A pilot study to assess [11C]elacridar and [11C]tariquidar as two positron emission tomography radiotracers for visualization of P-glycoprotein in humans. - [11C]inhibitors

开始日期2010-11-03

申办/合作机构-

NCT00082368

/ Completed临床2期IIT

A Pilot Study of Tc-94m Sestamibi PET MDR Imaging

Background:
* Tc-94m sestamibi is a radioactive imaging drug approved by the Food and Drug Administration to help photograph and study bodily functions.
* Tc-94m sestamibi accumulates in tumor cells and is eliminated from them in much the same way that some chemotherapy drugs are eliminated from cancer cells in patients with drug resistance.
* P-glycoprotein is a protein found on the surface of some cancer cells. The protein causes the cells to pump out, or reject, some types of chemotherapy drugs. P-glycoprotein also makes the cells reject sestamibi.
* Some drugs, including a drug called tariquidar, may block the pumping action of P-glycoprotein, giving the chemotherapy more time to work. Tariquidar can also help sestamibi stay in the cells longer.
Objectives:
-To evaluate the use of sestamibi for determining if chemotherapy is being rejected and if enough of the blocking drugs are present to stop the rejection.
Eligibility:
-Patients18 years of age and older with a tumor 2 cm or larger who are enrolled in or are eligible for enrollment in an active National Cancer Institute treatment protocol.
Design:
* Patients have two scans, one before receiving any drugs and a second 1-2 hours after receiving tariquidar. The second scan is done 72 or more hours after the first. For both scans, Tc-94m sestamibi is injected into a vein and a series of pictures are taken with an imaging camera called a PET (positron emission tomography) scanner. The pictures show where the sestamibi distributes in the body and monitors the effects of tariquidar on drug resistance. Blood samples are collected during the scan to examine the effect of tariquidar on P-glycoprotein in normal cells.
* Some patients may be asked to undergo a tumor biopsy to test for the presence of the P-glycoprotein on their cancer cells. This will be requested only in patients whose tumor is easily accessible and in whom a biopsy can be done with minimal risk.

开始日期2004-05-16

申办/合作机构

National Cancer Institute

100 项与 Tariquidar 相关的临床结果

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100 项与 Tariquidar 相关的转化医学

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100 项与 Tariquidar 相关的专利（医药）

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项与 Tariquidar 相关的文献（医药）

2025-12-01·EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY

Discovery of a heterocyclic aromatic amide based P-gp inhibitor as coadjutant regulating autophagy against drug resistance in breast cancer

Article

作者: Ge, Gong-Hui ; Yu, Han ; Lu, Peng-Fei ; Zhang, Ting-Jian ; Guo, Shuai ; Zhang, Xu ; Xue, Wen-Han ; Man, Ru-Yi ; Meng, Fan-Hao ; Liu, Hong-Ye

P-glycoprotein (P-gp) plays a vital role in the development of multidrug resistance (MDR) during chemotherapy, which mediated lysosomal sequestration of ADM, leading to the development of drug resistance. Lysosomes fuse with autophagosomes to generate autolysosomes in which contents are degraded, thereby achieving the metabolic needs of the cell itself and the renewal of organelles. In this work, a series of N-(3-cyano-4-(alkoxy)phenyl)heterocyclic aromatic amide derivatives (A1-A48) were designed and synthesized as novel P-gp inhibitors. Among them, compound A38 showed low cytotoxicity and excellent reversal activity, which was considered the most promising P-gp inhibitor. P-gp ATPase assay, MOE and CETSA revealed that A38 interacts with P-gp. ADM accumulation assay and other studies were conducted to verify that compound A38 inhibits P-gp function. Further investigation indicated that A38 in combination with ADM significantly promoted apoptosis and markedly suppressed the proliferation, migration and invasion ability in drug resistant breast cancer. mCherry-GFP-LC3B puncta formation assay verified that P-gp inhibitor A38 blocks the formation of autophagic flux and ADM combined with A38 results in the accumulation of autophagosomes, thereby inducing drug-resistant breast cancer cell death. In in vivo and in vitro tumor model experiments, the antitumor activity of ADM combined with P-gp inhibitor A38 was superior to that of tariquidar. The effectiveness of compound A38 and its role in regulating autophagy provided a new reference for the development of P-gp inhibitors and the clinical treatment of drug-resistant breast cancer.

