伯舒替尼(Bosutinib Monohydrate) - 药物靶点：Bcr-Abl x SRC_在研适应症：费城染色体阳性慢性粒细胞白血病，加速期慢性骨髄性白血病，急性转化期慢性粒细胞性白血病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile、BOSUTINIB、Bosutinib Hydrate

+ [9]

靶点

Bcr-Abl x SRC

作用机制

Bcr-Abl抑制剂(bcr-abl酪氨酸激酶抑制剂)、SRC抑制剂(酪氨酸蛋白激酶SRC抑制剂)

治疗领域

肿瘤血液及淋巴系统疾病神经系统疾病+ [2]

在研适应症

费城染色体阳性慢性粒细胞白血病加速期慢性骨髄性白血病急性转化期慢性粒细胞性白血病+ [1]

非在研适应症

急性肾损伤晚期乳腺癌晚期胆道癌+ [16]

原研机构

Pfizer Inc.

在研机构

Pfizer Inc.PF Prism CVPfizer Europe MA EEIG

+ [1]

非在研机构

Wyeth AB

Roche Farma SA

Excella GmbH

最高研发阶段批准上市

首次获批日期

美国 (2012-09-04),

费城染色体阳性慢性粒细胞白血病

最高研发阶段(中国)终止

特殊审评特殊审批 (中国)、孤儿药 (日本)、加速批准 (美国)

登录后查看首次获批时间轴

结构

分子式C26H31Cl2N5O4

InChIKeyBXPOSPOKHGNMEP-UHFFFAOYSA-N

CAS号918639-08-4

查看全部结构式(2)

关联

88

项与伯舒替尼相关的临床试验

NCT06297161 / Not yet recruitingN/A

Post Marketing Surveillance Study to Observe Safety and Effectiveness of BOSULIF

The purpose of this study is to look at how safe and effective is bosulif in routine clinical practice.
This study is seeking for participants who are:
Adult Patients who are just confirmed to have Chronic Myeloid Leukemia (CML) defined in Local Product Document (LPD). CML is a type of cancer that starts in the blood-forming cells of the bone marrow and invades the blood. LPD explains what a medicine's benefits and problems are. LPD also explains how to use the medicine correctly in Korea.
willing to take part in the study after being informed about the study. All participants in this study will receive bosulif. All participants who have entered this study should meet the usual prescribing criteria for bosulif as per the LPD. The participants will be treated with bosulif under routine clinical practice in Korea.
The study will look at the experiences of people receiving the study medicine. This will help to see if the study medicine is safe and effective.
In this study all treatment and checking of the patients will be done as per the study doctor. The study can be performed in Korean health care centers where bosulif is prescribed to treat CML after the patients have agreed to take part in the study.

开始日期2024-03-01

申办/合作机构

Pfizer Inc.

NCT04655391 / Withdrawn临床1期IIT

A Pilot/Phase 1b Study of Glasdegib-Based Treatment Combinations in Adult Patients With Relapsed AML Post Allogeneic Hematopoietic Cell Transplantation

This phase Ib trial evaluates the best dose and effect of glasdegib in combination with venetoclax and decitabine, or gilteritinib, bosutinib, ivosidenib, or enasidenib in treating patients with acute myeloid leukemia that has come back (relapsed) after stem cell transplantation. Chemotherapy drugs, such as venetoclax and decitabine, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Glasdegib, bosutinib, ivosidenib, and enasidenib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Glasdegib inhibits the Sonic the Hedgehog gene. Venetoclax inhibits BCL-2 gene. Bosutinib is a tyrosine kinase inhibitor that inhibits BCR-ABL gene fusion. Ivosidenib inhibits isocitrate dehydrogenase-1 gene or IDH-1. Enasidenib inhibits isocitrate dehydrogenase-2 gene or IDH-2. This study involves an individualized approach that may allow doctors and researchers to more accurately predict which treatment plan works best for patients with relapsed acute myeloid leukemia.

