A Phase I/II Non-Randomized, Open-Label, Dose-Finding Study of Ispinesib (SB-715992) Followed By a Fixed-Dose Study in Chemotherapy-Naïve Patients With Metastatic Breast Cancer (MBC).

The Phase I portion was a dose-escalation study designed to assess safety and tolerability in patients with metastatic breast cancer. Phase II was intended to measure response rate in patients with metastatic breast cancer but did not enroll because the Phase I portion was halted prior to Maximum Tolerated Dose (MTD) determination.

开始日期2007-12-01

申办/合作机构

Cytokinetics, Inc.

NCT00363272

/ Completed临床1期IIT

A PHASE 1 STUDY OF ISPINESIB (SB-715992) IN PEDIATRIC PATIENTS WITH RELAPSED OR REFRACTORY SOLID TUMORS

This phase I trial is studying the side effects and best dose of ispinesib in treating young patients with relapsed or refractory solid tumors or lymphoma. Drugs used in chemotherapy, such as ispinesib, work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing

开始日期2006-06-01

申办/合作机构

National Cancer Institute

NCT00354250

/ Completed临床2期IIT

A Phase II Study of SB-715992 (NSC-727990, IND-70273) in Advanced Renal Cell Cancer

This phase II trial is studying how well ispinesib works in treating patients with metastatic or unresectable kidney cancer. Ispinesib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

开始日期2006-05-01

申办/合作机构

National Cancer Institute

100 项与伊匹尼塞相关的临床结果

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100 项与伊匹尼塞相关的转化医学

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100 项与伊匹尼塞相关的专利（医药）

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项与伊匹尼塞相关的文献（医药）

2024-12-01·iScience

Resistance to spindle inhibitors in glioblastoma depends on STAT3 and therapy induced senescence

Article

作者: Dovas, Athanassios ; Zarco, Natanael ; Nagaiah, Naveen K H ; Kenchappa, Rajappa S ; Sims, Peter A ; Haddock, Ashley ; Meyer, Christian T ; de Araujo Farias, Virginea ; Rosenfeld, Steven S ; Nagaiah, Naveen KH. ; Hambardzumyan, Dolores ; Canoll, Peter

While mitotic spindle inhibitors specifically kill proliferating tumor cells without the toxicities of microtubule poisons, resistance has limited their clinical utility. Treating glioblastomas with the spindle inhibitors ispinesib, alisertib, or volasertib creates a subpopulation of therapy induced senescent cells that resist these drugs by relying upon the anti-apoptotic and metabolic effects of activated STAT3. Furthermore, these senescent cells expand the repertoire of cells resistant to these drugs by secreting an array of factors, including TGFβ, which induce proliferating cells to exit mitosis and become quiescent-a state that also resists spindle inhibitors. Targeting STAT3 restores sensitivity to each of these drugs by depleting the senescent subpopulation and inducing quiescent cells to enter the mitotic cycle. These results support a therapeutic strategy of targeting STAT3-dependent therapy-induced senescence to enhance the efficacy of spindle inhibitors for the treatment of glioblastoma.

2024-05-01·Cell reports

Multiplexed single-cell lineage tracing of mitotic kinesin inhibitor resistance in glioblastoma

Article

作者: Canoll, Peter ; Banu, Matei A ; Sims, Peter A ; Cheng, Yim Ling ; Zhao, Wenting ; Rosenfeld, Steven S

Glioblastoma (GBM) is a deadly brain tumor, and the kinesin motor KIF11 is an attractive therapeutic target with roles in proliferation and invasion. Resistance to KIF11 inhibitors, which has mainly been studied in animal models, presents significant challenges. We use lineage-tracing barcodes and single-cell RNA sequencing to analyze resistance in patient-derived GBM neurospheres treated with ispinesib, a potent KIF11 inhibitor. Similar to GBM progression in patients, untreated cells lose their neural lineage identity and become mesenchymal, which is associated with poor prognosis. Conversely, cells subjected to long-term ispinesib treatment exhibit a proneural phenotype. We generate patient-derived xenografts and show that ispinesib-resistant cells form less aggressive tumors in vivo, even in the absence of drug. Moreover, treatment of human ex vivo GBM slices with ispinesib demonstrates phenotypic alignment with in vitro responses, underscoring the clinical relevance of our findings. Finally, using retrospective lineage tracing, we identify drugs that are synergistic with ispinesib.

