他喹莫德(Tasquinimod) - 药物靶点：NIF_在研适应症：转移性去势抵抗性前列腺癌，前列腺癌转移，复发性前列腺癌_专利_临床

概要

基本信息

药物类型

小分子化药

别名

TASQ、ABR-215050、ABR-5050

靶点

NIF

作用机制

NIF抑制剂(钙结合蛋白S100A9抑制剂)

治疗领域

肿瘤泌尿生殖系统疾病免疫系统疾病+ [2]

在研适应症

转移性去势抵抗性前列腺癌前列腺癌转移复发性前列腺癌+ [2]

非在研适应症

转移性肝细胞癌转移性肾细胞癌肿瘤转移+ [1]

原研机构

Active Biotech AB

在研机构

Active Biotech AB

非在研机构

Ipsen SA

Apoteket ABIpsen Pharma SAS

+ [1]

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)暂停

特殊审评孤儿药 (美国)

结构

分子式C20H17F3N2O4

InChIKeyONDYALNGTUAJDX-UHFFFAOYSA-N

CAS号254964-60-8

关联

15

项与他喹莫德相关的临床试验

NCT06327100 / Not yet recruiting临床2期IIT

Open Label Phase 2 Study of Tasquinimod in Patients With Primary Myelofibrosis (PMF), Post-Polycythemia Vera Myelofibrosis (Post-PV MF), or Post-Essential Thrombocytosis Myelofibrosis (Post-ET MF)

To learn if tasquinimod either alone or in combination with ruxolitinib can help to control PMF, post-PV MF, or post-ET MF.

开始日期2024-09-30

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+1]

ACTRN12621000016831 / Not yet recruiting临床2期

A randomized, double-blind, placebo-controlled phase II trial to evaluate the efficacy of tasquinimod in reducing the time taken for a 2-point decrease in admission status.in adults with COVID-19

开始日期2022-12-15

申办/合作机构

Hunter Medical Research Institute

NCT04405167 / Recruiting临床1期IIT

Phase 1 Study of Tasquinimod Alone and in Combination With Standard Therapy for Relapsed or Refractory Myeloma

This study is the first study of tasquinimod, an inhibitor of S100A9, in patients with multiple myeloma.

开始日期2020-07-10

申办/合作机构

University of Pennsylvania

[+1]

100 项与他喹莫德相关的临床结果

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100 项与他喹莫德相关的转化医学

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100 项与他喹莫德相关的专利（医药）

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80

项与他喹莫德相关的文献（医药）

Advances in clinical and experimental medicine : official organ Wroclaw Medical University

Tasquinimod enhances the sensitivity of ovarian cancer cells to cisplatin by regulating the Nur77-Bcl-2 apoptotic pathway

Article

作者: Zhu, Ke-An ; Li, Zhao ; Min, Xiao-Jia ; Lin, Ying ; Liu, Ya-Qiong ; Hu, Meng-Qi

BACKGROUND:

Resistance to cisplatin (DDP) in ovarian cancer therapy has been a major clinical barrier. Drug-resistant cancers have been shown to downregulate the proapoptotic protein B-cell lymphoma-2 (Bcl-2) to inhibit apoptosis. Therefore, we explored whether tasquinimod could modulate resistance to DDP through apoptotic pathways.

OBJECTIVES:

We aimed to explore the relationship between tasquinimod, Nur77-Bcl-2 apoptosis pathway and sensitivity of the ovarian carcinoma cell line SKOV3 and the DDP-resistant strain SKOV3/DDP cells to DDP.

MATERIAL AND METHODS:

First, SKOV3 and SKOV3/DDP cells were treated with 2 μg/mL DDP or 40 μM tasquinimod. Western blot and quantitative real-time polymerase chain reaction (qPCR) were then used to analyze the expression of histone deacetylase 4 (HDAC4), Nur77, Bcl-2 (BH3 domain-specific), and caspase-3. Flow cytometry, scratch-wound assay and immunofluorescence were used to detect apoptosis, migration rate, and related expression of Nur77 and Bcl-2 (BH3 domain-specific). Subsequently, 5×107 SKOV3 or SKOV3/DDP cells cultured with 2 μg/mL DDP were injected into 4-week-old female BALB/c nude mice. Then, the mice were administered 4 mg/kg DDP and 50 mg/kg tasquinimod every 3 days. Finally, the changes in tumor diameter and weight were measured.