2025-11-01·EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES

Effect of Different Doses of Dexamethasone on the Penetration of Acyclovir Across the Blood-Brain Barrier

Article

作者: Nie, Zhiyong ; Wang, Mengyao ; Cen, Yuying ; Liu, Yuxuan ; Zhang, Jiatang ; Zhuang, Tiantian ; Shan, Yuheng ; Zhao, Jiahua ; Xie, Jianwei ; Li, Yibing

Acyclovir (ACV) is a widely used antiviral agent for the treatment of herpes simplex virus encephalitis. Dexamethasone (DEX) is often co-administered as an adjunctive therapy. Tariquidar (TQD), a potent and selective inhibitor of P-glycoprotein, has been demonstrated to enhance the brain accumulation of ACV. This study is designed to systematically investigate the impact of varying DEX dosages on the blood-brain barrier (BBB) transport of ACV, elucidate the mechanisms involved, and evaluate the therapeutic potential of TQD in the management of herpes simplex virus encephalitis. Microdialysis, coupled with high-performance liquid chromatography, was employed to measure unbound ACV concentrations in blood and brain tissue at pre-determined time intervals. The effects of low (0.5 mg/kg), moderate (1 mg/kg), and high (3 mg/kg) doses of DEX, administered continuously for 4 days, on the pharmacokinetic parameters of ACV were evaluated in the presence and absence of tariquidar (TQD, P-glycoprotein inhibitor, 8 mg/kg). The BBB transport of ACV was assessed by calculating the ratio of the area under the unbound brain drug concentration-time curve to the area under the unbound blood drug concentration over time, to reflect changes in the BBB transport (K_p,uu,brain) of ACV. The mean of the area under the unbound brain and blood drug concentration-time curve, and K_p,uu,brain in rats of the solvent control (SC) group were 2674 ± 448 min·μg/mL, 564 ± 136 min·μg/mL, and 20.9%, respectively. In the low-dose DEX group, the K_p,uu,brain of ACV was 19.5%, with no statistically significant difference compared with the SC group (P > 0.05). In the moderate- and high-dose DEX groups, the K_p,uu,brain of ACV decreased to 17.0% and 14.0%, respectively, with a statistically significant difference compared with the SC group (P < 0.001). Pairwise comparisons further revealed significant differences in the K_p,uu,brain of ACV among different DEX dose groups. Conversely, TQD administration increased the K_p,uu,brain of ACV by 1.40-fold (P < 0.001). The K_p,uu,brain in the TQD plus low-dose DEX group was 27.1%, significantly higher than that of the SC group (P < 0.001). The K_p,uu,brain of the TQD plus moderate-dose DEX and TQD plus high-dose DEX groups was 21.6% and 18.4%, respectively, with no significant difference compared to the SC group (P > 0.05). Low-dose DEX does not significantly alter the BBB transport of ACV. However, moderate to high doses of DEX exhibit a dose-dependent reduction in ACV penetration across the BBB. Co-administration of TQD with DEX counteracts this effect, and even enhancing the BBB transport of ACV.

2025-09-03·ACS Chemical Neuroscience

Evaluation of [¹⁸F]F-CNBI and [¹⁸F]F-CNPI PET Probes in GSK-3β Transgenic Mice

Article

作者: Gundam, Surendra Reddy ; Lim, Do Young ; Baker, Darren J. ; Bansal, Aditya ; Wootla, Bharath ; Larson, Nicholas B. ; Giri, Sharmila ; Rivera, Andy Gonzalez ; Lowe, Val J. ; Kethamreddy, Manasa ; Pandey, Mukesh K.

The present study explores the noninvasive positron emission tomography (PET) imaging for the detection of GSK-3β overexpression using [¹⁸F]F-CNPI and [¹⁸F]F-CNBI in a GSK-3β overexpressing transgenic mouse model. Herein, we validated GSK-3β overexpression in different brain regions by genotyping and Western blot. PET scans and ex vivo biodistribution were performed in normal mice and early stage and late-stage GSK-3β transgenic mice with and without the P-gp inhibitor, Tariquidar. Both probes are found in the substrate of the P-gp transporter. [¹⁸F]F-CNPI showed significantly higher brain uptake in normal and GSK-3β overexpressing mice with the P-gp inhibitor compared to those without the P-gp inhibitor. The uptake of [¹⁸F]F-CNBI was lower in all the groups compared to that of [¹⁸F]F-CNPI. The late-stage GSK-3β transgenic mice having higher GSK-3β expression showed higher uptake of [¹⁸F]F-CNPI in the brain as compared to normal and early stage GSK-3β transgenic mice brains. To the best of our knowledge, this is the first report evaluating any GSK-3 PET probe in a GSK-3β overexpressing transgenic mouse model. The developed GSK-3β overexpressing transgenic mouse model can be efficiently employed to evaluate an array of GSK-3 PET probes.

