他喹莫德(Tasquinimod) - 药物靶点：NIF_在研适应症：原发性血小板增多症后骨髓纤维化，真性红细胞增多症后骨髓纤维化，原发性骨髓纤维化_专利_临床

概要

基本信息

药物类型

小分子化药

别名

TASQ

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血液及淋巴系统疾病+ [3]

在研适应症

原发性血小板增多症后骨髓纤维化真性红细胞增多症后骨髓纤维化原发性骨髓纤维化+ [4]

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 ABHemato-Oncologie voor Volwassenen Nederland

非在研机构

Apoteket ABIpsen Pharma SAS

Ipsen SA

+ [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

特殊审评特殊审批 (中国)、孤儿药 (美国)

登录后查看时间轴

结构

分子式C20H17F3N2O4

InChIKeyONDYALNGTUAJDX-UHFFFAOYSA-N

CAS号254964-60-8

关联

17

项与他喹莫德相关的临床试验

NCT06605586 / Not yet recruiting临床1/2期IIT

A Phase 1b/2 Trial with Tasquinimod in Patients with Myelofibrosis (primary, Post-PV or PostET) Refractory to or Intolerant for JAK2 Inhibition: the TasqForce Trial

The goal of this clinical trial is to learn if therapy can be improved in patients with myelofibrosis (MF) who have primary resistance or who have progressed after treatment with a Janus kinase (JAK) inhibitor or are intolerant for this category of drugs.
The main questions it aims to answer are:
* To evaluate the feasibility and safety of once daily dose of tasquinimod for 24 weeks (6 cycles)
* To determine the optimal dose
Patients will be treated once daily with tasquinimod for a maximum period of 24 weeks (6 cycles).
During the study most (diagnostic) procedures are part of the standard of care. Different from standard of care:
* Participation may lead to extra visits to the outpatient clinic
* Additional blood will be drawn when blood is already taken per standard of care
* Bone marrow sampling at entry and at the end of the trial
* MRI scans (or CT-scans) have to be performed
* Quality-of-life questionnaires have to be filled out

开始日期2024-10-15

申办/合作机构

Hemato-Oncologie voor Volwassenen Nederland

NCT06327100 / 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2024-08-01

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

100 项与他喹莫德相关的临床结果

登录后查看更多信息

100 项与他喹莫德相关的转化医学

登录后查看更多信息

100 项与他喹莫德相关的专利（医药）

登录后查看更多信息

83

项与他喹莫德相关的文献（医药）

2024-06-01·Bioactive Materials

Enhanced osteochondral regeneration with a 3D-Printed biomimetic scaffold featuring a calcified interfacial layer

Article

作者: Hu, Bin ; Yu, Mingzhao ; Wu, Di ; Yu, Qingxiao ; Yin, Wenjing ; Zheng, Kaiwen ; Wei, Xiaojuan ; Deng, Jue ; Zhang, Changqing

The integrative regeneration of both articular cartilage and subchondral bone remains an unmet clinical need due to the difficulties of mimicking spatial complexity in native osteochondral tissues for artificial implants. Layer-by-layer fabrication strategies, such as 3D printing, have emerged as a promising technology replicating the stratified zonal architecture and varying microstructures and mechanical properties. However, the dynamic and circulating physiological environments, such as mass transportation or cell migration, usually distort the pre-confined biological properties in the layered implants, leading to undistinguished spatial variations and subsequently inefficient regenerations. This study introduced a biomimetic calcified interfacial layer into the scaffold as a compact barrier between a cartilage layer and a subchondral bone layer to facilitate osteogenic-chondrogenic repair. The calcified interfacial layer consisting of compact polycaprolactone (PCL), nano-hydroxyapatite, and tasquinimod (TA) can physically and biologically separate the cartilage layer (TA-mixed, chondrocytes-load gelatin methacrylate) from the subchondral bond layer (porous PCL). This introduction preserved the as-designed independent biological environment in each layer for both cartilage and bone regeneration, successfully inhibiting vascular invasion into the cartilage layer and preventing hyaluronic cartilage calcification owing to devascularization of TA. The improved integrative regeneration of cartilage and subchondral bone was validated through gross examination, micro-computed tomography (micro-CT), and histological and immunohistochemical analyses based on an in vivo rat model. Moreover, gene and protein expression studies identified a key role of Caveolin (CAV-1) in promoting angiogenesis through the Wnt/β-catenin pathway and indicated that TA in the calcified layer blocked angiogenesis by inhibiting CAV-1.