开始日期2022-06-25

申办/合作机构

City of Hope National Medical Center

[+1]

JPRN-jRCT2051220002 / Not yet recruiting临床2期

Phase 1/2 Study of Bosutinib in Patients with Amyotrophic Lateral Sclerosis (ALS)

开始日期2022-05-22

申办/合作机构-

100 项与伯舒替尼相关的临床结果

登录后查看更多信息

100 项与伯舒替尼相关的转化医学

登录后查看更多信息

100 项与伯舒替尼相关的专利（医药）

登录后查看更多信息

702

项与伯舒替尼相关的文献（医药）

2024-02-23·Blood

Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: The role of kinase type and SH3 domain.

Article

作者: Inge van Outersterp ; Sarah K Tasian ; Caitlin Ej Reichert ; Aurélie Boeree ; Hester A de Groot-Kruseman ; Gabriele Escherich ; Judith M Boer ; Monique L den Boer

Acute lymphoblastic leukemia (ALL) with fusions of ABL-class tyrosine kinase genes other than BCR::ABL1 occurs in approximately 3% of children with ALL. The tyrosine kinase genes involved in this BCR::ABL1-like (Ph-like) subtype include ABL1, PDGFRB, ABL2, and CSF1R, which each have up to ten described partner genes. ABL-class ALL resembles BCR::ABL1-positive ALL by a similar gene expression profile, a poor response to chemotherapy, and sensitivity to tyrosine kinase inhibitors (TKIs). There is a lack of comprehensive data regarding TKI sensitivity for the heterogeneous group of ABL-class ALL. We observed variability in TKI sensitivity both within and amongst each ABL-class tyrosine kinase gene subgroup. We showed that ALL samples with fusions of any of the four tyrosine kinase genes were relatively sensitive to imatinib. In contrast, PDGFRB-fused ALL samples were less sensitive to dasatinib and bosutinib. Variation in ex vivo TKI response within the subset of samples with the same ABL-class tyrosine kinase gene was not associated with ALL immunophenotype, 5' fusion partner, the presence or absence of the Src-homology-2/3 domains, or deletions of IKZF1, PAX5, or CDKN2A/B. In conclusion, the tyrosine kinase gene involved in ABL-class ALL is the main determinant for TKI sensitivity and is relevant for specific TKI selection.

2024-02-23·BMC pharmacology & toxicology

Pharmacovigilance study of BCR-ABL1 tyrosine kinase inhibitors: a safety analysis of the FDA adverse event reporting system.

Article

作者: Dehua Zhao ; Xiaoqing Long ; Jisheng Wang

BACKGROUND:

With the increased use of BCR-ABL1 tyrosine kinase inhibitors (TKIs) in cancer patients, adverse events (AEs) have garnered considerable interest. We conducted this pharmacovigilance study to evaluate the AEs of BCR-ABL1 TKIs in cancer patients using the Food and Drug Administration Adverse Event Reporting System (FAERS) database.

METHODS:

To query AE reports from the FAERS database, we used OpenVigil 2.1. Descriptive analysis was then employed to describe the characteristics of TKIs-associated AE reports. We also utilized the disproportionality analysis to detect safety signals by calculating the proportional reporting ratio (PRR) and reporting odds ratios (ROR).

RESULTS:

From the FAERS database, a total of 85,989 AE reports were retrieved, with 3,080 significant AE signals identified. Specifically, imatinib, nilotinib, dasatinib, bosutinib, and ponatinib had significant AE signals of 1,058, 813, 232, 186, and 791, respectively. These significant signals were further categorized into 26 system organ classes (SOCs). The AE signals of imatinib and ponatinib were primarily associated with general disorders and administration site conditions. On the other hand, nilotinib, dasatinib, and bosutinib were mainly linked to investigations, respiratory, thoracic and mediastinal disorders, and gastrointestinal disorders, respectively. Notably, new signals of 245, 278, 47, 55, and 253 were observed in imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, respectively.

CONCLUSIONS:

The results of this study demonstrated that AE signals differ among the five BCR-ABL1 TKIs. Furthermore, each BCR-ABL1 TKI displayed several new signals. These findings provide valuable information for clinicians aiming to reduce the risk of AEs during BCR-ABL1 TKI treatment.

2024-02-08·Nature communications

UPP1 promotes lung adenocarcinoma progression through the induction of an immunosuppressive microenvironment.

