Resminostat is a potent, orally available inhibitor of Class I, IIb and IV histone deacetylases (HDACs), including a pronounced activity against HDAC6. Resminostat targets epigenetic changes observed in tumour cells and has the potential to provide significant benefit to patients with advanced malignancies by inhibiting tumour progression and metastasis or even inducing tumour regression.
This will be a Phase 1, open-label, non-randomized, single dose study of the absorption, metabolism, excretion of [14C] resminostat following a single oral dose in healthy male participants.
The purpose of this study is to determine the absorption, metabolism, and excretion (AME) of [14C] resminostat and to characterize and determine the metabolites present in plasma, urine, and, where possible, faeces in healthy male participants following a single oral administration. Knowledge of the metabolism and excretion of parent drug and its metabolites is useful for evaluating the Metabolites in Safety Testing requirements elucidated in the International Conference on Harmonisation (ICH) M3, and the likelihood of effects of renal or hepatic impairment on the disposition of resminostat, and the likelihood for drug-drug interactions with resminostat. The results from this study may guide future study designs using special populations or evaluating the potential for drug-drug interactions.

开始日期2021-10-12

申办/合作机构

4SC AG

NCT02953301

/ Completed临床2期

A Multicentre, Double Blind, Randomised, Placebo-controlled, Phase II Trial to Evaluate Resminostat for Maintenance Treatment of Patients With Advanced Stage (Stage IIB-IVB) Mycosis Fungoides (MF) or Sézary Syndrome (SS) That Have Achieved Disease Control With Systemic Therapy - the RESMAIN Study

The purpose of this study is to determine whether resminostat will be able to delay or prevent worsening of disease in patients with advanced stage mycosis fungoides or Sézary Syndrome that have recently achieved disease control with previous systemic therapy.

开始日期2016-11-01

申办/合作机构

4SC AG

100 项与 Resminostat 相关的临床结果

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100 项与 Resminostat 相关的转化医学

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100 项与 Resminostat 相关的专利（医药）

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项与 Resminostat 相关的文献（医药）

2025-08-01·ACTA BIOCHIMICA ET BIOPHYSICA SINICA

Exploring DNA topoisomerase II alpha in adrenocortical carcinoma through multi-omics analysis: a potential biomarker and therapeutic targetTOP2A in ACC

Article

作者: Zhuo, Yangjia ; Cai, Chao ; Ye, Jianheng ; Deng, Junhong ; Lu, Jianming ; Wu, Zhenjie ; Han, Zhaodong ; Deng, Pei ; Zhong, Weide ; Chen, Jiahong ; Zhang, Le ; Wu, Yongding ; Tang, Jiaojiao ; Liang, Yingke ; Liang, Yuxiang ; Xie, Wenjie ; Cai, Zhouda

Adrenocortical carcinoma (ACC) is a rare but aggressive cancer. Recent studies identified DNA Topoisomerase II Alpha (TOP2A) as a potential biomarker for ACC, which can provide new avenues for targeted therapy and improve clinical outcomes. This study aims to elucidate the role of TOP2A in ACC by exploring its prognostic value and identifying inhibitors for ACC therapy. Utilizing RNA sequencing data, mutation data, and clinical information from The Cancer Genome Atlas (TCGA-ACC) and additional datasets from the Gene Expression Omnibus (GEO), differential expression and prognostic analyses are conducted to assess the significance of TOP2A in ACC. Immunohistochemistry and cell assays, including cell viability, colony formation, and transwell assays, are conducted to validate the oncogenic effects of TOP2A. The "IOBR" R package is used to examine the relationship between TOP2A expression and CD8 ⁺ T-cell infiltration. The CMap platform is used to identify potential TOP2A inhibitors. In vivo assays verify the therapeutic effect of TOP2A inhibitors on ACC. Our findings indicate that TOP2A is significantly overexpressed in ACC and is associated with poor prognosis. Immunohistochemistry and cell assays confirm the oncogenic role of TOP2A. Furthermore, distinct gene expression patterns related to different TOP2A expression levels are identified, influencing the response to immunotherapy. Potential inhibitors targeting TOP2A are discovered, and the therapeutic effects of resminostat and etoposide are confirmed via in vivo assays, suggesting new therapeutic strategies for ACC treatment. In conclusion, TOP2A serves as a crucial biomarker in ACC and is associated with adverse clinical outcomes and a diminished immune response. The identification of potential inhibitors against TOP2A opens new avenues for the development of targeted therapies for ACC patients.