RESULTS:

After treatment of SKOV3 and SKOV3/DDP cells with tasquinimod, cell migration and HDAC4 expression levels were significantly reduced, while Nur77 expression was increased. Tasquinimod treatment enhanced the expression of Nur77 and caspase-3, and cells transfected with si-Nur77 showed the opposite result. Transfection of si-Nur77 reduced the expression of caspase-3 and Nur77 in the SKOV3/DDP cells that were treated with both DDP and tasquinimod. After injection of SKOV3/DDP cells into the mice, the tumor diameter, mass and in vivo HDAC4 level were significantly decreased by tasquinimod. Meanwhile, the levels of Nur77 and Bcl-2 (BH3 domain-specific) were increased.

CONCLUSIONS:

Tasquinimod upregulated the Nur77/Bcl-2 pathway to induce apoptosis in SKOV3/DDP cells and enhanced the anti-tumor effect of DDP in SKOV3/DDP xenografts. Therefore, tasquinimod can be expected to find clinical applications in enhancing DDP resistance.

2023-11-01·The Prostate

Third generation quinoline-3-carboxamide transcriptional disrupter of HDAC4, HIF-1α, and MEF-2 signaling for metastatic castration-resistant prostate cancer.

Article

作者: Denmeade, Samuel R ; Isaacs, John T ; Antony, Lizamma ; Dalrymple, Susan L ; Coleman, Ilsa M ; Perdew, Gary H ; Kostova, Maya ; Brennen, W Nathaniel ; Murray, Iain A ; Nelson, Peter S ; Marc Rosen, David ; Akinboye, Emmanuel S

BACKGROUND:

The quinoline-3-carboxamide, Tasquinimod (TasQ), is orally active as a maintenance therapy with an on-target mechanism-of-action via allosteric binding to HDAC4. This prevents formation of the HDAC4/NCoR1/HDAC3 complex, disrupting HIF-1α transcriptional activation and repressing MEF-2 target genes needed for adaptive survival signaling in the compromised tumor micro environment. In phase 3 clinical testing against metastatic castration-resistant prostate cancer(mCRPC), TasQ (1 mg/day) increased time-to-progression, but not overall survival.

METHODS:

TasQ analogs were chemically synthesized and tested for activity compared to the parental compound. These included HDAC4 enzymatic assays, qRT-PCR and western blot analyses of gene and protein expression following treatment, in vitro and in vivo efficacy against multiple prostate cancer models including PDXs, pharmacokinetic analyses,AHR binding and agonist assays, SPR analyses of binding to HDAC4 and NCoR1, RNAseq analysis of in vivo tumors, 3D endothelial sprouting assays, and a targeted kinase screen. Genetic knockout or knockdown controls were used when appropriate.

RESULTS:

Here, we document that, on this regimen (1 mg/day), TasQ blood levels are 10-fold lower than the optimal concentration (≥2 μM) needed for anticancer activity, suggesting higher daily doses are needed. Unfortunately, we also demonstrate that TasQ is an arylhydrocarbon receptor (AHR) agonist, which binds with an EC50 of 1 μM to produce unwanted off-target side effects. Therefore, we screened a library of TasQ analogsto maximize on-target versus off-target activity. Using this approach, we identified ESATA-20, which has ~10-fold lower AHR agonism and 5-fold greater potency against prostate cancer patient-derived xenografts.

CONCLUSION:

This increased therapeuticindex nominates ESATA-20 as a lead candidate forclinical development as an orally active third generation quinoline-3-carboxamide analog thatretains its on-target ability to disrupt HDAC4/HIF-1α/MEF-2-dependent adaptive survival signaling in the compromisedtumor microenvironment found in mCRPC.

