover, we detected that both CHEK1 and AURKA were overexpressed in patients with TNBC and negatively correlated with patient survival.

CONCLUSIONS:

Our findings suggested that AURKAi in combination with CHK1i enhanced TNBC radiosensitivity in preclinical models, potentially providing a novel strategy of precision treatment for patients with TNBC.

项与 Alisertib 相关的新闻（医药）

2024-04-18

·BioSpace

Puma Biotechnology to Host Conference Call to Discuss First Quarter 2024 Financial Results

LOS ANGELES--(BUSINESS WIRE)-- Puma Biotechnology Inc. (NASDAQ: PBYI), a biopharmaceutical company, will host a conference call at 1:30 p.m. PDT/4:30 p.m. EDT on Thursday, May 2, 2024, following the release of its first quarter 2024 financial results. The call may be accessed by dialing 1-877-709-8150 (domestic) or 1-201-689-8354 (international). Please dial in at least 10 minutes in advance and inform the operator that you would like to join the “Puma Biotechnology Conference Call.” A live webcast of the conference call and presentation slides may be accessed on the Investors section of the Puma Biotechnology website at . A replay of the call will be available approximately one hour after completion of the call and will be archived on Puma’s website for 90 days. 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. Further information about Puma Biotechnology may be found at .

上市批准引进/卖出财报

2024-04-05

·精准药物

中山大学报道肿瘤药物治疗新靶点

本文为转化医学网原创，转载请注明出处作者：Jerry导读：AURKA是肿瘤治疗的既定靶点; 然而，其抑制剂在临床试验中的疗效受到不同肿瘤亚型缓解率差异的阻碍。3月23日，中山大学研究团队在期刊《Cell Death&Disease》上发表了研究论文，题为“AURKA emerges as a vulnerable target for KEAP1-deficient non-small cell lung cancer by activation of asparagine synthesis”。本研究中，研究人员证明了AURKA调节氨基酸合成，使其成为KEAP1缺陷非小细胞肺癌(NSCLC)的脆弱靶点。从机制上讲，AURKA与eIF2α激酶GCN2相互作用，并保持其磷酸化，以调节eIF2α-ATF4介导的氨基酸生物合成。AURKA抑制抑制了天冬酰胺合成酶(ASNS)的表达，使得KEAP1-缺陷的NSCLC细胞易受AURKA抑制剂的影响，其中ASNS高表达。本研究揭示了AURKA在氨基酸代谢中的关键作用，并确定了AURKA抑制剂的特定代谢适应症。这些发现还为KEAP1-突变/缺陷NSCLC提供了新的临床治疗靶点，该疾病的特点是对放疗、化疗和靶向治疗具有耐药性。https://www.nature.com/articles/s41419-024-06577-x#Sec9研究背景 01 Aurora kinase A (AURKA)是一种重要的有丝分裂激酶，它的激活在多种癌症中发挥重要作用。前期研究发现，AURKA在乳腺癌中的高表达促进了细胞增殖、侵袭、干性及化疗耐药。此外，AURKA在非小细胞肺癌(NSCLC)中也显著上调，并与不良预后相关。抑制AURKA会导致纺锤体形成异常和有丝分裂缺陷，最终导致肿瘤细胞死亡。目前已有几种AURKA抑制剂，包括阿立塞替(MLN8237)、达努塞替和ENMD-2076，在多种肿瘤类型中均有一定的抗肿瘤效果。然而，MLN8237在复发性外周T细胞淋巴瘤中的III期临床试验被宣告失败，与对照化疗药物相比未显示出生存优势。因此，AURKA抑制剂的临床应用面临停滞。研究进展 02 为了确定AURKA抑制剂的代谢适应性，研究人员使用代谢文库在肺癌和乳腺癌细胞中进行了CRISPR/Cas9筛选。为了验证KEAP1突变或缺陷对AURKA抑制剂的增敏作用，研究人员首先在癌症药物敏感性基因组学数据库GDSC中分析了具有野生型或突变型KEAP1的NSCLC细胞系对AURKA抑制剂的敏感性。随后，研究人员选择了KEAP1野生型NSCLC细胞株H1975、H3122、H1650和KEAP1突变型NSCLC细胞株H2122(F211C)、HCC44(A170-R204del)进行进一步验证，使用CCK8实验检测这些细胞株在不同浓度MLN8237下的细胞活力，也证实了KEAP1突变使NSCLC细胞对MLN8237敏感。此外，研究人员在KEAP1野生型NSCLC细胞株H1975和H3122中敲低KEAP1后进行了克隆形成实验，观察到这两个细胞株对AURKA抑制剂的敏感性显著增强。在MDA-MB-231细胞中也获得了类似的结果。最后，使用H1975野生型和KEAP1-敲低细胞在裸鼠皮下成瘤实验中进一步证实了KEAP1敲低后NSCLC细胞对AURKA抑制剂MLN8237的敏感性显著增强。为了研究NRF2的激活是否介导了KEAP1的敲低对AURKA抑制剂的增敏作用，我们在KEAP1缺陷细胞中敲低了NRF2。克隆形成结果证实了NRF2的敲低对KEAP1的敲低对AURKA抑制剂的增敏作用的缓解作用。此外，在KEAP1突变细胞系HCC44(KEAP1-F211C)中敲低NRF2显著降低了细胞对AURKA抑制剂的敏感性。总之，KEAP1缺陷增强了NSCLC细胞对AURKA抑制的敏感性，并且这种作用依赖于NRF2通路的激活。KEAP1缺陷通过NRF2激活使NSCLC细胞对AURKA抑制敏感研究结论 03在本研究中，研究人员采用CRISPR代谢筛选技术，发现了携带代谢相关基因突变的特定肿瘤亚型对AURKA抑制剂MLN8237表现出敏感性。研究结果表明，MLN8237对KEAP1突变或缺陷的肿瘤细胞的生长抑制效果尤为显著。此外，研究人员阐明了AURKA的抑制下调了天冬酰胺的合成，从而增强了KEAP1缺陷的NSCLC对MLN8237的敏感性。因此，本研究揭示了KEAP1突变或缺陷肿瘤的一个有前途的药物靶点，并探索了AURKA抑制剂的新型临床应用。参考资料：https://www.nature.com/articles/s41419-024-06577-x#Sec9声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