2024-04-23·ACS Omega

Development of Half-Sandwich Ru, Os, Rh, and Ir Complexes Bearing the Pyridine-2-ylmethanimine Bidentate Ligand Derived from 7-Chloroquinazolin-4(3H)-one with Enhanced Antiproliferative Activity

Article

作者: Makal, Anna ; Plażuk, Damian ; Łomzik, Michał ; Błauż, Andrzej ; Tchoń, Daniel ; Rychlik, Błażej

Kinesin spindle protein (KSP) inhibitors are one of the most promising anticancer agents developed in recent years. Herein, we report the synthesis of ispinesib-core pyridine derivative conjugates, which are potent KSP inhibitors, with half-sandwich complexes of ruthenium, osmium, rhodium, and iridium. Conjugation of 7-chloroquinazolin-4(3H)-one with the pyridine-2-ylmethylimine group and the organometallic moiety resulted in up to a 36-fold increased cytotoxicity with IC₅₀ values in the micromolar and nanomolar range also toward drug-resistant cells. All studied conjugates increased the percentage of cells in the G₂/M phase, simultaneously decreasing the number of cells in the G₁/G₀ phase, suggesting mitotic arrest. Additionally, ruthenium derivatives were able to generate reactive oxygen species (ROS); however, no significant influence of the organometallic moiety on KSP inhibition was observed, which suggests that conjugation of a KSP inhibitor with the organometallic moiety modulates its mechanism of action.