Article

作者: Yin Li ; Manling Jiang ; Ling Aye ; Li Luo ; Yong Zhang ; Fengkai Xu ; Yongqi Wei ; Dan Peng ; Xiang He ; Jie Gu ; Xiaofang Yu ; Guoping Li ; Di Ge ; Chunlai Lu

The complexity of the tumor microenvironment (TME) is a crucial factor in lung adenocarcinoma (LUAD) progression. To gain deeper insights into molecular mechanisms of LUAD, we perform an integrative single-cell RNA sequencing (scRNA-seq) data analysis of 377,574 cells from 117 LUAD patient samples. By linking scRNA-seq data with bulk gene expression data, we identify a cluster of prognostic-related UPP1^high tumor cells. These cells, primarily situated at the invasive front of tumors, display a stronger association with the immunosuppressive components in the TME. Our cytokine array analysis reveals that the upregulation of UPP1 in tumor cells leads to the increased release of various immunosuppressive cytokines, with TGF-β1 being particularly prominent. Furthermore, this UPP1 upregulation also elevates the expression of PD-L1 through the PI3K/AKT/mTOR pathway, which contributes to the suppression of CD8 + T cells. Cytometry by time-of-flight (CyTOF) analysis provides additional evidence of the role of UPP1 in shaping the immunosuppressive nature of the TME. Using patient-derived organoids (PDOs), we discover that UPP1^high tumors exhibit relatively increased sensitivity to Bosutinib and Dasatinib. Collectively, our study highlights the immunosuppressive role of UPP1 in LUAD, and these findings may provide insights into the molecular features of LUAD and facilitate the development of personalized treatment strategies.

43

项与伯舒替尼相关的新闻（医药）

2024-02-29

·Pharmaceutical Technology

Every Cure receives ARPA-H grant for drug repurposing

The funding will support the development of an AI-powered platform. Credit: tilialucida / Shutterstock.com. Every Cure has received a three-year $48.3m contract from the US Advanced Research Projects Agency for Health (ARPA-H), marking a significant federal investment in drug repurposing. The funding will support the development of an artificial intelligence (AI)-powered platform, ML/AI-enabled Therapeutic Repurposing In eXtended uses (MATRIX) to enhance the potential of existing therapies to treat a broader range of diseases. Every Cure plans to leverage the ARPA-H funding to create an open-source drug repurposing database and build a portal for contributions from researchers, physicians and patients. The company also intends to publicly launch predictive efficacy scores for all therapies against all diseases and choose drugs to address neglected ailments. Traditional drug discovery and repurposing typically focus on one disease or drug, limiting the scope of potentially life-saving treatments. See Also: Biotechs heed political headwinds for drug pricing negotiations and partnerships Biotech execs say IRA is causing unintended effects for cancer drug development Every Cure’s approach will analyse a range of drugs and diseases simultaneously, quantifying the strength of links to identify promising new treatments. The MATRIX project builds on previous work by the National Center for Advancing Translational Sciences (NCATS) Biomedical Data Translator Program. Last year, Every Cure collaborated with NCATS-funded investigator David Koslicki at Penn State University, and other Translator Program members to create pilot rankings for all 3,000 drugs approved by the FDA for all human diseases. By using new AI techniques to assess worldwide biomedical knowledge, the company aims to detect 100 potential therapy opportunities over the five years to 2028. It plans to progress 25 of them into further research, including studies. Early promising leads include arginine to treat sickle cell disease, folinic acid for autism spectrum disorder and bosutinib for amyotrophic lateral sclerosis. The latest development comes after Every Cure secured funding from the Chan Zuckerberg Initiative, the Elevate Prize Foundation, Flagship Pioneering and Lyda Hill Philanthropies. Every Cure co-founder and CEO Grant Mitchell stated: “Society’s greatest life-saving resource is the trove of medicines we already have. Leveraging a systematic, disease-agnostic approach for drug repurposing enables us to rapidly unlock new diseases they can treat and confirm the validity of AI discoveries in patients. “We’re excited to make our research tools available to the public, advancing data-driven discovery and offering hope to patients worldwide.”