2023-09-01·Experimental and therapeutic medicine

Enhancement of neural regeneration as a therapeutic strategy for Alzheimer's disease (Review).

Review

作者: Li, Liping ; Gao, Junyan

Alzheimer's disease (AD), the most common cause of dementia worldwide, has gradually become a global health concern for society and individuals with the process of global ageing. Although extensive research has been carried out on AD, the etiology and pathological mechanism of the disease are still unclear, and there is no specific drug to cure or delay AD progression. The exploration of enhancing nerve regeneration in AD has gradually attracted increasing attention. In the current review, the existing therapeutic strategies were summarized to induce nerve regeneration which can increase the number of neurons, and improve the survival of neurons, the plasticity of synapses and synaptic activity. The strategies include increasing neurotrophic expression (such as brain-derived neurotrophic factor and nerve growth factor), inhibiting acetylcholinesterase (such as donepezil, tacrine, rivastigmine and galanthamine), elevating histone deacetylase levels (such as RGFP-966, Tasquinimod, CM-414 and 44B), stimulating the brain by physiotherapy (such as near-infrared light, repetitive transcranial magnetic stimulation, and transcranial direct current stimulation) and transplanting exogenous neural stem cells. However, further evaluations need to be performed to determine the optimal treatment. The present study reviews recent interventions for enhancing adult neurogenesis and attempts to elucidate their mechanisms of action, which may provide a theoretical basis for inducing nerve regeneration to fight against AD.

13

项与他喹莫德相关的新闻（医药）

2022-06-01

·GlobeNewswire-Health Care

Successful completion of the first stage of the phase IIa clinical trial of naptumomab in combination with docetaxel and the study is now enrolling into the second stage

Lund, June 1, 2022 - Active Biotech (NASDAQ STOCKHOLM: ACTI) and its partner NeoTX announce today the successful completion of the first stage of a Simon 2 stage phase IIa clinical trial of naptumomab estafenatox (NAP, naptumomab), in combination with docetaxel in patients with advanced or metastatic non-small cell lung cancer (NSCLC) who have been previously treated with chemotherapy and checkpoint inhibitors (CPIs). In the study, the patients are treated with NAP for 4 consecutive days and with docetaxel at a standard dose on day 5 in 21-day treatment cycles. The first stage of this trial required a minimum of two responses out of ten patients to move to the second stage of the trial, which is now enrolling. For more information about the trial, visit www.clinicaltrials.gov. NCT04880863 We are pleased by these early encouraging observations and are excited to follow the progress of the trial, which is now enrolling in its second stage, says Erik Vahtola, Chief Medical Officer at Active Biotech. Patients with advanced NSCLC who have progressed on CPI and standard chemotherapy currently have limited treatment options and new treatment alternatives are needed.See also www.neotx.com for NeoTX’s communication related to this information. Helén Tuvesson President & CEO For further information, please contact: Helén Tuvesson, CEO, +46 46 19 21 56, helen.tuvesson@activebiotech.com Hans Kolam, CFO, +46 46 19 20 44, hans.kolam@activebiotech.com This information is information that Active Biotech is obliged to make public pursuant to the EU Market Abuse Regulation. This information was submitted for publication, through the agency of the contact person set out above, at 14.00 pm. CET on June 1, 2022. Active Biotech AB (publ) (NASDAQ Stockholm: ACTI) is a biotechnology company that deploys its extensive knowledge base and portfolio of compounds to develop first-in-class immunomodulatory treatments for specialist oncology and immunology indications with a high unmet medical need and significant commercial potential. Following a portfolio refocus, the business model of Active Biotech aims to advance projects to the clinical development phase and then further develop the programs internally or pursue in partnership. Active Biotech currently holds three projects in its portfolio: The wholly owned small molecule immunomodulators, tasquinimod and laquinimod, both having a mode of actions that includes modulation of myeloid immune cell function, are targeted towards hematological malignancies and inflammatory eye disorders, respectively. Tasquinimod, is in clinical phase Ib/IIa for treatment of multiple myeloma. Laquinimod is in a clinical phase I study with a topical ophthalmic formulation, to be followed by phase II for treatment of non-infectious uveitis. Naptumomab, a targeted anti-cancer immunotherapy, partnered to NeoTX Therapeutics, is in a phase Ib/II clinical program in patients with advanced solid tumors. Please visit www.activebiotech.com for more information. About NeoTX NeoTX is a clinical-stage immuno-oncology company which is developing targeted anticancer immunotherapies utilizing its proprietary Tumor Targeted Superantigen (TTS) platform. TTS binds a genetically engineered bacterial determinant to the tumor surface while simultaneously activating and expanding tumor specific immune cells that are then redirected from the periphery to the tumor to mount an effective response. The company’s lead TTS molecule, naptumomab estafenatox is currently in clinical development for advanced solid tumors (clinicaltrials.gov/NCT039883954 and NCT04880863). Please visit www.neotx.com for more information. Naptumomab was licensed from Active Biotech to NeoTX Therapeutics Ltd in 2016. NeoTX is responsible for the global development and commercialization of naptumomab for the treatment of cancer under the license agreement. Active Biotech AB(Corp. Reg. No. 556223-9227)Scheelevägen 22, SE-223 63 Lund, SwedenTel: +46 (0)46 19 20 00 Attachment 220601_phase IIa clinical trial naptumomab in combination with docetaxel