项与伊匹尼塞相关的新闻（医药）

2024-05-15

·精准药物

JMC | 基于ATTEC技术开发DDR1降解剂

2024年5月7日，药物化学权威期刊Journal of Medicinal Chemistry在线发表了中国科学院上海有机化学研究所丁克教授和王震研究员团队的最新研究成果“Discovery of LLC355 as an Autophagy-Tethering Compound for the Degradation of Discoidin Domain Receptor 1”。该研究基于自噬小体绑定化合物(ATTEC)技术开发了一类降解DDR1的降解剂，代表性化合物LLC355在NCI-H23细胞中通过溶酶体介导的自噬途径有效降解DDR1。跨膜受体酪氨酸激酶Discoidin domain receptors（DDR1和DDR2）在细胞增殖和细胞分化等过程中发挥关键作用，是治疗癌症、纤维化疾病和炎症的潜在靶点。尽管一些选择性的DDR抑制剂和DDR1/2双靶点抑制剂在小鼠模型中展现出有希望的治疗效果，但目前尚无DDR抑制剂进入到临床研究阶段。已有研究表明除了DDR1的激酶功能，DDR1非酶结构域介导的功能在肿瘤的发生发展、转移和免疫排斥过程中发挥重要作用。因此，传统的DDR1抑制剂只能有效抑制DDR1的激酶功能，无法阻断DDR1非激酶结构域所介导的功能。目前需要探索新的方法来靶向DDR1的非酶结构域。与PROTAC类似，近年来发展起来的一种靶向蛋白质降解技术自噬小体绑定化合物(ATTEC)通过将靶蛋白招募至自噬关键蛋白LC3并最终经溶酶体途径诱导靶蛋白降解提供了一种潜在的策略。为了开发一类降解DDR1的ATTEC类降解剂，作者以高亲和力和选择性DDR1抑制剂作为靶蛋白配体，并通过Docking模拟了其与DDR1的结合模式。结果显示DDR1抑制剂化合物1的N-甲基哌嗪部分处于溶剂暴露区，是连接LC3配体的合适位点（图1）。在LC3配体部分，作者分别探索了已被成功用于ATTEC设计的GW5074和ispinesib。同时作者设计了合理的方案合成了一系列降解DDR1的ATTEC。图1 降解DDR1的ATTEC的设计首先，作者分析了这类ATTECs诱导DDR1降解的构效关系，化合物的DDR1降解效率在NCI-H23细胞中通过免疫印迹评估。结果显示以GW5074为LC3配体的ATTECs的降解效率相对较低，最有效的化合物10g在1 μM浓度下诱导60%的DDR1降解，在0.3 μM浓度下未观察到明显的DDR1降解。而以ispinesib为LC3配体的ATTECs的降解效率更高，10l − 10o在1 μM浓度下对DDR1的降解率超过70%。其中化合物10n (LLC355)的DDR1降解能力最强，在0.3 μM浓度下诱导40%的DDR1降解，而在1 μM浓度下诱导92%的DDR1降解。因此，作者以LLC355作为代表性化合物用于后续的研究。作者进一步分析了LLC355在NCI-H23细胞中诱导DDR1降解的效率。结果表明LLC355以剂量依赖的方式诱导DDR1降解，DC50 = 150.8 nM（图2A 和2B），但LLC355对DDR2的表达量没有明显影响（图2C）。此外，LLC355诱导DDR1降解呈时间依赖性，在24 h达到最大降解效率（图2D）。最后，作者还在两株胰腺癌ANC-1和MIA-PaCa-2细胞中观察到LLC355对DDR1降解（图2E）。这些结果充分证明了LLC355是一个有效的DDR1降解剂。图2 LLC355在肿瘤细胞中诱导DDR1降解为了进一步探究LLC355诱导DDR1降解的机制，作者通过qPCR分析了经LLC355处理后NCI-H23细胞中DDR1的mRNA的变化，结果表明在0.3 μM和1 μM两个浓度条件下均未观察到DDR1的mRNA水平的显著改变（图3A）。而在cycloheximide处理的NCI-H23细胞中，LLC355处理组DDR1的半衰期明显缩短（图3B）。为了验证LLC355是基于ATTEC的机制诱导了DDR1的降解，作者发现在自噬抑制剂bafilomycin A1和chloroquine处理的NCI-H23细胞中，LLC355诱导DDR1降解的效率被显著抑制（图3D）。而在自噬激动剂rapamycin处理的细胞中，LLC355诱导DDR1降解的效率被进一步增强（图3E）。这些结果共同表明了ATTEC化合物LLC355是通过溶酶体-自噬途径实现了对DDR1的降解。随后作者通过蛋白质组学分析探究了LLC355的选择性，经10 μM LLC355处理6小时的NCI-H23细胞虽然在Western blotting实验中观察到明显的DDR1降解，但在全蛋白质分析中并没观察到DDR1蛋白的显著改变。图3 LLC355通过溶酶体途径诱导DDR1降解最后，作者评估了LLC355诱导DDR1降解的细胞表型。Transwell实验显示LLC355在0.3μM浓度条件下显著抑制了NCI-H23细胞的迁移和侵袭，而DDR1抑制剂1无法产生明显的抗迁移效果（图4A）。进一步探究发现LLC355能够抑制EMT过程关键标志物N-cadherin（图4B）。此外，作者还探究了LLC355对细胞凋亡标志物cleaved-PARP的影响，结果显示0.3 μM LLC355对cleaved-PARP未产生影响，但1 μM LLC355能够导致NCI-H23细胞中cleaved-PARP水平的显著升高（图4C）。作者还通过集落形成实验评估了LLC355的抑瘤能力，结果显示DDR1抑制剂1和LLC355都能够明显抑制NCI-H23细胞的集落形成，但降解剂LLC355抑制集落形成能力优于DDR1抑制剂化合物1（图4D）。图4 LLC335抑制NCI-H23细胞的迁移、侵袭和集落形成原文链接：https://doi-org.libproxy1.nus.edu.sg/10.1021/acs.jmedchem.4c00162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↓