2024-02-28

·PRNewswire

Every Cure to Receive $48.3M from ARPA-H to Develop AI-Driven Platform to Revolutionize Future of Drug Development and Repurposing

ARPA-H contract will supercharge Every Cure's work to identify existing medicines that can be repurposed to treat currently untreated diseases. Initial progress utilizing a pilot version of the AI platform and stakeholder engagement has led to the identification of potential treatments for sickle cell disease, ALS, and autism spectrum disorder. NEW YORK, Feb. 28, 2024 /PRNewswire/ -- Every Cure, a nonprofit on a mission to save lives by repurposing existing medicines, announced today significant funding from the Advanced Research Projects Agency for Health (ARPA-H). The three-year, $48.3 million contract was unveiled at the White House this evening and represents a substantial federal investment in drug repurposing. It will accelerate Every Cure's mission to unlock the full potential of existing drugs to treat more diseases through the development of an AI-powered platform, called ML/AI-enabled Therapeutic Repurposing In eXtended uses (MATRIX). "I'm alive and in remission from my rare disease thanks to a repurposed drug that I discovered. While Ozempic is a recent example of drug repurposing, the concept is not new," said David Fajgenbaum, MD, MBA, MSc, Co-Founder and President of Every Cure and Associate Professor of Medicine at the University of Pennsylvania. "Through Every Cure, we are working tirelessly to unlock the full potential of FDA-approved drugs to treat many more diseases. This funding comes at a pivotal time, allowing us to scale our approach across diseases to pioneer new treatments for millions of people around the world without options." Established in 2022 by the Biden-Harris Administration, ARPA-H is a new federal agency that aims to advance high-potential, high-impact biomedical and health research that cannot be readily accomplished through traditional research or commercial activity. The ARPA-H funding will enable Every Cure to: Develop an open-source drug repurposing database. Establish a portal for physicians, researchers, and patients to contribute repurposing ideas. Publicly release predictive efficacy scores for all drugs against all diseases. Select numerous drugs for advancement to address neglected diseases in neglected populations. "Rather than the current, one-step-at-a-time drug discovery process, we have an opportunity to use artificial intelligence to rapidly understand how already approved drugs could be effective against other diseases," said ARPA-H Director Renee Wegrzyn, Ph.D. "Through this project, we hope to unlock the full potential of existing medicines to quickly and safely bring therapies to people with rare or currently untreatable diseases." New drug discovery and traditional drug repurposing begins with one disease or one drug and seeks to identify the most promising matches for it, thus limiting the potential for finding the most promising life-saving treatments across all opportunities. Every Cure looks across all drugs and all diseases simultaneously and then quantifies the strength of those connections to find the most promising new treatments to help patients. The MATRIX project builds upon previous work led by the National Center for Advancing Translational Sciences (NCATS) Biomedical Data Translator Program to structure biomedical data and perform targeted queries. In 2023, Every Cure partnered with an NCATS funded investigator at Penn State University, David Koslicki and other members of the Translator Program, to generate pilot rankings for all 3,000 FDA-approved drugs to treat all human diseases. One of the top hits was for a drug that was recently used to save a patient's life. By leveraging novel AI techniques to analyze the world's biomedical knowledge, Every Cure is working to identify 100 potential treatment opportunities in the next five years and advance 25 into further research, including clinical trials. Promising early leads include arginine for sickle cell disease, folinic acid for autism spectrum disorder, and bosutinib for ALS. Within the last year, Every Cure has received funding from leading organizations such as the Chan Zuckerberg Initiative, Flagship Pioneering, Elevate Prize Foundation, and Lyda Hill Philanthropies. With government and philanthropic support, Every Cure is seeking partnerships with healthcare organizations that may be open to sharing data and well-positioned to bring cures to patients who need them most. " Society's greatest life-saving resource is the trove of medicines we already have. Leveraging a systematic, disease agnostic approach for drug repurposing enables us to rapidly unlock new diseases they can treat and confirm the validity of AI discoveries in patients," says Grant Mitchell, MD, MBA, Co-Founder & CEO of Every Cure. "We're excited to make our research tools available to the public, advancing data-driven discovery and offering hope to patients worldwide." For more information or to express interest in partnering with Every Cure, please contact Brent Shaw ([email protected]) About Every Cure Every Cure is a nonprofit organization dedicated to unlocking the full potential of every existing medicine to treat every disease possible. Repurposing existing drugs is the fastest and most efficient way to treat diseases with the greatest return on investment for saving lives. However, systemic barriers impede repurposing, so patients suffer while potential treatments are not fully utilized. Every Cure overcomes these barriers to systematically identify and advance promising repurposing opportunities and save lives. Every Cure is taking a revolutionary and disruptive approach to overcome these systemic barriers by developing a comprehensive, open-source data engine to generate predictive efficacy scores for all 3,000 drugs against all 12,000 diseases and rapidly advance treatments to patients. In partnership with academia, industry, and government, Every Cure is integrating proprietary and public data into a comprehensive dataset, optimizing AI ranking algorithms, validating the most promising drug-disease matches, performing clinical trials, and works to ensure optimal and equitable access to effective therapies. For more information, please visit EveryCure.org or connect with us on Twitter, LinkedIn, Facebook, and Instagram. SOURCE Every Cure