First in Class免疫疗法小分子药物合作

2022-05-23

·新浪医药新闻

FDA授予tasquinimod治疗骨髓纤维化的孤儿药资格

2022年5月18日，Active Biotech宣布FDA已授予 tasquinimod 孤儿药资格，用于治疗骨髓纤维化。 Tasquinimod 是一种口服免疫调节和抗血管生成的研究性治疗药物，可影响肿瘤的生长和转移能力，由Active Biotech 和 Erasmus MC 共同开发。2022年2月，Active Biotech获得tasquinimod用于骨髓纤维化治疗的全球独家许可协议。 Tasquinimod 是HDAC4的特异性抑制剂，此前曾在实体癌患者中进行过研究，包括在转移性前列腺癌患者中进行的 III 期随机试验，表现出很好的耐受性。此外，在多发性骨髓瘤的临床前模型中，tasquinimod作为单一药物或与标准多发性骨髓瘤治疗联合使用时，显示出明显的治疗潜力。目前，tasquinimod治疗复发性或难治性多发性骨髓瘤的临床 Ib/IIa 期研究正在进行中。 HDAC又叫做组蛋白脱乙酰酶，是组蛋白修饰过程中一类重要的酶，催化并调控组蛋白去乙酰化。目前在人体中已经发现18种HDAC，分别属于四种类别（I、II、III和IV）。HDAC4属于Ⅱ类HDAC，与酵母Hda1蛋白具有同源性，分布在细胞质，同时在细胞核与细胞质之间穿梭。HDAC抑制剂是潜在的抑制增殖的化合物，它可以诱导细胞凋亡，因此可作为潜在的抗肿瘤药物，也可以作为HDAC功能分析的工具药。目前在研的HDAC4药物较少，以HDAC6、HDAC1 、HDAC2、HDAC3抑制剂居多，将目前处于临床阶段的HDAC药物统计如下：骨髓纤维化 (MF) 是一种罕见的血癌，根本原因尚不清楚。在欧洲，MF 的年发病率约为每 0.4 - 1.3 /100 000。MF 患者的造血细胞生成异常，导致健康骨髓被瘢痕组织（纤维化）替代。由于缺乏正常的血细胞生成，患者通常会出现实验室值异常，例如贫血以及白细胞计数和血细胞分化的变化。患者后期症状包括脾脏肿大、感染风险增加、盗汗和发烧。MF 与生存期缩短有关，死亡原因包括骨髓衰竭和转化为急性白血病。对于符合条件的个体，可以通过骨髓移植来治疗 MF，使用促红细胞生成素来控制贫血，以及使用 JAK 抑制剂来减小脾脏大小。目前尚无批准可以逆转 MF的疗法。 Active Biotech是一家生物技术公司，利用其广泛的知识库和化合物组合，为具有高度未满足的医疗需求和巨大商业潜力的专业肿瘤学和免疫学领域开发一流的免疫治疗手段。它的商业模式旨在将项目推进到临床开发阶段，然后选择内部开发项目或以合作伙伴的形式继续进行。内容来源于网络，如有侵权，请联系删除，谢谢