蛋白降解靶向嵌合体

2023-04-21

·SYNAPSE

着手淋巴瘤治疗领域，Vincerx Pharma展示自研ADC药物VIP924临床前数据

4月20日，Vincerx Pharma在2023年美国癌症研究协会（AACR）年会上展示了其自研药物VIP924的临床前数据。据Vincerx Pharma宣称，CXCR5是一个非常有潜力的药物靶点，用于开发治疗淋巴瘤患者的抗体-药物偶联物（antibody-drug conjugates，ADC）。淋巴瘤是起源于淋巴造血系统的恶性肿瘤，主要表现为无痛性淋巴结肿大，肝脾肿大，全身各组织器官均可受累。根据瘤细胞分为非霍奇金淋巴瘤（NHL）和霍奇金淋巴瘤（HL）两类。病理学特征在霍奇金淋巴瘤为瘤组织内含有淋巴细胞、嗜酸性粒细胞、浆细胞和特异性的里-斯（Reed-Steinberg）细胞，HL按照病理类型分为结节性富含淋巴细胞型和经典型，后者包括淋巴细胞为主型、结节硬化型、混合细胞型和淋巴细胞消减型。 NHL发病率远高于HL，是具有很强异质性的一组独立疾病的总和，病理上主要是分化程度不同的淋巴细胞、组织细胞或网状细胞，根据NHL的自然病程，可以归为三大临床类型，即高度侵袭性、侵袭性和惰性淋巴瘤。根据不同的淋巴细胞起源，可以分为B细胞、T细胞和NK细胞淋巴瘤。 VIP924由抗CXCR5的人源化单克隆抗体组成，该药物含有一个独特的肽序列，能被肿瘤相关的溶酶体蛋白酶legumain特异性裂解。在肿瘤细胞内，当legumain裂解时，活性载荷成分VIP716被释放。VIP716是一种新型的，高效且特异的纺锤体驱动蛋白（KSPi）抑制剂，通过被修饰为亲水的CellTrapper™分子，以减少药物膜渗透性，而降低药物的负面效应。这种修饰使VIP716在CXCR5+肿瘤细胞中的细胞质内积聚，以提供更大的疗效，并防止药物渗透到健康组织中，减少毒性。 Vincerx Pharma的数据显示：通过免疫组化法观察到CXCR5在新发和再发弥漫性大B细胞淋巴瘤（DLBCL）、滤泡性淋巴瘤（FL）、套细胞淋巴瘤（MCL）和慢性淋巴细胞白血病（CLL）样本中的高表达；而在健康组织中表达有限。 VIP924在不同的非霍奇金淋巴瘤细胞系中显示出卓越的体外细胞毒性，与其他偶联相同化学效应物的B细胞淋巴瘤靶向抗体，包括CD19-KSPi、CD22-KSPi和CD70-KSPi相比， VIP924（10mg/kg）在两种DLBCL衍生的动物肿瘤模型中产生了明显的肿瘤生长抑制作用：在一个低CXCR5表达的模型中为68%，在一个高CXCR5表达的模型中为87%。在两个VIP924治疗的动物模型中，动物存活时间均延长。在VIP924治疗的小鼠中没有观察到对药物体重的影响或任何不良反应。为了确定VIP924对较大规模肿瘤的疗效，在移植了HBL-1淋巴瘤细胞系的小鼠中，给予单次10mg/kg的VIP924剂量。3只小鼠中的2只观察到完全反应，在治疗第26天没有观察到可测量的肿瘤。24和48小时后，在肿瘤中检测到VIP924代谢物VIP716的积累，而在血浆中没有检测到。 KSP抑制导致有丝分裂停止，并形成特征性的单极纺锤体（monoasters）。与可渗透的小分子KSPi Ispinesib相比，VIP924治疗淋巴瘤细胞系中产生了更高的水平和更长的单体形成时间。 Vincerx公司首席执行官Ahmed Hamdy医学博士评论："我们很高兴能用我们最新的我们的生物标记平台继续推进ADC药物VIP924的研究。VIP924在一组淋巴瘤细胞系以及细胞系衍生和患者衍生的淋巴瘤小鼠模型中显示了有意义的临床前活性。最值得注意的是，植入淋巴瘤患者肿瘤细胞的小鼠模型在VIP924治疗后显示出明显的肿瘤生长抑制和生存期延长。在植入患者肿瘤细胞的小鼠模型（也称为PDX模型）中显示出药物活性有特别意义，因为PDX模型比细胞系的试验结果更能代表人类癌症的复杂性。" 参考资料：https://investors.vincerx.com/news-releases/news-release-details/vincerx-pharma-presents-preclinical-data-vip924-first-class