2024-02-01

·药融圈

辉瑞公布2023年业绩：营收同比下降42%，净利润同比下降93%

▲3月7-8日成都生物医药创新者峰会 · 点击立即报名注：本文不构成任何投资意见和建议，以官方/公司公告为准；本文仅作医疗健康相关药物介绍，非治疗方案推荐（若涉及），不代表平台立场。任何文章转载需得到授权。1月30日，辉瑞公布了2023年四季度和全年业绩。全年营收584.96亿美元，同比下降42%，其中四季度营收142.49亿美元，同比下降41%。2023年实现净利润21.19亿美元，同比下降93%，其中四季度净亏损33.69亿美元，是全年业绩拉胯的主要原因。根据辉瑞官方的解释，业绩下滑的主要原因是新冠疫苗Comirnaty和抗新冠病毒药Paxlovid销售额大幅萎缩41%，如果排除这两大产品，则营收反而同比增长7%。而利润下降，业是跟两个新冠药物有关。辉瑞旗下拥有4大业务部门，分别为普药、专科药和抗肿瘤和创新服务。普药部门全年营收305.89亿美元，同比下降58%；专科药部门全年营收149.70亿美元，同比增长8%；抗肿瘤业务营收116.27亿美元，同比下降4%；年初新设立的创新服务部门营收达13.1亿美元，同比下降2%。值得一提的是，辉瑞还从事CDMO和原料药供应的生意。普药部门方面，新冠疫苗营收112.20亿美元，同比下降70%，虽然销售额大幅下滑，但并没有出现新冠疫苗“没人打了”的现象；阿哌沙班销售额67.47亿美元，同比增长4%；肺炎疫苗家族营收64.40亿美元，同比增长2%；P药卖出12.97亿美元，同比下降93%；口服CGRP抑制剂Rimegepant销售比较抢眼，达9.28亿美元，相比2022年的2.13亿美元翻了4倍有余；呼吸道合胞病毒(RSV)二价疫苗 Abrysvo首年上市就卖出8.90亿美元，表现秒杀90%以上的药物；其余的管线产品基本是辉瑞的成熟产品，销售额主要以萎缩为主。专科药业务方面，罕见病药物氯苯唑酸(Vyndaqel)堪称吸金神器，2023年为辉瑞奉献了33.21亿美元的销售额，同比增长36%；托法替布因为速释制剂专利悬崖，销售额下降5%至17.03亿美元；老药依拉西普销售额8.3亿美元，同比下降17%；抗生素舒普深居然仍有7.57亿美元的销售额（同比下降4%），估计过半来自中国；注射用头孢他啶阿维巴坦钠(思福妥)卖出5.11亿美元，同比上涨24%，值得一提的是，该产品是2010年以来，首个销售额突破5亿美元的头孢类抗生素；其余的管线产品基本是辉瑞的成熟产品，销售额没有太大变化，更多产品2023和2022年销售额如下表所示。抗肿瘤业务方面，帕博西利全年营收47.53亿美元，同比下降7%；恩扎鲁胺营收11.91亿美元，同比下降1%；阿西替尼销售额10.36亿美元，同比增长3%；博舒替尼营收6.45亿美元，同比增长12%……虽然辉瑞抗肿瘤管线产品较多，但严重缺乏超级重磅炸弹，而且多个产品面临专利悬崖业绩压力较大。整体而言，辉瑞的管线缺乏足够的亮点，老产品、小产品较多，加之新冠药物逐渐转冷，业绩压力较大，2023年股价一直不“高”，最新市值仅有1551.6亿美元，远低于默沙东（3073.3亿美元）、强生(3836.2亿美元）、礼来（6123.0亿美元）、艾伯维（2894.6亿美元）等相似规模的美国制药巨头。版权声明：本文转自药事纵横，如不希望被转载的媒体或个人可与我们联系，我们将立即删除活动推荐 3月 • NDC x 2024新药创新者峰会关键词： ADC，改良型新药，小分子新药，GLP-1药物（点击下方图片查看详情）▼【关于药融圈】药融圈PRHub旨在帮助生物医药科技型企业进行品牌推广及商务拓展服务，针对客户的真实需求制定系统化解决方案，通过“翻译-降维-场景化”将客户的品牌信息以直白易懂的方式被公众知悉，同时在流量渠道覆盖100万+垂直用户基础上实现合作目的，帮助合作伙伴完成从品牌开始到商务为终的闭环营销服务。我们已经完成了数十场线下1000人规模的生物医药研发类会议，涵盖小分子新药，大分子新药，改良型新药，BD跨境交易等多个领域，服务了百余家上市/独角兽/生物技术/制药企业。