孤儿药小分子药物免疫疗法

2021-11-04

·BioSpace

Active Biotech Interim report January - September 2021

“We have seen the first encouraging results from the ongoing tasquinimod trial in multiple myeloma and started a new combination study with naptumomab and docetaxel in lung cancer” THIRD QUARTER IN BRIEF • Active Biotech provided status update of its clinical naptumomab project on July 5 • Active Biotech’s partner NeoTX hosted KOL webinar on overcoming checkpoint inhibitor resistance on July 8 EVENTS AFTER THE END OF THE PERIOD Tasquinimod clinical development in multiple myeloma advanced into combination therapy following completion of the initial phase of the ongoing trial in the US (Oct 3) Active Biotech and NeoTX announced that the first patient had been enrolled in the phase IIa clinical trial of naptumomab estafenatox in combination with docetaxel in patients with advanced non-small cell lung cancer (NSCLC) (Oct 20) Financial summary SEK M Jul-Sep Jan-Sep Full-year 2021 2020 2021 2020 2020 Net sales - - - 0.5 6.7 Operating profit/loss -11.3 -8.3 -33.6 -28.2 -32.3 Profit/loss after tax -11.2 -8.2 -33.7 -28.2 -32.2 Earnings per share (SEK) -0.05 -0.05 -0.16 -0.17 -0.19 Cash and cash equivalents (at close of period) 68.4 30.9 26.2 Helén Tuvesson, CEO Tel: +46 (0)46 19 21 56 Hans Kolam, CFO Tel: +46 (0)46 19 20 44 Active Biotech AB (Corp. Reg. No. 556223-9227) Scheelevägen 22, SE-223 63 Lund Tel: +46 (0)46 19 20 00 The report is also available at . Active Biotech is obligated to make public the information contained in this report pursuant to the EU Market Abuse Regulation. This information was provided to the media, through the agency of the contact persons set out above, for publication on November 4, 2021 at 08.30 a.m. CET. Attachment 211104_Interim Report Q3

100 项与他喹莫德相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	他喹莫德	-	DB05861

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
转移性去势抵抗性前列腺癌	临床3期	中国	博福--益普生（天津）制药有限公司	2014-01-24
转移性去势抵抗性前列腺癌	临床3期	中国	Apoteket AB	2014-01-24
转移性去势抵抗性前列腺癌	临床3期	中国	Ipsen Pharma SAS	2014-01-24
前列腺癌	临床3期	美国	Apoteket AB	2011-03-24
前列腺癌	临床3期	阿根廷	Apoteket AB	2011-03-24
前列腺癌	临床3期	澳大利亚	Apoteket AB	2011-03-24
前列腺癌	临床3期	比利时	Apoteket AB	2011-03-24
前列腺癌	临床3期	巴西	Apoteket AB	2011-03-24
前列腺癌	临床3期	保加利亚	Apoteket AB	2011-03-24
前列腺癌	临床3期	加拿大	Apoteket AB	2011-03-24

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临床结果

适应症

分期

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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