2023-04-20

·BioSpace

Vincerx Pharma Presents Preclinical Data on VIP924, a First-in-Class Antibody-Drug Conjugate (ADC), at the 2023 American Association for Cancer Research (AACR) Annual Meeting

PALO ALTO, Calif., April 19, 2023 (GLOBE NEWSWIRE) -- Vincerx Pharma Inc. (Nasdaq: VINC), a biopharmaceutical company aspiring to address the unmet medical needs of patients with cancer through paradigm-shifting therapeutics, today presented a poster of VIP924 preclinical data at the 2023 American Association for Cancer Research (AACR) Annual Meeting. VIP924 consists of an anti-CXCR5 humanized monoclonal antibody with a novel linker containing a unique peptide sequence specifically cleaved by legumain—a tumor-associated lysosomal protease. Inside the tumor cell, upon legumain cleavage, the active payload, VIP716, is released. VIP716 is a novel highly potent and selective kinesin spindle protein inhibitor (KSPi), which has been modified with a hydrophilic CellTrapper™ moiety to reduce membrane permeability without having a negative impact on efficient target binding. This modification allows for intracellular accumulation of VIP716 in CXCR5+ tumor cells, providing greater efficacy, and prevents cellular penetration into healthy tissues, reducing toxicity. “We are thrilled to continue advancing our bioconjugation platform with our newest ADC, VIP924,” said Ahmed Hamdy M.D., Chief Executive Officer of Vincerx. “At AACR, VIP924 showed meaningful preclinical activity in a panel of lymphoma cell lines and in cell line-derived and patient-derived lymphoma mouse models. Most notably, mouse models implanted with tumor cells from lymphoma patients demonstrated significant tumor growth inhibition and prolonged survival after VIP924 treatment. Showing activity in mouse models implanted with tumor cells from patients, also known as PDX models, is particularly meaningful because PDX models are more representative of the complexity of human cancer than results seen with cell lines.” Dr. Hamdy continued, “Despite progress in the treatment of B-cell malignancies, there is still an unmet medical need, especially for patients with relapsed or refractory disease. The results presented at AACR, together with our previous efficacy findings of durable complete tumor regression in CXCR5-positive, ibrutinib-refractory lymphoma models, suggest that VIP924 has the potential to be a treatment option for relapsed and refractory patients. Looking at the totality of preclinical data we’ve generated, including the data we presented at ASH that showed how our next generation linker, payload, and CellTrapper™ technology significantly improved the safety and efficacy of the approved ADC, Mylotarg™, we can’t help but be excited about the future of our ADC programs. We look forward to filing the IND for VIP924 in mid-2024.” Key Presentation Highlights: Poster presentation, titled, CXCR5 is a very promising drug target for the development of antibody-drug conjugates to treat patients with lymphoma, presented by Tibor Schomber, Ph.D., Vincerx Pharma GmbH, Monheim, Germany, include: High expression of CXCR5 was observed by immunohistochemistry on naive and previously treated diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), mantle cell lymphoma (MCL), and chronic lymphocytic leukemia (CLL) samples; with limited expression in healthy tissues. VIP924 showed superior in vitro cytotoxicity across different non-Hodgkin lymphoma cell lines compared with other B-cell lymphoma targeting antibodies conjugated to the same effector chemistry including, CD19-KSPi, CD22-KSPi, and CD70-KSPi. VIP924 (10mg/kg) resulted in significant tumor growth inhibition in two DLBCL patient-derived tumor models: 68% in a low CXCR5-expressing model and 87% in a high CXCR5-expressing model. Prolonged survival of VIP924-treated animals was observed in both models. No effect on body weight or any adverse effects in the VIP924-treated mice were observed. To determine the efficacy of VIP924 in large, established tumors, a single VIP924 dose of 10mg/kg was administered in mice transplanted with the HBL-1 lymphoma cell line. Complete responses were observed in 2 out