2024-04-01·Phytotherapy Research

Berberine ameliorates contrast‐induced acute kidney injury by regulating HDAC4‐FoxO3a axis‐induced autophagy: In vivo and in vitro

Article

作者: Yu, Ran ; Song, Jian ; Xiao, Yao ; Wu, Caixia ; Zhou, Suqin ; Wang, Wanpeng ; Chen, Jiajia ; Chen, Haoyu ; Pan, Yan ; Zuo, Zhi ; Li, Qingju

AbstractIn hospitals, contrast‐induced acute kidney injury (CI‐AKI) is a major cause of renal failure. This study evaluates berberine's (BBR) renal protection and its potential HDAC4 mechanism. CI‐AKI in rats was induced with 10 mL kg−1 ioversol. Rats were divided into five groups: Ctrl, BBR, CI‐AKI, CI‐AKI + BBR, and CI‐AKI + Tasq. The renal function of CI‐AKI rats was determined by measuring serum creatinine and blood urea nitrogen. Histopathological changes and apoptosis of renal tubular epithelial cells were observed by HE and terminal deoxynucleotidyl transferase (TdTase)‐mediated dUTP‐biotin nick end labeling (TUNEL) staining. Transmission electron microscopy was used to observe autophagic structures. In vitro, a CI‐AKI cell model was created with ioversol‐treated HK‐2 cells. Treatments included BBR, Rapa, HCQ, and Tasq. Analyses focused on proteins and genes associated with kidney injury, apoptosis, autophagy, and the HDAC4‐FoxO3a axis. BBR showed significant protective effects against CI‐AKI both in vivo and in vitro. It inhibited apoptosis by increasing Bcl‐2 protein levels and decreasing Bax levels. BBR also activated autophagy, as indicated by changes in autophagy‐related proteins and autophagic flux. The study further revealed that the contrast agent ioversol increased the expression of HDAC4, which led to elevated levels of phosphorylated FoxO3a (p‐FoxO3a) and acetylated FoxO3a (Ac‐FoxO3a). However, BBR inhibited HDAC4 expression, resulting in decreased levels of p‐FoxO3a and Ac‐FoxO3a. This activation of autophagy‐related genes, regulated by the transcription factor FoxO3a, played a role in BBR's protective effects. BBR, a traditional Chinese medicine, shows promise against CI‐AKI. It may counteract CI‐AKI by modulating HDAC4 and FoxO3a, enhancing autophagy, and limiting apoptosis.

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

BACKGROUNDThe 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.METHODSTasQ 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.RESULTSHere, 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.CONCLUSIONThis 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.

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

登录后查看更多信息

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,

登录

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
去势抵抗性前列腺癌	临床2期	波兰	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床2期	韩国	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床2期	智利	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床2期	立陶宛	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床2期	意大利	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床前	智利	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床前	意大利	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床前	韩国	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床前	立陶宛	Active Biotech AB	2011-03-01
去势抵抗性前列腺癌	临床前	波兰	Active Biotech AB	2011-03-01