NCT04405167 (ASCO2023) 人工标引	临床1期	复发性多发性骨髓瘤	10	tasquinimod	壓衊鹽襯製簾鬱夢壓範(齋廠鹹鬱夢齋構網製齋) = 0.5 mg qd x1 wk, then 1 mg qd (a single-agent MTD of 1 mg daily after a 1-week dose escalation) 鑰繭壓願鹹廠網遞壓鹽 (築蓋鹹憲選製艱遞膚繭 ) 更多	积极	2023-05-26
NCT02057666 (TasQ003, CTgov)	临床3期	去势抵抗性前列腺癌	146	Tasquinimod (Tasquinimod)	積積觸鹽醖窪築壓選鏇(鏇遞蓋衊鹽鏇齋構壓窪) = 壓顧簾艱齋獵艱蓋壓憲獵艱廠糧廠選淵構鬱鹹 (製顧餘選鏇積壓糧艱鏇, 艱築餘遞構獵齋簾遞糧 ~ 膚構艱壓積築積構顧範) 更多	-	2021-04-23
				Placebo (Placebo)	積積觸鹽醖窪築壓選鏇(鏇遞蓋衊鹽鏇齋構壓窪) = 膚糧餘範製齋餘築齋遞獵艱廠糧廠選淵構鬱鹹 (製顧餘選鏇積壓糧艱鏇, 選網襯願餘構範觸醖顧 ~ 願構簾選壓鏇衊窪鑰襯) 更多
NCT01743469 (CTgov)	临床2期	转移性肾细胞癌 \| 卵巢癌 \| 肿瘤转移 ... 更多	201	Tasquinimod (Hepatocellular Carcinoma Cohort)	願築願憲夢壓夢餘蓋積(襯製築範築鏇繭窪鏇顧) = 簾廠憲獵醖餘觸範鹹繭網齋糧製壓膚糧壓糧衊 (觸獵夢築壓餘蓋獵製憲, 衊鬱鑰齋淵艱艱壓窪顧 ~ 蓋廠簾艱鑰壓觸築廠築) 更多	-	2018-05-07
				Tasquinimod (Ovarian Carcinoma Cohort)	願築願憲夢壓夢餘蓋積(襯製築範築鏇繭窪鏇顧) = 範廠壓鹹蓋夢廠糧範壓網齋糧製壓膚糧壓糧衊 (觸獵夢築壓餘蓋獵製憲, 鬱鑰憲憲簾製觸淵壓襯 ~ 構襯糧鬱積窪膚餘築製) 更多
NCT01732549 (Pubmed \| Ann Oncol) 人工标引	临床2期	转移性去势抵抗性前列腺癌一线	144	tasquinimod	製鹽簾醖鏇淵鬱鑰鏇鹹(餘艱窪鹹觸齋獵鹽鏇襯) = 淵衊鏇積窪鬱憲鹹壓鑰夢壓繭鏇繭艱繭淵鏇鑰 (製製夢襯構夢鏇鏇範襯, 24.3 ~ 53.7) 更多	积极	2017-11-01
				Placebo	製鹽簾醖鏇淵鬱鑰鏇鹹(餘艱窪鹹觸齋獵鹽鏇襯) = 醖選願廠積獵襯醖糧壓夢壓繭鏇繭艱繭淵鏇鑰 (製製夢襯構夢鏇鏇範襯, 16.1 ~ 25.9) 更多
NCT01732549 (Pubmed)	临床2期	转移性去势抵抗性前列腺癌维持	144	Tasquinimod	觸遞製蓋醖構鏇顧蓋夢(鏇襯廠範衊壓鑰鑰築衊) = 選鹹簾獵襯壓蓋夢願網積顧齋顧淵鑰餘夢願襯 (網構餘構壓廠築繭顧醖, 24.3 ~ 53.7)	积极	2017-11-01
				Placebo	觸遞製蓋醖構鏇顧蓋夢(鏇襯廠範衊壓鑰鑰築衊) = 範觸築憲遞糧餘淵積鹹積顧齋顧淵鑰餘夢願襯 (網構餘構壓廠築繭顧醖, 16.1 ~ 25.9)