2025-05-01·BIOORGANIC & MEDICINAL CHEMISTRY

Design, synthesis and biological evaluation of novel hydroxamic acid-derived histone deacetylase inhibitors bearing a 2-oxoindoline scaffold as potential antitumor agents

Article

作者: Thien, Nguyen Duc ; Anh, Duong Tien ; Kim, Ji Su ; Dung, Do Thi Mai ; Thang, Nguyen Quoc ; Nam, Nguyen-Hai ; Han, Sang-Bae ; Oanh, Dao Thi Kim ; Kim, Jiyeon ; Kang, Jong Soon ; Huong, Tran Thi Lan ; Kim, Hwa Kyung ; Tung, Truong Thanh

Histone deacetylases (HDACs) have emerged as compelling targets in developing anticancer therapeutics. This study outlines the development, synthesis, and biological evaluation of novel hydroxamic acid derivatives featuring a 2-oxoindoline scaffold, which exhibit high HDAC inhibitory activity and potential anticancer effects. Three series of N-hydroxycinnamamides, N-hydroxyheptanamides, and N-hydroxybenzamides were synthesized and assessed for their biological activity. The results of the biological activity evaluation indicated that the synthesized derivatives exhibited notable inhibitory effects against SW620 (colon cancer) and HCT116 (human colorectal carcinoma). Compound N-hydroxy-7-(2-oxoindolin-1-yl)heptanamide (6a) exhibited remarkable HDAC inhibitory activity, achieving sub-nanomolar potency with an IC₅₀ value of less than 0.001 µM. While this potent HDAC inhibition suggests strong enzymatic activity, the anticancer activity of 6a against SW620 and HCT116 was comparable to that of SAHA (IC₅₀ of 0.101 µM). Analysis of selected compound 6a also revealed that this compound effectively triggered both early and late stages of apoptosis and caused cell cycle arrest at the G2/M phase in SW620 cells. Finally, docking studies and molecular dynamics study conducted on the HDAC isoforms for series 6a-e identified key structural features that play a significant role in the inhibitory activity of the synthesized compounds.

2025-03-01·VIROLOGY

A high-throughput, microplate reader-based method to monitor in vitro HIV latency reversal in the absence of flow cytometry

Article

作者: Nkwelle, Chantal Emade ; Esemu, Seraphine N ; Ndip, Roland N ; Liang, Kimberly ; Ntie-Kang, Fidele ; Tietjen, Ian ; Cassel, Joel ; Stephens, Unique ; Salvino, Joseph M ; Montaner, Luis J

J-Lat cells are derivatives of the Jurkat CD4⁺ T cell line that contain a non-infectious, inducible HIV provirus with a GFP tag. While these cells have substantially advanced our understanding of HIV latency, their use by many laboratories in low and middle-income countries is restricted by limited access to flow cytometry. To overcome this barrier, we describe a modified J-Lat assay using a standard microplate reader that detects HIV-GFP expression following treatment with latency-reversing agents (LRAs). We show that HIV reactivation by control LRAs like prostratin and romidepsin is readily detected with dose dependence and with significant correlation and sensitivity to standard flow cytometry. For example, 10 μM prostratin induced a 20.1 ± 3.3-fold increase in GFP fluorescence in the microplate reader assay, which corresponded to 64.2 ± 5.0% GFP-positive cells detected by flow cytometery. Similarly, 0.3 μM prostratin induced a 1.7 ± 1.2-fold increase compared to 8.7 ± 5.7% GFP-positive cells detected. Using this method, we screen 79 epigenetic modifiers and identify CUDC-101, molibresib, and quisinostat as novel LRAs. This microplate reader-based method offers accessibility to researchers in resource-limited regions to work with J-Lat cells and more actively participate in global HIV cure research efforts.