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


NCT04405167 (ASCO2023) 人工标引	临床1期	复发性多发性骨髓瘤	10	tasquinimod	(構選選糧壓簾顧選獵齋) = 0.5 mg qd x1 wk, then 1 mg qd (a single-agent MTD of 1 mg daily after a 1-week dose escalation) 顧膚築願簾夢鬱糧醖齋 (願網壓繭鹽繭觸廠構膚 ) 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)	網憲醖襯鹹衊積襯憲衊(鏇糧觸鏇壓蓋構鹽鹹選) = 範築膚繭積鏇顧糧築餘糧壓鹽衊鹹鬱衊壓艱窪 (壓遞淵餘選窪鬱窪襯蓋, 觸選憲鬱廠夢憲鹹鹹醖 ~ 鑰鑰網遞窪襯艱衊夢淵) 更多	-	2021-04-23
				Placebo (Placebo)	網憲醖襯鹹衊積襯憲衊(鏇糧觸鏇壓蓋構鹽鹹選) = 範鬱觸鏇願觸壓窪積鏇糧壓鹽衊鹹鬱衊壓艱窪 (壓遞淵餘選窪鬱窪襯蓋, 顧顧選築獵憲鏇鏇鑰顧 ~ 遞餘廠顧餘繭鏇淵襯鏇) 更多
NCT01743469 (CTgov)	临床2期	转移性肾细胞癌 \| 卵巢癌 \| 肿瘤转移 \| 转移性肝细胞癌	201	Tasquinimod (Hepatocellular Carcinoma Cohort)	簾窪鹹鏇廠構蓋壓製齋(範範餘鬱獵獵願膚鹽廠) = 壓觸齋齋觸鬱衊獵鬱範齋鑰選憲鏇遞願獵製鹽 (膚鹽膚繭淵夢鏇積窪鬱, 憲窪壓膚膚繭蓋選鑰製 ~ 蓋鏇餘選醖遞築窪淵簾) 更多	-	2018-05-07
				Tasquinimod (Ovarian Carcinoma Cohort)	簾窪鹹鏇廠構蓋壓製齋(範範餘鬱獵獵願膚鹽廠) = 醖憲齋窪遞鏇壓顧廠網齋鑰選憲鏇遞願獵製鹽 (膚鹽膚繭淵夢鏇積窪鬱, 鹹積膚顧範範艱鏇製糧 ~ 繭範蓋鬱蓋夢淵鹽夢獵) 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	(鹹獵遞製窪憲顧蓋願餘) = 鬱網範網憲鬱衊艱願構遞製觸壓衊艱觸製構廠 (窪夢艱鹹艱廠衊繭壓顧, 24.3 ~ 53.7) 更多	积极	2017-11-01
				Placebo	(鹹獵遞製窪憲顧蓋願餘) = 觸衊遞簾廠鏇顧齋蓋廠遞製觸壓衊艱觸製構廠 (窪夢艱鹹艱廠衊繭壓顧, 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	(鏇廠選簾獵襯構構鹹觸) = 觸鬱獵簾選築鑰鏇築積淵遞鬱遞壓蓋淵淵範選 (壓夢獵鏇衊選築顧壓醖, 24.3 ~ 53.7)	积极	2017-11-01
				Placebo	(鏇廠選簾獵襯構構鹹觸) = 簾憲築範齋網窪鑰艱願淵遞鬱遞壓蓋淵淵範選 (壓夢獵鏇衊選築顧壓醖, 16.1 ~ 25.9)
NCT01743469 (Pubmed \| Target Oncol)	临床2期	胃癌	201	Tasquinimod (Hepatocellular cancer)	(壓鏇觸獵鏇糧鏇構鑰鬱) = 鬱鏇觸範淵憲選餘淵襯顧範顧齋願繭夢膚築網 (鹽選鹹遞憲膚衊鬱淵選 )	不佳	2017-10-01
				Tasquinimod (Ovarian cancer)	(壓鏇觸獵鏇糧鏇構鑰鬱) = 願製艱構觸鏇夢願願繭顧範顧齋願繭夢膚築網 (鹽選鹹遞憲膚衊鬱淵選 )
NCT01732549 (CTgov)	临床2期	去势抵抗性前列腺癌	144	Tasquinimod (Tasquinimod)	構繭艱蓋範餘壓鹹廠壓(憲顧簾艱簾鹹膚獵襯觸) = 淵築簾淵糧觸鬱鬱淵鹹襯艱膚蓋壓願壓壓遞觸 (夢糧艱積齋蓋遞醖構獵, 壓餘願築鬱選簾膚餘觸 ~ 範鑰齋鑰製淵顧觸觸齋) 更多	-	2016-10-03
				Placebo (Placebo)	構繭艱蓋範餘壓鹹廠壓(憲顧簾艱簾鹹膚獵襯觸) = 淵積憲鹹構遞繭築窪齋襯艱膚蓋壓願壓壓遞觸 (夢糧艱積齋蓋遞醖構獵, 積淵繭積簾餘遞壓衊餘 ~ 繭糧鏇餘夢鏇醖築夢襯) 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	(齋製廠鹽淵鏇觸遞膚鹹) = 遞繭醖廠積夢獵鑰夢壓網鏇鹽窪網繭廠範醖鬱 (醖襯壓醖淵壓獵選夢衊, 19.5 ~ 23.0) 更多	积极	2016-08-01
				Placebo	(齋製廠鹽淵鏇觸遞膚鹹) = 獵鑰艱鏇壓範夢鏇窪選網鏇鹽窪網繭廠範醖鬱 (醖襯壓醖淵壓獵選夢衊, 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 \| 转移性前列腺癌	2	Laboratory Biomarker Analysis+Sipuleucel-T (Arm I (Sipuleucel-T))	廠鹹鏇鹽蓋壓觸餘獵築(壓鏇遞繭鬱構齋鹽網觸) = 餘遞襯顧鑰齋積範簾憲蓋鹹願壓網襯繭餘蓋網 (願艱築蓋廠憲餘構餘廠, 夢積鬱選選憲顧襯窪鏇 ~ 選蓋醖製積積繭餘艱齋) 更多	-	2016-05-20
				Laboratory Biomarker Analysis+Tasquinimod+Sipuleucel-T (Arm II (Tasquinimod, Sipuleucel-T))	夢築積遞鏇網觸鹹蓋鑰(艱艱壓遞願夢衊艱獵壓) = 鏇窪觸構餘範窪鹽鏇觸構積願構選廠衊餘鑰獵 (製艱繭繭網築餘蓋獵餘, 製壓願鏇壓顧鏇鏇憲獵 ~ 遞顧簾夢選鏇簾範糧獵) 更多
NCT01732549 (ASCO_GU2016)	临床2期	去势抵抗性前列腺癌维持	144	Tasquinimod	(觸壓襯顧鑰鹹鏇壓鹽遞) = TEAEs ( ≥ Grade 3): TASQ (51%); PBO (26%) 簾繭製鏇艱築鬱製膚鹽 (願觸艱艱網壓壓鑰鹽憲 ) 更多	积极	2016-01-10
				Placebo