临床研究临床结果基因疗法

2024-03-25

·今日头条

克服耐药！中山大学再发文：发现肿瘤药物治疗新靶点

本文为转化医学网原创，转载请注明出处作者：Jerry 导读： AURKA是肿瘤治疗的既定靶点; 然而，其抑制剂在临床试验中的疗效受到不同肿瘤亚型缓解率差异的阻碍。 3月23日，中山大学研究团队在期刊《Cell Death&Disease》上发表了研究论文，题为“AURKA emerges as a vulnerable target for KEAP1-deficient non-small cell lung cancer by activation of asparagine synthesis”。本研究中，研究人员证明了AURKA调节氨基酸合成，使其成为KEAP1缺陷非小细胞肺癌(NSCLC)的脆弱靶点。从机制上讲，AURKA与eIF2α激酶GCN2相互作用，并保持其磷酸化，以调节eIF2α-ATF4介导的氨基酸生物合成。AURKA抑制抑制了天冬酰胺合成酶(ASNS)的表达，使得KEAP1-缺陷的NSCLC细胞易受AURKA抑制剂的影响，其中ASNS高表达。本研究揭示了AURKA在氨基酸代谢中的关键作用，并确定了AURKA抑制剂的特定代谢适应症。这些发现还为KEAP1-突变/缺陷NSCLC提供了新的临床治疗靶点，该疾病的特点是对放疗、化疗和靶向治疗具有耐药性。 https://www.nature.com/articles/s41419-024-06577-x#Sec9 研究背景 01 Aurora kinase A (AURKA)是一种重要的有丝分裂激酶，它的激活在多种癌症中发挥重要作用。前期研究发现，AURKA在乳腺癌中的高表达促进了细胞增殖、侵袭、干性及化疗耐药。此外，AURKA在非小细胞肺癌(NSCLC)中也显著上调，并与不良预后相关。抑制AURKA会导致纺锤体形成异常和有丝分裂缺陷，最终导致肿瘤细胞死亡。目前已有几种AURKA抑制剂，包括阿立塞替(MLN8237)、达努塞替和ENMD-2076，在多种肿瘤类型中均有一定的抗肿瘤效果。然而，MLN8237在复发性外周T细胞淋巴瘤中的III期临床试验被宣告失败，与对照化疗药物相比未显示出生存优势。因此，AURKA抑制剂的临床应用面临停滞。研究进展 02 为了确定AURKA抑制剂的代谢适应性，研究人员使用代谢文库在肺癌和乳腺癌细胞中进行了CRISPR/Cas9筛选。为了验证KEAP1突变或缺陷对AURKA抑制剂的增敏作用，研究人员首先在癌症药物敏感性基因组学数据库GDSC中分析了具有野生型或突变型KEAP1的NSCLC细胞系对AURKA抑制剂的敏感性。随后，研究人员选择了KEAP1野生型NSCLC细胞株H1975、H3122、H1650和KEAP1突变型NSCLC细胞株H2122(F211C)、HCC44(A170-R204del)进行进一步验证，使用CCK8实验检测这些细胞株在不同浓度MLN8237下的细胞活力，也证实了KEAP1突变使NSCLC细胞对MLN8237敏感。此外，研究人员在KEAP1野生型NSCLC细胞株H1975和H3122中敲低KEAP1后进行了克隆形成实验，观察到这两个细胞株对AURKA抑制剂的敏感性显著增强。在MDA-MB-231细胞中也获得了类似的结果。最后，使用H1975野生型和KEAP1-敲低细胞在裸鼠皮下成瘤实验中进一步证实了KEAP1敲低后NSCLC细胞对AURKA抑制剂MLN8237的敏感性显著增强。为了研究NRF2的激活是否介导了KEAP1的敲低对AURKA抑制剂的增敏作用，我们在KEAP1缺陷细胞中敲低了NRF2。克隆形成结果证实了NRF2的敲低对KEAP1的敲低对AURKA抑制剂的增敏作用的缓解作用。此外，在KEAP1突变细胞系HCC44(KEAP1-F211C)中敲低NRF2显著降低了细胞对AURKA抑制剂的敏感性。总之，KEAP1缺陷增强了NSCLC细胞对AURKA抑制的敏感性，并且这种作用依赖于NRF2通路的激活。 KEAP1缺陷通过NRF2激活使NSCLC细胞对AURKA抑制敏感研究结论 03 在本研究中，研究人员采用CRISPR代谢筛选技术，发现了携带代谢相关基因突变的特定肿瘤亚型对AURKA抑制剂MLN8237表现出敏感性。研究结果表明，MLN8237对KEAP1突变或缺陷的肿瘤细胞的生长抑制效果尤为显著。此外，研究人员阐明了AURKA的抑制下调了天冬酰胺的合成，从而增强了KEAP1缺陷的NSCLC对MLN8237的敏感性。因此，本研究揭示了KEAP1突变或缺陷肿瘤的一个有前途的药物靶点，并探索了AURKA抑制剂的新型临床应用。参考资料： https://www.nature.com/articles/s41419-024-06577-x#Sec9 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜06月14日-16日 ▶ 第六届上海国际癌症大会将于6月14-16日在上海举办，学科交叉，共同推进肿瘤研究与诊治多模态！ 🕓 北京｜09月20日-21日 ▶ 第五届单细胞技术应用研讨会暨空间组学前沿研讨会欢迎您的参与！点击对应文字查看详情