项与 Resminostat 相关的新闻（医药）

2026-01-11

·今日头条

脑胶质瘤治疗指南：化疗与靶向药的明智选择

医学进步正让“脑内顽疾”从绝症变为可控的慢性病。在神经外科病房里，每天都有患者家属拿着检查报告询问：“医生，我家人这种情况该选择化疗还是靶向药？”这不仅是一个治疗选择，更是一场生死抉择。随着医学进步，脑胶质瘤治疗已从“一刀切”进入精准医疗时代。最新数据显示，我国恶性脑肿瘤年新发病例约8.75万人，面对这一“脑内顽疾”，科学治疗方案的制定尤为重要。中国脑胶质瘤协作组推出的最新指南，为患者提供了明确的治疗路径。化疗：基石药物的精准应用化疗作为脑胶质瘤治疗的基石，其应用已从经验用药走向精准选择。替莫唑胺（TMZ）作为一线药物，通过破坏肿瘤细胞DNA发挥抗肿瘤作用。化疗的成功应用关键在于把握“ 时间密码 ”——同步放化疗+辅助化疗的STUPP方案。这一方案将患者中位生存期从单纯手术的12个月延长至14.6个月，部分患者甚至能存活超过5年。分子标记物检测是实现精准化疗的关键。MGMT启动子甲基化状态是预测TMZ疗效的“风向标”。MGMT蛋白能修复被TMZ破坏的DNA，而甲基化会“关闭”MGMT基因，使癌细胞对TMZ更敏感。研究表明，MGMT甲基化阳性患者接受TMZ治疗生存获益更显著。对于低级别胶质瘤，PCV方案（丙卡巴肼+洛莫司汀+长春新碱）显示出卓越疗效。研究证实，接受PCV辅助化疗的WHO 2级胶质瘤患者，中位生存期由单纯放疗后的7.8年延长至13.3年。靶向治疗：精准打击的“生物导弹” 与传统化疗“杀敌一千，自损八百”不同，靶向药像是给药物装上了导航系统，变成精准打击肿瘤细胞的“生物导弹”。 IDH抑制剂为低级别胶质瘤患者带来新希望。Vorasidenib作为首个具有较高脑渗透性的IDH1/2双靶点抑制剂，Ⅲ期INDIGO研究显示，相较于安慰剂，Vorasidenib能明显改善低级别胶质瘤患者的无进展生存期。针对MET融合基因的伯瑞替尼成为我国脑胶质瘤靶向治疗的里程碑。II/Ⅲ期FUGEN研究表明，与化疗组相比，伯瑞替尼单药组的死亡风险降低48%，基线肿瘤直径≤3cm的患者OS从4.2个月增至32.5个月。对于BRAF V600E突变患者，达拉非尼+曲美替尼联合方案提供了新的治疗选择。这类突变在毛细胞型星形细胞瘤、多形性黄色星形细胞瘤中检出率较高，靶向药物能精准抑制突变基因活性。个体化治疗：从分子分型到方案制定现代脑胶质瘤治疗强调“ 量体裁衣 ”式的个体化策略。通过检测肿瘤组织的分子标记物，医生能为患者定制最佳治疗方案。