of 3 mice with no measurable tumors on treatment day 26. After 24 and 48 hours, accumulation of VIP716 (ie, payload; “metabolite”) was observed in the tumors but not in plasma. KSP inhibition resulted in mitotic arrest and the formation of characteristic monopolar spindles (monoasters). VIP924 treatment produced higher levels and longer duration of monoaster formation in a lymphoma cell line compared to the permeable, small molecule KSPi, ispinesib. The poster can be accessed on the presentations section of the Vincerx website. About Vincerx Pharma, Inc. Vincerx Pharma, Inc. (Vincerx) is a clinical-stage biopharmaceutical company committed to developing differentiated and novel therapies to address the unmet medical needs of patients with cancer. Vincerx has assembled a seasoned management team with a proven track record of successful oncology drug development, approvals, and value creation. The company’s diverse pipeline consists of enitociclib, currently in Phase 1, and a proprietary modular bioconjugation platform, which includes a small molecule drug-conjugate, VIP236, in Phase 1, and preclinical next-generation antibody drug conjugates, VIP943 and VIP924. Vincerx is based in Palo Alto, Calif., and has a research facility in Monheim, Germany. For more information, please visit . Cautionary Statement This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as amended, that are intended to be covered by the “safe harbor” created by those sections. Forward-looking statements, which are based on certain assumptions and describe future plans, strategies, expectations and events, can generally be identified by the use of forward-looking terms such as “believe,” “expect,” “may,” “will,” “should,” “would,” “could,” “suggest,” “seek,” “intend,” “plan,” “goal,” “potential,” “on-target,” “on track,” “project,” “estimate,” “anticipate,” or other comparable terms. All statements other than statements of historical facts included in this press release are forward-looking statements. Forward-looking statements include, but are not limited to: Vincerx’s business model, pipeline, strategy, timeline, product candidates and attributes, and preclinical and clinical development, timing, and results. Forward-looking statements are neither historical facts nor assurances of future performance or events. Instead, they are based only on current beliefs, expectations and assumptions regarding future business developments, future plans and strategies, projections, anticipated events and trends, the economy and other future conditions. Forward-looking statements are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Actual results, conditions and events may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause actual results, conditions, and events to differ materially from those indicated in the forward-looking statements include, but are not limited to: general economic, financial, legal, political, and business conditions; the potential effects of health epidemics and pandemics, including COVID-19; risks associated with preclinical or clinical development and trials, including those conducted prior to Vincerx’s in-licensing; failure to realize the benefits of Vincerx’s license agreement with Bayer; risks related to the rollout of Vincerx’s business and the timing of expected business milestones; changes in the assumptions underlying Vincerx’s expectations regarding its future business or business model; Vincerx’s ability to develop and commercialize product candidates; Vincerx’s capital requirements and availability and uses of capital; and the risks and uncertainties set forth in Forms 10-K, 10-Q, and 8-K most recently filed with or furnished to the SEC by Vincerx. Forward-looking statements speak only as of the date hereof, and Vincerx disclaims any obligation to update any forward-looking statements. Vincerx and the Vincerx logo are our trademarks. This press release also contains trademarks and trade names that are the property of their respective owners. Contacts Gabriela Jairala Vincerx Pharma, Inc. gabriela.jairala@vincerx.com Bruce Mackle LifeSci Advisors, LLC 646-889-1200 bmackle@lifesciadvisors.com