项与 Tariquidar 相关的新闻（医药）

2025-11-24

·精准药物

【JMC】第二代靶向AURKA的PROTACs在治疗神经母细胞瘤中的应用

AURKA是一种已明确的致癌因子，也是神经母细胞瘤的治疗靶点，归因于其在有丝分裂和MYCN蛋白稳定性方面所起的作用。2025年11月18日比利时根特大学的研究者在Journal of Medicinal Chemistry上发表题为“Second-Generation AURKA-Targeting PROTACs: Structural Optimization toward in Vivo Degradation in Neuroblastoma”的文章。文章中作者以先前发表的AURKA降解剂SK2188作为先导化合物进行构效关系研究，包括连接子刚性化以及引入替代性的CRBN配体和AURKA招募配体，由此得到了两种优化后的PROTACs，分别是SK4454和SK5527。这两种化合物均能快速且特异性地降解AURKA。重要的是，在神经母细胞瘤异种移植小鼠模型中，单次静脉注射任一降解剂均可在体内有效降低AURKA水平。此外，SK4454和SK5527在药代动力学特性方面也得到改善，值得进一步开展临床前评估。 1 研究背景神经母细胞瘤是儿童最常见的颅外实体肿瘤。尽管采用了包括手术、化疗、放疗、免疫疗法和干细胞移植在内的多模式密集治疗，但一半的高危患者最终仍因疾病去世，凸显了新治疗策略的紧迫需求。虽然神经母细胞瘤形成的确切起源和机制尚不明确，但MYCN致癌基因的扩增是高风险疾病和整体生存率较低的最强标志之一。然而，由于缺乏明确的结合口袋，直接抑制MYCN仍是一大挑战。 AURKA是一种丝氨酸/苏氨酸激酶，通过催化活性在中心体成熟、纺锤组装和有丝分裂进入中起着关键作用。AURKA的失调已被认为是多种癌症类型中的关键致癌驱动因素，使其成为一种有吸引力的治疗靶点。在神经母细胞瘤中，AURKA直接与MYCN相互作用，并阻止其被E3泛素连接酶SCFFBXW7识别从而保护MYCN免受蛋白酶体降解。该AURKA/MYCN复合物的形成还被证明在通过CDK12磷酸化缓解S期转录-复制冲突中起关键作用。另一项研究揭示了AURKA在与TPX2复合物中调节DNA损伤修复和复制叉稳定性的额外激酶非依赖功能。鉴于这些多样功能，开发AURKA降解剂的兴趣日益增长，能够同时靶向激酶依赖性和非依赖性活性。 2 研究内容优化药代动力学性质，发现新的AURKA PROTACs 作者在前期研究中开发了AURKA降解剂SK2188和SK3277，由于其血浆稳定性低、小鼠肝微粒体中高周转率，以及SK2188存在高静脉清除率（图1）。为解决这个问题，作者继续进行结构优化，以生成具有更好药代动力学特性的新型AURKA降解剂。共合成并筛选了38个新型PROTACs，根据不同的优化策略分为4个系列：（1）连接子刚性，（2）探索芳氨基戊二酰胺和（3）基于二氢尿嘧啶的CRBN配体，以及（4）使用类LY3295668 AURKA配体。所有化合物均在体外使用MYCN扩增的神经母细胞瘤细胞系NGP进行筛选。使用IncuCyte活细胞成像来测量抗增殖效果（GI50）和Simple Western用于监测24小时处理后AURKA蛋白水平的下降情况。对于有潜力的候选化合物，采用Simple Western技术更精准地评估其降解效力（DC₅₀、Dₘₐₓ）并委托Eurofins Discovery Services检测其在血浆中的稳定性（血浆半衰期t₁/₂）、小鼠肝微粒体中的内在清除率、肝细胞内在清除率及小鼠肝匀浆中的相关指标。图2显示了部分优选化合物的结构和生物活性。图1 先前开发的AURKA降解剂SK2188和SK3277以及相关的参数图2 在PROTAC结构优化研究中开发的关键化合物及其相应的体外和体内参数。关键化合物根据不同的优化策略被分类为不同系列 SK4454和SK5527是快速、强效和选择性AURKA降解剂采用了纳米荧光素酶生物发光共振能量转移技术检测了降解剂在细胞内AURKA的结合作用，结果发现在通透化处理的细胞裂解液中，SK4454和SK5527能够以约20 nM的IC₅₀值取代与NanoLuc-AURKA融合蛋白结合的荧光探针。接下来，作者采用Simple Western技术，在神经母细胞瘤细胞系中评估了SK4454和SK5527降解AURKA的潜力。两种PROTACs均诱导了相当程度的AURKA降解，并伴随MYCN降解（图3A和B），其中在MYCN扩增的IMR-32、NGP和SJNB-8细胞系中效果最为显著，DC₅₀ < 25 nM。在MYCN扩增的SK-N-BE(2)-C细胞系以及非MYCN扩增的SK-N-AS和SJNB-1细胞系中，降解效果较弱。重要的是SK4454和SK5527均在1小时后即诱导显著的AURKA降解，而MYCN的降解在暴露后24小时才达到约50%（图3C），表明MYCN的减少是AURKA降解的次级后果，而非PROTAC的直接作用。