分子分型包括IDH突变、1p/19q联合缺失、MGMT启动子甲基化、TERT突变等指标。不同分子分型的肿瘤对手术切除、放疗和化疗、免疫靶向治疗具有不同的敏感性。例如，IDH突变型低级别胶质瘤患者对PCV方案反应更好，部分患者甚至可通过化疗延缓手术。而MGMT甲基化阴性的患者，可考虑TMZ剂量密集方案或联合用药策略来克服耐药。中国脑胶质瘤协作组建议，所有疑似或已明确的儿童低级别胶质瘤、成人少见类型胶质瘤，以及影像学上呈特殊生长模式的高级别胶质瘤均应进行分子检测，以指导后续治疗。未来展望：创新疗法与组合策略肿瘤电场治疗（TTFields）作为一种新型物理疗法，通过贴敷于头皮的转换片产生交变电场而发挥控瘤作用。EF-14研究显示，TTFields联合TMZ相比单用TMZ，中位总生存期有显著获益（20.9个月 vs. 16.0个月）。免疫治疗也在探索中前进。虽然PD-1/PD-L1抑制剂在常规胶质瘤中疗效有限，但对MSI-H/dMMR等罕见亚群仍提供了关键选择。CAR-T、肿瘤疫苗等新型免疫疗法正通过临床试验展现潜力。针对替莫唑胺耐药这一临床难题，最新研究发现小分子化合物Resminostat能够特异性破坏HDAC1-CTCF凝聚体，在耐药GBM的模型中显著恢复TMZ敏感性，为克服肿瘤耐药提供了新思路。治疗指南：科学选择的关键因素中国脑胶质瘤协作组建议，治疗选择应综合考虑以下因素：肿瘤级别与分子特征：低级别与高级别胶质瘤治疗策略不同，分子标记物如IDH突变、MGMT甲基化状态直接影响药物选择。患者基本情况：年龄、KPS评分、器官功能状况决定治疗耐受性。年老或体弱者可选择短疗程放疗或单纯TMZ化疗。治疗史：初治与复发患者方案不同，复发胶质瘤需考虑既往治疗类型与反应情况。药物可及性：一些新药虽证实有效，但需考虑医保政策与经济负担。中国工程院院士江涛强调：“未来10年是我国医药创新‘弯道超车’黄金期。随着精准医疗的发展，脑胶质瘤治疗正迎来前所未有的机遇。” 面对脑胶质瘤这一复杂疾病，化疗与靶向治疗各展所长。传统化疗作为基石治疗，在精准应用下仍发挥重要作用；靶向治疗作为新兴力量，为特定患者群带来突破性获益。医学进步让脑胶质瘤治疗从“一刀切”走向个体化精准医疗。通过分子分型指导下的科学选择，患者能够获得最适合的治疗方案，实现生存期与生活质量的平衡。正如专家所言，这是一场“多兵种协同作战”——神经外科、放疗科、肿瘤内科、病理科通力合作，共同为患者制定最佳治疗方案。相信随着医学发展，更多患者能够实现长期生存，与瘤共存。