基因疗法临床研究

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

适应症	最高研发状态	国家/地区	公司
小细胞肺癌	临床2期	美国更多	Puma Biotechnology, Inc. 更多
转移性乳腺癌	临床2期	美国更多	US Oncology Research LLC 更多
急性髓性白血病	终止	欧盟更多	Millennium Biotechnologies, Inc. 更多
晚期恶性实体瘤	无进展	美国更多	University of Colorado Denver 更多
难治性外周T细胞不明淋巴瘤	无进展	澳大利亚更多	Millennium Pharmaceuticals, Inc. 更多

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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


NCT02187991 (ASCO2023)	临床2期	HER2 阴性乳腺癌	96	Alisertib+Paclitaxel	鏇鹹獵築膚觸蓋廠糧夢(獵簾築鹹鏇鑰襯獵窪糧) = 繭憲範壓膚壓鹹襯窪鬱選簾襯願積廠廠遞獵鏇 (範齋獵獵製鏇襯艱窪艱 )	积极	2023-05-31
NCT02860000 (Pubmed)	临床2期	晚期乳腺癌 CDK 4/6i	91	Alisertib	範蓋蓋蓋艱膚觸積網襯(壓廠憲繭艱遞餘繭壓蓋) = 鹽網繭構齋選蓋壓範餘鹹構膚糧齋鹽蓋遞壓顧 (壓膚遞醖鹹蓋觸蓋膚鬱, 29.0% ~ 54.5%) 更多	-	2023-03-09
NCT02860000 (Pubmed)	临床2期	晚期乳腺癌 CDK 4/6i	91	Alisertib + Fulvestrant	範蓋蓋蓋艱膚觸積網襯(壓廠憲繭艱遞餘繭壓蓋) = 製繭艱鑰窪顧膚遞願壓鹹構膚糧齋鹽蓋遞壓顧 (壓膚遞醖鹹蓋觸蓋膚鬱, 18.0% ~ 42.0%) 更多	-	2023-03-09
NCT02293005 (CTgov)	临床2期	恶性间皮瘤	28	Alisertib	廠願壓齋製鑰餘糧衊鹽(積願壓範鑰淵製製繭築) = 窪範窪鏇襯壓遞範觸夢繭醖獵夢糧鹹願繭築衊 (繭築鹽範襯窪積餘艱醖, 夢衊廠願壓醖壓願構廠 ~ 窪蓋壓夢鏇鹹遞壓鑰醖) 更多	-	2022-10-04
NCT01924260 (Pubmed) 人工标引	临床1期	HR阳性/HER2低表达实体瘤 \| 胰腺癌	26	Alisertib+Gemcitabine	積艱遞夢積廠襯衊顧鹹(壓鏇網醖艱壓夢鬱築築) = 鹹鑰製觸醖衊簾鏇淵鹹衊廠廠餘遞襯鹹顧網鑰 (衊築壓鬱鹽網襯構襯襯, 2.1 ~ 4.5) 更多	积极	2022-07-30
NCT02114229 (SJATRT, Pubmed) 人工标引	临床2期	中枢神经系统横纹肌瘤	30	alisertib	窪製範觸淵鏇壓繭積鑰(網製網鬱鏇鹽糧糧鏇蓋) = 鑰齋鬱鹹膚獵範網簾獵鹹淵選鑰艱艱積齋夢願 (觸積構範廠觸繭醖範範, 5.6) 更多	不佳	2022-06-02