为验证作用机制，作者合成了SK5527的两种甲基化类似物，分别设计用于破坏其与CRBN（SK5527-CRBi）或AURKA（SK5527-AURi）的结合。正如预期，两种对照化合物均未能降解AURKA（图3D）。图3 SK4454和SK5527的蛋白降解活性 SK4454和SK5527在体外细胞系中显示出强烈的抗增殖活性利用IncuCyte活细胞成像技术，评估SK4454和SK5527在一系列神经母细胞瘤细胞系中的抗增殖效果，并将其与SK2188以及AURKA抑制剂TAS-119、LY3295668和MK-5108进行了对比（图4A），在暴露于SK4454和SK5527 72小时后，IMR-32、NGP和SJNB-8细胞系显示出最强的抗增殖效果，GI₅₀ < 100 nM，这与观察到的强效AURKA降解作用相一致。此外，两种PROTACs在抑制神经母细胞瘤细胞生长方面总体上比SK2188更为有效（图4B）。 MDR1介导的药物外排是SK4454和SK5527体外敏感性的关键限制因素此前已有研究指出，药物外排泵是限制PROTAC在癌细胞中敏感性的关键因素。因此，作者推测SK4454和SK5527在SK-N-BE(2)-C、SK-N-SH和SJNB-1细胞系中活性降低（图3A和图4A）的原因可能是药物外排，因为这些细胞系中由ABCB1基因编码的多药耐药蛋白1（MDR1）表达水平较高（图4C）。这一发现促使作者评估在MDR1抑制剂Tariquidar存在的情况下，新型PROTACs降解AURKA的潜力。在MDR1表达水平最高的SK-N-BE(2)-C细胞系中，与Tariquidar（1 μM）联合治疗显著增强了SK4454和SK5527降解AURKA的能力（图4D）。同时，这一联合治疗还显著提高SK-N-BE(2)-C细胞系的凋亡诱导率，而在缺乏MDR1表达的NGP细胞系中则未观察到此差异（图4E）。在直接对比实验中，当Tariquidar联合治疗消除药物外排作用后，SK4454和SK5527展现出的生长抑制活性与AURKA抑制剂TAS-119相当，各细胞系中的GI₅₀值几乎一致（图4F）。图4 SK4454和SK5527的体外抗增殖活性和MDR1介导的药物外排对SK4454和SK5527治疗效果的影响 SK4454和SK5527可在体内诱导AURKA蛋白降解如前所述，与作者先前报道的PROTAC分子SK2188相比，SK4454和SK5527在静脉（IV）给药后小鼠体内的清除率有所降低。此外，作者还对这两种降解剂进行了腹腔（IP）和口服（PO）给药后的小鼠药代动力学（PK）研究。两种PROTAC的腹腔给药药代动力学特征与其静脉给药特征极为相似（图5A）。口服生物利用度相对较低，SK4454为7%，SK5527为11%，这在一定程度上可能归因于它们易受MDR1介导的外排作用影响。作者在IMR-32神经母细胞瘤细胞系来源的异种移植（CDX）小鼠中，静脉和腹腔给予15 mg/kg的SK4454或SK5527。给药后4、8和24小时采集肿瘤组织，将AURKA蛋白水平可视化，并与t=0小时的基线水平进行比较。结果显示，单次静脉给药后4和8小时，两种PROTAC在体内均显著降低了AURKA蛋白水平，至24小时则恢复至基线水平（图5B）。图5 体内PK曲线以及蛋白降解活性研究 3 研究结果鉴于作者前期报道的AURKA降解剂SK2188，因其血浆和代谢稳定性差、体内清除率高，在进一步体内应用中表现欠佳。因此在本研究中，作者通过采用更刚性的连接链，并探索替代性的CRBN配体与AURKA招募配体，发现了PROTAC分子SK4454和SK5527。与SK2188相比，这两种分子展现出更优的血浆和代谢稳定性，且静脉清除率降低。SK4454和SK5527均保留了强效且选择性的AURKA降解能力。在神经母细胞瘤异种移植小鼠模型中进行药效动力学研究证实，静脉单次给予15 mg/kg剂量的SK4454和SK5527，均能在体内有效降解AURKA。然而，相同浓度的单次腹腔给药并未检测到AURKA降解，尽管其全身暴露量相当。这一差异可能归因于静脉给药后达到的更高初始血浆浓度，该浓度可能促进肿瘤内更快、更有效的靶标结合。需进一步研究以确定更高剂量或重复腹腔给药能否在体内实现相当的AURKA降解，从而支持进一步的临床前疗效和安全性评估。总体而言，尽管合理设计原则可指导PROTAC优化并克服关键药代动力学挑战，但发现过程最终仍高度依赖经验。尽管如此，本研究中展示的优化分子SK4454和SK5527，为持续开展临床前研究奠定了坚实基础，旨在验证AURKA降解作为神经母细胞瘤及其他AURKA驱动性恶性肿瘤治疗策略的有效性。全文链接：https://pubs.acs.org/doi/10.1021/acs.jmedchem.5c01271 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↓