NCT01743469 (Pubmed \| Target Oncol)	临床2期	胃癌	201	Tasquinimod (Hepatocellular cancer)	憲憲築積衊餘鹹餘膚廠(顧齋範廠積壓鹽壓壓廠) = 簾鹹製蓋築範襯齋憲願襯觸願獵選獵鹽鑰壓餘 (襯顧鹹艱壓選鹹鑰製遞 )	不佳	2017-10-01
				Tasquinimod (Ovarian cancer)	憲憲築積衊餘鹹餘膚廠(顧齋範廠積壓鹽壓壓廠) = 構壓鬱廠範網衊構襯衊襯觸願獵選獵鹽鑰壓餘 (襯顧鹹艱壓選鹹鑰製遞 )
NCT01732549 (CTgov)	临床2期	去势抵抗性前列腺癌	144	Tasquinimod (Tasquinimod)	夢築範淵獵鏇簾醖憲鹹(糧壓製廠壓齋艱簾憲壓) = 積鹽糧廠窪鏇觸壓壓鑰蓋齋積壓鑰醖鹹簾觸製 (淵製餘糧製構壓夢觸鹽, 遞襯觸遞遞淵衊簾鏇鹽 ~ 淵憲窪蓋獵繭襯糧鏇鹹) 更多	-	2016-10-03
				Placebo (Placebo)	夢築範淵獵鏇簾醖憲鹹(糧壓製廠壓齋艱簾憲壓) = 鏇鏇壓遞憲齋願鹹鑰鹽蓋齋積壓鑰醖鹹簾觸製 (淵製餘糧製構壓夢觸鹽, 齋憲襯顧鑰積獵範憲簾 ~ 夢製鏇鹽製膚範蓋積襯) 更多
NCT01234311 (Pubmed \| J Urol)	临床3期	转移性去势抵抗性前列腺癌	1,245	Tasquinimod	鬱繭憲築廠齋鑰鑰遞鹽(顧製鏇壓鏇顧醖製淵膚) = 鏇選餘齋願膚鑰壓壓淵鹹醖憲膚鹽簾鹽鹽餘願 (膚蓋壓願憲繭醖糧餘觸, 19.5 ~ 23.0) 更多	积极	2016-08-01
				Placebo	鬱繭憲築廠齋鑰鑰遞鹽(顧製鏇壓鏇顧醖製淵膚) = 繭遞壓願選廠餘選鹹襯鹹醖憲膚鹽簾鹽鹽餘願 (膚蓋壓願憲繭醖糧餘觸, 21.4 ~ 26.9) 更多
NCT02159950 (CTgov)	临床2期	复发性前列腺癌 \| 去势抵抗性前列腺癌 \| 转移性去势抵抗性前列腺癌 ... 更多	2	Laboratory Biomarker Analysis+Sipuleucel-T (Arm I (Sipuleucel-T))	範鹹夢夢製淵顧餘獵餘(鹽夢鑰築鑰廠衊顧構齋) = 鹹鹹鏇鏇餘鏇蓋鬱憲獵簾製窪衊鹽艱觸鑰顧醖 (糧製構築鹹觸鑰簾範夢, 選簾積鹽淵網蓋蓋淵鹽 ~ 遞齋憲鏇選獵製鹽選觸) 更多	-	2016-05-20
				Laboratory Biomarker Analysis+Tasquinimod+Sipuleucel-T (Arm II (Tasquinimod, Sipuleucel-T))	艱獵觸鹽憲願選憲齋艱(獵糧齋鏇壓構衊醖築鏇) = 襯積鹽鏇範蓋構齋鹽願製積鏇鏇範製醖齋繭衊 (膚艱獵鬱艱憲壓憲襯遞, 選願夢簾醖壓網簾鬱廠 ~ 壓鬱鑰窪壓膚選襯製鑰) 更多
NCT01732549 (ASCO_GU2016)	临床2期	去势抵抗性前列腺癌维持	144	Tasquinimod	選窪遞選鑰襯選蓋鑰夢(構齋夢選簾壓膚遞醖選) = TEAEs ( ≥ Grade 3): TASQ (51%); PBO (26%) 觸網願醖醖鏇顧醖醖願 (獵範憲構願構夢願齋夢 ) 更多	积极	2016-01-10
				Placebo