财报疫苗

100 项与伯舒替尼相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D09728	伯舒替尼	L01XE14	DB06616

研发状态

适应症	最高研发状态	国家/地区	公司
费城染色体阳性慢性粒细胞白血病	批准上市	日本更多	Pfizer Japan, Inc. 更多
慢性期慢性髓性白血病	临床3期	墨西哥更多	Pfizer Inc. 更多
局部晚期乳腺癌	终止	马来西亚更多	Pfizer Inc. 更多
晚期乳腺癌	终止	英国更多	Pfizer Inc. 更多
常染色体显性多囊肾病	无进展	斯洛伐克更多	Pfizer Inc. 更多

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT02130557 (BFORE, ASH2022) 人工标引	临床3期	费城染色体阳性慢性粒细胞白血病一线	536	Bosutinib	(選選膚廠鏇夢網簾鑰膚) = 觸築願糧遞廠壓顧構願艱獵繭廠壓鹹觸窪憲獵 (憲艱選顧襯網鹽壓膚觸, 40.7 ~ 52.6) 更多	优效	2022-11-15
				Imatinib	(選選膚廠鏇夢網簾鑰膚) = 壓構網廠選壓餘簾艱顧艱獵繭廠壓鹹觸窪憲獵 (憲艱選顧襯網鹽壓膚觸, 30.4 ~ 41.9) 更多
NCT03854903 (ASCO2023) 人工标引	临床1期	转移性HER2阴性乳腺癌 HR Positive \| HER2 Negative	18	Bosutinib + Palbociclib + Fulvestrant	(齋齋築糧襯構艱糧簾膚) = Most common AEs were G1/2 (9 pts) and G3/4 (7 pts) neutropenia (no neutropenic fever); G1 nausea (8 pts); G1/2 (12pts) and G3 (1pt) diarrhea; G1/2 rash (4 pts), and no G5 events. 鹹鹽夢廠衊積簾築簾窪 (蓋憲簾膚築膚獵艱選獵 ) 更多	积极	2023-05-31
NCT02130557 (BFORE, ASH2018) 人工标引	临床3期	费城染色体阳性慢性粒细胞白血病一线	536	Bosutinib (≥65 years)	(遞獵鑰鏇窪顧襯鹹糧構) = 鹹簾壓襯廠鑰餘艱醖鏇餘廠築鑰積繭廠窪構醖 (獵獵醖鹹築鏇憲鑰襯夢 ) 更多	积极	2018-11-29
				Bosutinib (<65 years)	(遞獵鑰鏇窪顧襯鹹糧構) = 憲艱齋簾膚齋鑰餘憲淵餘廠築鑰積繭廠窪構醖 (獵獵醖鹹築鏇憲鑰襯夢 ) 更多
NCT02130557 (BFORE, Pubmed) 人工标引	临床3期	慢性期慢性髓性白血病一线	533	Bosutinib	鏇窪遞觸襯觸鬱繭窪淵(憲製顧製網範蓋鹽鑰構) = 醖選鹹積醖遞鑰醖壓製餘繭選蓋製憲窪鬱憲簾 (膚襯選獵鏇願鏇壓齋製 ) 更多	优效	2022-05-28
				imatinib	鏇窪遞觸襯觸鬱繭窪淵(憲製顧製網範蓋鹽鑰構) = 淵繭壓衊願鏇範糧鹽鹹餘繭選蓋製憲窪鬱憲簾 (膚襯選獵鏇願鏇壓齋製 ) 更多