临床2期核酸药物

2026-01-10

·BioArt

Nat Chem Biol | 赵蔚/董鹏团队揭示Resminostat靶向HDAC1凝聚体克服肿瘤耐药的药理机制

胶质母细胞瘤（Glioblastoma，GBM）是成人中最常见且侵袭性最强的原发性脑肿瘤之一，患者预后极差，中位总生存期通常不足两年【1,2】。替莫唑胺（Temozolomide，TMZ）是目前唯一被广泛应用的一线化疗药物，可在一定程度上延长患者生存，但约90%的初始敏感病例最终会因获得性耐药而导致肿瘤复发【3】。如何有效克服TMZ耐药仍是临床治疗中的重大挑战。 2026年1月9日，赵蔚教授与董鹏教授团队合作在Nature Chemical Biology 发表了题为Deacetylase-Independent HDAC1 Condensation Defines Temozolomide Response in Glioblastoma的研究论文。该研究发现，替莫唑胺（TMZ）治疗可诱导胶质母细胞瘤（GBM）细胞形成HDAC1-CTCF凝聚体，从而导致染色质结构重塑和DNA修复活性增强，促进TMZ获得性耐药的发生。更为重要的是，研究团队鉴定出小分子化合物Resminostat能够特异性靶向该凝聚体，在耐药GBM的患者来源异种移植（PDX）模型中显著恢复TMZ敏感性，有效克服肿瘤耐药。研究团队首先利用董鹏教授自主研发的高通量三维超分辨成像技术3D-ATAC-STORM，发现TMZ耐药GBM细胞的染色质可及性显著降低，并系统描绘了其三维基因组结构特征。进一步的机制研究表明，耐药细胞染色质可及性降低主要归因于TMZ处理诱导HDAC1-CTCF凝聚体的形成，该凝聚体在染色质上聚集并限制局部开放性。为探索药物干预策略，研究团队建立了针对HDAC1-CTCF凝聚体的高内涵筛选体系，发现小分子化合物Resminostat能够特异性破坏该凝聚体的形成。在TMZ耐药GBM的PDX模型中，Resminostat显著逆转肿瘤对TMZ的耐药性，促进DNA损伤反应并抑制肿瘤进展。进一步的机制研究表明，Resminostat对HDAC1-CTCF凝聚体的作用并不依赖于抑制HDAC1的经典组蛋白去乙酰化酶活性，而是通过干扰其固有无序区域（Intrinsically Disordered Region, IDR）介导的相分离过程实现。Resminostat可破坏 HDAC1-CTCF 凝聚体的形成与稳定性，从而抑制其介导的DNA修复复合物在损伤位点的组装，降低DNA损伤修复效率并增强TMZ诱导的DNA损伤积累，最终有效克服肿瘤细胞的耐药性。本研究系统揭示了HDAC1-CTCF凝聚体介导的染色质重塑与DNA修复在胶质母细胞瘤替莫唑胺耐药中的关键作用机制，拓展了对HDAC1生物学作用模式的理解。该研究证实小分子化合物Resminostat可通过破坏HDAC1-CTCF凝聚体从而恢复TMZ敏感性，为靶向肿瘤凝聚体以克服肿瘤耐药提供了新的理论依据。值得强调的是，Resminostat 已在皮肤 T 细胞淋巴瘤（ClinicalTrials ID: NCT02953301）、肝细胞癌（NCT02400788）及霍奇金淋巴瘤（NCT01037478）等多种肿瘤中开展过早期临床研究，相关结果显示，其安全性特征较为明确，整体耐受性处于可管理范围内。虽然其在GBM中用于克服TMZ耐药的疗效尚未开展临床验证，但本研究为其转化应用提供了坚实的理论与实验基础。未来研究可进一步优化Resminostat的血脑屏障通透性与脑内药代动力学特征，以期实现其在GBM中的精准递送与有效治疗。本研究由中山大学中山医学院、中国科学院深圳先进技术研究院、南方科技大学、广东省人民医院及中南大学湘雅医院等单位联合完成。中山大学张钦凯博士、邱茹博士与南方医科大学鲁冰教授为论文共同第一作者。中南大学湘雅医院刘庆教授、龙文勇医生及黄蒙医生为本研究提供了重要的GBM临床样本与临床数据支持。原文链接： https://www.nature.com/articles/s41589-025-02123-8 制版人：十一参考文献 1. Michael Weller, Guido Reifenberger. et al. Glioma. Nat Rev Dis Primers. 2024 May 9;10(1):33. 2. Lauren R Schaff, Ingo K Mellinghoff. Glioblastoma and Other Primary Brain Malignancies in Adults: A Review. JAMA. 2023 Feb 21;329(7):574-587. 3. Chia-Hung Chien. et al. Dissecting the mechanism of temozolomide resistance and its association with the regulatory roles of intracellular reactive oxygen species in glioblastoma. J Biomed Sci. 2021 Mar 8;28(1):18. 学术合作组织（*排名不分先后）战略合作伙伴（*排名不分先后） · 转载须知【非原创文章】本文著作权归文章作者所有，欢迎个人转发分享，未经作者的允许禁止转载，作者拥有所有法定权利，违者必究。 BioArt Med Plants 人才招聘近期直播推荐点击主页推荐活动关注更多最新活动！