AACR会议临床1期抗体药物偶联物

100 项与伊匹尼塞相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB06188

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
复发性卵巢癌	临床2期	美国	GSK Plc	2004-12-01
晚期乳腺癌	临床2期	美国	GSK Plc	2004-06-30
晚期乳腺癌	临床2期	比利时	GSK Plc	2004-06-30
晚期乳腺癌	临床2期	马来西亚	GSK Plc	2004-06-30
晚期乳腺癌	临床2期	新加坡	GSK Plc	2004-06-30
晚期乳腺癌	临床2期	英国	GSK Plc	2004-06-30
转移性乳腺癌	临床2期	美国	GSK Plc	2004-06-30
转移性乳腺癌	临床2期	比利时	GSK Plc	2004-06-30
转移性乳腺癌	临床2期	马来西亚	GSK Plc	2004-06-30
转移性乳腺癌	临床2期	新加坡	GSK Plc	2004-06-30

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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


NCT00089973 (CTgov)	临床2期	转移性乳腺癌 \| 晚期乳腺癌	50	Ispinesib	構繭製顧積淵窪願鬱遞(淵齋選鹽範餘憲網鏇鏇) = 鹽網衊鏇積鑰壓鏇獵鑰選憲願繭鹽鬱觸壓製窪 (夢醖範鹹鹹構淵艱糧衊, 遞範構網憲淵憲選窪顧 ~ 製夢鑰鏇夢壓鑰繭襯餘) 更多	-	2018-02-26
NCT00095628 (CTgov)	临床2期	口腔鳞状细胞癌复发 \| 口咽部鳞状细胞癌 \| 下咽部鳞状细胞癌 ... 更多	21	pharmacological study+ispinesib	遞觸艱製顧膚遞餘醖蓋(窪壓網鹹膚窪夢襯製顧) = 廠憲觸窪鹹繭範鏇蓋鏇製積膚繭構艱壓壓憲鹹 (襯壓選窪廠窪餘窪糧簾, 鑰膚獵醖夢範獵壓構選 ~ 簾構獵齋顧積觸廠膚願) 更多	-	2017-03-06
NCT00103311 (CTgov)	临床2期	复发性结肠癌 \| 直肠癌 \| 结肠转移性腺癌	64	laboratory biomarker analysis+ispinesib (Arm I)	衊夢壓窪衊繭遞鹹選鑰(憲鏇齋醖膚製觸繭鏇餘) = 鏇網淵網鬱觸鹹繭鹹觸鏇繭遞獵憲鹹願網積遞 (顧糧鹽鑰選壓鏇繭繭鏇, 繭餘膚夢積顧壓醖蓋鬱 ~ 壓蓋遞衊糧鬱築繭齋築) 更多	-	2015-03-02
NCT00103311 (CTgov)	临床2期	复发性结肠癌 \| 直肠癌 \| 结肠转移性腺癌	64	laboratory biomarker analysis+ispinesib (Arm II)	衊夢壓窪衊繭遞鹹選鑰(憲鏇齋醖膚製觸繭鏇餘) = 襯窪鏇蓋鑰襯製齋廠鹽鏇繭遞獵憲鹹願網積遞 (顧糧鹽鑰選壓鏇繭繭鏇, 鹹獵醖餘齋衊鹽願鬱淵 ~ 範築積艱顧願壓簾糧憲) 更多	-	2015-03-02