免疫疗法蛋白降解靶向嵌合体AACR会议

2023-10-02

·Science Daily

Breakthrough in the fight against resistance in metastatic breast cancer

A team of researchers has discovered that dormant tumor cells surviving chemotherapy can be targeted through the inhibition of a specific protein called P-glycoprotein (P-gp). This discovery opens up new possibilities for delaying relapse and is particularly relevant for aggressive triple-negative breast cancer (TNBC), for which there are currently few effective treatments. A team of researchers at the Medical University of Vienna has discovered that dormant tumor cells surviving chemotherapy can be targeted through the inhibition of a specific protein called P-glycoprotein (P-gp). This discovery opens up new possibilities for delaying relapse and is particularly relevant for aggressive triple-negative breast cancer (TNBC), for which there are currently few effective treatments. The findings, published in the journal Drug Resistance Updates, could represent a step forward in the treatment of this type of cancer. So-called "triple-negative breast cancer" is a particularly dangerous form of breast cancer. It is characterised by an early relapse and a poor survival rate. Until now, there have only been limited treatment options, and chemotherapy protocols are often not sufficiently effective. Therapy resistance, where cancer cells do not respond to conventional treatments, has long been a major problem. A research team at MedUni Vienna's Center for Cancer Research has now discovered why this happens and how it can be prevented. Certain cancer cells evade chemotherapy by entering a dormant cell state. Such cancer cells can persist undetected for several months or even years before they start to proliferate again to give rise to tumor relapse. Although cytotoxic agents are less effective against nondividing cells, drug tolerant persister cells must come up with additional protective measures to cope with the toxic effects of chemotherapy. Researchers led by Gergely Szakács at MedUni Vienna's Center for Cancer Research found that this partially happens through the activation of a protein called P-glycoprotein (P-gp), which helps to clean cells from secondary damage inflicted by chemotherapy. "P-gp has been well-known as a protein that can export chemotherapeutic drugs from the cells, but its role in protecting dormant cancer cells has not been proven. The discovery that P-gp contributes to the removal of toxic lipids from rare surviving cancer cells represents a vulnerability that can be exploited to prevent relapse. The good thing is that there are already drugs that can block this protein, so we were able to test our hypothesis." explains Gergely Szakács, the lead author of the study. In a mouse model of triple-negative breast cancer, prolonged inhibition of P-gp prior to the onset of resistance with a drug called tariquidar significantly prolonged the survival of mice, indicating that the critical population of drug-tolerant cancer cells can be targeted by blocking P-glycoprotein. These results could mean that patients with triple-negative breast cancer have a better chance of being cured in the future. Researchers are now working to translate these findings into clinical practice to better treat patients.