NCT02311998 (EHA2020) 人工标引	临床1/2期	费城染色体阳性急性淋巴细胞白血病复发 \| 急性转化期慢性粒细胞性白血病	18	Inotuzumab ozogamicin+Bosutinib	(繭觸壓築簾鬱糧顧網鏇) = rash (n=3), reversible ALT elevation (n=1) and hyponatremia (n=1). No pts had veno-occlusive disease. 獵淵遞鏇窪積製願憲夢 (憲簾鬱襯築窪鬱衊鬱鹹 ) 更多	积极	2020-05-14
NCT04258943 (ITCC-054/COG-AAML1921, ASCO2023) 人工标引	临床1/2期	费城染色体阳性慢性粒细胞白血病一线	24	Bosutinib	(鏇選顧遞觸範願構簾遞) = non-hematological (AEs) were diarrhea (n = 16, Grade (Gr) ≤ 2 = 13), abdominal pain (n = 10, Gr ≤ 2 = 10), and nausea/vomiting (n = 8/8, Gr ≤ 2 = 7/8). hematological AEs included platelet count decrease (n = 11, Gr ≤ 2 = 5), and anemia (n = 10, Gr ≤ 2 = 4). 齋製窪艱積襯觸遞餘鹽 (壓壓糧願範膚醖構鑰範 )	积极	2023-05-31
NCT00574873 (BELA, ESMO2018) 人工标引	临床3期	慢性期慢性髓性白血病一线	502	bosutinib (Indian pts)	(積夢夢壓鏇壓鬱鬱襯壓) = 構醖窪廠憲醖觸鹽膚簾鹹夢範鑰選選壓鏇憲憲 (網蓋壓憲鹽遞淵簾顧鏇, 54–90) 更多	积极	2018-10-20
				imatinib (Indian pts)	(積夢夢壓鏇壓鬱鬱襯壓) = 選築蓋鹹齋鏇選艱憲繭鹹夢範鑰選選壓鏇憲憲 (網蓋壓憲鹽遞淵簾顧鏇, 74–99) 更多
NCT02228382 (BYOND, ASCO2022) 人工标引	临床4期	费城染色体阳性慢性粒细胞白血病末线	-	Bosutinib (Resistant pts)	(觸齋壓蓋蓋鑰觸積廠願) = 願網製夢餘繭鑰艱淵顧醖襯鑰窪膚構簾醖壓簾 (鑰壓夢醖範壓餘觸醖鹽, 4.0 ~ 45.6) 更多	积极	2022-06-02
				Bosutinib (Intolerant pts)	(觸齋壓蓋蓋鑰觸積廠願) = 構鬱膚鑰願鏇憲範觸艱醖襯鑰窪膚構簾醖壓簾 (鑰壓夢醖範壓餘觸醖鹽, 37.4 ~ 74.5) 更多
NCT00261846 (Pubmed) 人工标引	临床1/2期	白血病 Ph positive	570	bosutinib (dose-reduced to bosutinib 400 mg/day)	(齋繭願願築繭蓋壓膚餘) = The incidence of treatment-emergent AEs was lower after dose reductions, particularly for gastrointestinal events. 餘遞鬱餘獵膚願選構鏇 (餘製鹽膚範窪繭網齋製 )	积极	2021-12-01
				bosutinib (without reduction to 300 mg/day)
NCT03128411 (Pubmed \| Int J Hematol) 人工标引	临床2期	慢性期慢性髓性白血病一线	60	bosutinib	(簾蓋膚憲鬱繭願構繭鹽) = 願憲築窪膚築簾夢夢壓遞構艱鏇鬱艱窪鹽夢鑰 (鬱鑰壓壓選選蓋衊簾鑰, 44.4 ~ 65.6)	积极	2020-07-01