ASCO2009	临床1/2期	晚期乳腺癌	16	Ispinesib	鏇夢鹽範鬱鬱夢繭鏇鏇(構網壓鹽鑰廠選窪餘簾) = 壓範鹽網餘願鹹顧鏇鏇鹹齋糧製窪鬱鹽顧鑰壓 (構糧糧夢廠製壓積鹹齋 ) 更多	-	2009-05-20
NCT00095992 (NCIC CTG IND.168, Pubmed \| Invest New Drugs)	临床2期	转移性肝细胞癌	15	SB-715992	壓壓網遞醖鏇築襯襯糧(衊遞鹹網醖壓網遞鹽窪) = 壓鏇觸壓積繭蓋齋夢壓餘遞夢願願糧襯繭築鏇 (艱製糧繭製遞獵艱憲齋, 1.31 ~ 3.94)	不佳	2008-06-01
ASCO2008	临床1/2期	局部晚期乳腺癌	-	Ispinesib	膚夢鹹窪網簾獵艱網範(糧繭鏇鏇糧廠糧簾憲鹹) = 鏇膚鹽膚願鹽鏇壓鹹鹹鏇遞遞選憲遞艱觸獵憲 (膚獵壓鏇艱築鹽蓋糧壓 )	-	2008-05-20
ASCO2008	临床1期	-	21	Ispinesib 9 mg/m2	窪鑰鬱蓋製糧製餘繭觸(構淵夢糧鹹鹽願齋鏇積) = 簾餘範膚繭繭醖鑰簾醖範鹽選製範餘鏇遞鑰憲 (遞簾淵簾範築糧膚壓餘 )	-	2008-05-20
ASCO2008	临床1期	-	21	Ispinesib 12 mg/m2	窪鑰鬱蓋製糧製餘繭觸(構淵夢糧鹹鹽願齋鏇積) = 齋積鑰網鹹鑰獵鏇鹽積範鹽選製範餘鏇遞鑰憲 (遞簾淵簾範築糧膚壓餘 )	-	2008-05-20
ASCO2006	临床1期	HR阳性/HER2低表达实体瘤	-	Ispinesib	衊糧範繭製廠獵獵艱衊(製艱網淵壓淵簾壓鹽醖) = 遞廠鹹襯壓齋膚膚選齋鬱糧積範衊遞蓋夢願憲 (鬱選淵窪鹹齋築齋鹹遞 )	-	2006-06-20
CCC-P (ASCO2006)	临床2期	转移性结直肠癌	64	Ispinesib 7 mg/m2 every week for 3 weeks, every 28 days	鹽憲壓願醖網窪齋艱獵(齋齋齋鏇遞簾糧艱積顧) = 淵繭鹽醖壓鏇選繭衊淵廠蓋積窪鑰夢蓋積獵襯 (窪獵鹹鹹糧築鏇壓蓋鹽, 44 ~ 51)	不佳	2006-06-20
CCC-P (ASCO2006)	临床2期	转移性结直肠癌	64	18 mg/m2 every 21 days	鹽憲壓願醖網窪齋艱獵(齋齋齋鏇遞簾糧艱積顧) = 獵願網廠壓淵獵衊糧範廠蓋積窪鑰夢蓋積獵襯 (窪獵鹹鹹糧築鏇壓蓋鹽, 35 ~ 42 days)	不佳	2006-06-20
ASCO2006	临床1期	HR阳性/HER2低表达实体瘤	24	Ispinesib	鬱願顧艱膚積膚壓糧鹽(鏇蓋衊簾築衊蓋鑰顧齋) = 醖遞繭鏇艱憲顧鑰築繭膚憲鏇選繭廠餘膚簾夢 (衊觸蓋鏇壓願簾齋鑰艱 ) 更多	-	2006-06-20