100 项与 Tariquidar 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D06008	Tariquidar	-	DB06240

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
转移性非小细胞肺癌	临床3期	-	QLT, Inc.	2002-06-01
非小细胞肺癌IIIB期	临床3期	-	QLT, Inc.	2002-06-01
乳腺癌	临床3期	-	Xenova Ltd.	-
乳腺癌	临床3期	-	National Cancer Institute	-
乳腺癌	临床3期	-	Novelion Therapeutics, Inc.	-
非小细胞肺癌	临床3期	-	National Cancer Institute	-
非小细胞肺癌	临床3期	-	Xenova Ltd.	-
肾上腺皮质肿瘤	临床2期	美国	National Cancer Institute	2003-10-01
肺癌	临床2期	美国	National Cancer Institute	2003-09-01
卵巢上皮癌	临床2期	美国	National Cancer Institute	2003-09-01

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临床结果

适应症

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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


NCT00011414 (Pubmed \| Cancer Chemother Pharmacol)	临床1期	实体瘤 P-glycoprotein	-	Tariquidar	範壓壓艱壓構鏇襯繭齋(簾醖淵鬱築廠憲夢繭鬱) = 構顧淵艱齋鹽願觸願遞艱鏇鹹衊選襯淵鏇範簾 (糧蓋積鏇淵艱顧膚鬱鹽 )	-	2015-12-01
NCT00069160 (CTgov)	临床2期	肺癌 \| 卵巢癌 \| 复发性卵巢癌 ... 更多	48	Docetaxel (Docetaxel Alone)	遞鏇襯壓窪選窪壓製範(鹽選艱膚壓簾鏇積鬱鏇) = 願構構積憲艱獵獵壓簾網遞選簾簾艱衊蓋遞範 (廠糧壓鏇壓簾網觸壓餘, 廠糧艱蓋壓壓襯鏇鹹窪 ~ 獵遞膚繭選鬱顧廠鑰觸) 更多	-	2012-10-12
NCT00069160 (CTgov)	临床2期	肺癌 \| 卵巢癌 \| 复发性卵巢癌 ... 更多	48	Tariquidar (With Tariquidar)	遞鏇襯壓窪選窪壓製範(鹽選艱膚壓簾鏇積鬱鏇) = 製糧繭膚網構夢鏇選餘網遞選簾簾艱衊蓋遞範 (廠糧壓鏇壓簾網觸壓餘, 醖顧範選夢繭願簾餘窪 ~ 襯願鑰窪糧築衊夢獵鑰) 更多	-	2012-10-12
NCT00071058 (CTgov)	临床2期	肾上腺皮质肿瘤	50	XR9576 (Tariquidar)	範觸艱鏇範醖顧獵網醖 = 壓觸淵襯繭簾齋憲繭選顧廠衊築鬱壓觸淵憲醖 (膚築衊鏇遞願蓋繭淵遞, 壓壓顧觸膚鬱簾製廠襯 ~ 廠觸鬱製範餘醖觸構鏇) 更多	-	2012-09-12
ASCO2004	临床1期	-	15	Tariquidar	願簾鹽選顧壓遞願遞夢(顧鑰觸壓鹹鏇鏇簾鬱膚) = 憲範膚餘艱憲醖鹹壓選膚鏇膚鏇憲網築製構窪 (製壓糧糧膚衊餘齋製鹹 ) 更多	-	2004-07-15
ASCO2004	临床1期	-	15	Doxorubicin	齋範夢憲顧鬱鹽餘鑰齋(顧鬱願鑰鏇選繭鏇鏇簾) = 憲壓壓鹽鬱願醖壓選襯觸積獵淵鑰鏇鬱顧構憲 (獵衊糧膚繭築簾顧網觸 )	-	2004-07-15