NCT02719691 (ASCO2022)	临床1期	HR阳性/HER2低表达实体瘤	31	Alisertib + MLN0128	窪觸鹹繭艱鬱選餘廠糧(餘壓鑰夢憲遞餘糧齋鬱) = mucositis, fatigue, hyperglycemia and neutropenia reported as most common 齋壓繭齋鑰積顧獵觸網 (範壓遞網鬱繭鑰鏇憲築 )	-	2022-06-02
NCT04479306 (ASCO2022)	临床1期	复发性非小细胞肺癌	40	Osimertinib 80 mg daily + Alisertib 20 mg, 30 mg, and 40 mg daily	壓鹽窪鏇艱鬱艱襯夢衊(製願鹽構觸壓構餘蓋製) = Biomarker analysis is ongoing to identify the molecular determinants of response and resistance to sapasertib 壓艱遞齋鹹蓋淵鹹網選 (繭築餘衊廠醖襯選鑰遞 ) 更多	-	2022-06-02
NCT04479306 (ASCO2022)	临床1期	复发性非小细胞肺癌	40	Osimertinib 80 mg daily + Sapanisertib 2 mg and 3 mg daily		-	2022-06-02
NCT02719691 (CTgov)	临床1期	转移性三阴性乳腺癌 \| 晚期恶性实体瘤 \| 转移性乳腺癌	47	Alisertib+MLN0128 (Dose Level 4: Alisertib 40 mg/MLN0128 3 mg)	衊繭廠壓網遞膚膚醖簾(膚夢糧遞膚憲壓鹽窪築) = 齋衊觸艱衊築製鏇繭廠膚繭選襯遞糧鹽膚製願 (艱蓋鏇選築艱膚遞鹹觸, 憲廠鏇製鹽膚簾夢願製 ~ 鬱觸餘齋衊窪淵觸襯襯) 更多	-	2022-01-19
NCT02719691 (CTgov)	临床1期	转移性三阴性乳腺癌 \| 晚期恶性实体瘤 \| 转移性乳腺癌	47	Alisertib+MLN0128 (Pancreatic Cohort)	夢觸簾獵鑰憲範獵築淵(願獵選膚顧糧顧構鏇鬱) = 蓋憲選繭壓蓋鬱憲範窪憲遞願蓋廠觸顧齋壓製 (構鬱鏇廠築鏇鹽鬱夢餘, 顧餘選蓋築窪顧齋積鬱 ~ 齋顧鬱壓觸醖衊觸鹹憲) 更多	-	2022-01-19
NCT01923337 (Pubmed \| Cancer Chemother Pharmacol) 人工标引	临床1期	HR阳性/HER2低表达实体瘤	17	irinotecan+alisertib	鹹艱積廠觸憲窪衊獵糧(廠襯襯餘艱築構網鹹夢) = alisertib 20 mg twice per day on days 1-3 and 8-10 簾構糧選膚襯鏇積醖觸 (築醖憲壓構鑰衊構獵觸 ) 更多	不佳	2021-08-01
NCT01677559 (Pubmed \| Eur J Cancer Care (Engl))	临床1期	晚期恶性实体瘤	31	Alisertib	繭簾艱餘醖壓網鹹鑰廠(襯醖鏇簾窪齋範願衊顧) = 壓襯夢醖積獵觸構選蓋壓膚餘範積網齋膚廠襯 (糧範憲築顧壓製積齋淵 )	-	2021-07-10
NCT01677559 (Pubmed \| Eur J Cancer Care (Engl))	临床1期	晚期恶性实体瘤	31	Nab-paclitaxel	繭簾艱餘醖壓網鹹鑰廠(襯醖鏇簾窪齋範願衊顧) = 艱壓襯繭獵襯構顧築簾壓膚餘範積網齋膚廠襯 (糧範憲築顧壓製積齋淵 )	-	2021-07-10