放射疗法

2025-05-23

·4sc.com

Resminostat (Kinselby) received a Negative CHMP Opinion in the EU

Planegg-Martinsried, Germany, 23 May 2025 – As already expected and announced on Tuesday, 20 May 2025, 4SC AG (“4SC”) (Frankfurt Stock Exchange, Prime Standard: VSC; ISIN: DE000A3E5C40) received a Negative Opinion on the Company’s Market Authorization Application for Resminostat (Kinselby) for the treatment of patients with advanced stage cutaneous T-cell lymphoma (CTCL) from the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA). Following an Oral Explanation on 20 May 2025, and the CHMP’s review of the data on quality, safety and efficacy for Resminostat (Kinselby) in the treatment of patients with advanced stage mycosis fungoides (MF) and Sézary syndrome (SS) that have achieved at least stable disease with at least one prior systemic therapy or Total Skin Electron Beam therapy (TSEB) – the CHMP considers by consensus that the efficacy of the above-mentioned medicinal product is not sufficiently demonstrated, and therefore, recommends the refusal of the granting of the marketing authorisation for Resminostat (Kinselby). As already communicated on 20 May 2025, 4SC will thus cease all efforts to develop and commercialize Resminostat (Kinselby). Currently, 4SC has at least a 12-month cash runway to finance the Company’s projected expenses as the Management and Supervisory Boards consider all options for the Company, including liquidation. Jason Loveridge, Ph.D., CEO of 4SC, commented: “We had hoped that the long wait for a maintenance treatment to help manage CTCL would soon be over. We are therefore deeply disappointed with this outcome as it is a further setback for people living with this rare and incurable disease.” For further information, please contact: 4SC AG ir-pr@4sc.com Optimum Strategic Communications Nick Bastin, Vareen Outhonesack Phone: +44 20 3922 0891 4SC@optimumcomms.com About 4SC 4SC is a biotech company focused on trying to improve the lives of patients suffering with advanced-stage cutaneous T-cell lymphoma (CTCL), a high unmet medical need. 4SC’s goal is to increase the value of the Company by advancing its own drug development programs through to market and entering into partnerships with pharmaceutical and biotech companies for the further development or commercialization of its drug candidates. 4SC is headquartered in Planegg-Martinsried near Munich, Germany. The Company had 15 employees as of 31 March 2025 and is listed on the Prime Standard of the Frankfurt Stock Exchange (FSE Prime Standard: VSC; ISIN: DE000A3E5C40). Information set forth in this press release contains forward-looking statements, which involve risks and uncertainties. The forward-looking statements contained herein represent the judgement of 4SC as of the date of this press release. Such forward-looking statements are neither promises nor guarantees but are subject to a variety of risks and uncertainties, many of which are beyond 4SC’s control, and which could cause actual results to differ materially from those contemplated in these forward-looking statements. 4SC expressly disclaims any obligation or undertaking to release any updates or revisions to any such statements to reflect any change in its expectations or any change in events, conditions or circumstances on which any such statement is based.

100 项与 Resminostat 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	Resminostat	-	DB12392

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
蕈样真菌病	临床2期	日本	4SC AG	2016-11-01
蕈样真菌病	临床2期	奥地利	4SC AG	2016-11-01
蕈样真菌病	临床2期	比利时	4SC AG	2016-11-01
蕈样真菌病	临床2期	法国	4SC AG	2016-11-01
蕈样真菌病	临床2期	德国	4SC AG	2016-11-01
蕈样真菌病	临床2期	希腊	4SC AG	2016-11-01
蕈样真菌病	临床2期	意大利	4SC AG	2016-11-01
蕈样真菌病	临床2期	荷兰	4SC AG	2016-11-01
蕈样真菌病	临床2期	波兰	4SC AG	2016-11-01
蕈样真菌病	临床2期	西班牙	4SC AG	2016-11-01

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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


NCT02953301 (RESMAIN, EORTC_CLTG2024)	临床2期	蕈样真菌病 \| 塞扎里综合征维持	201	Resminostat	網蓋鬱網觸鹽醖鹹鹹遞(願獵鬱壓廠願艱鹹膚夢) = 鹹襯構顧鹽衊廠憲壓積獵選廠鑰遞網膚觸衊壓 (膚鑰膚顧膚觸構鹹積襯 ) 更多	积极	2024-10-09
				Placebo	網蓋鬱網觸鹽醖鹹鹹遞(願獵鬱壓廠願艱鹹膚夢) = 壓簾艱願鹽憲衊糧糧積獵選廠鑰遞網膚觸衊壓 (膚鑰膚顧膚觸構鹹積襯 ) 更多
NCT02953301 (RESMAIN, Corporate Publications) 人工标引	临床2期	皮肤T细胞淋巴瘤维持	201	Resminostat	壓膚醖淵鬱選鬱鏇糧壓(築淵餘壓鹹憲鹽簾壓襯) = 選壓觸壓遞簾膚齋顧廠鑰醖齋膚網蓋膚淵簾襯 (築窪顧鬱夢鏇壓簾壓鹽 ) 更多	积极	2023-09-25
				Placebo	壓膚醖淵鬱選鬱鏇糧壓(築淵餘壓鹹憲鹽簾壓襯) = 製築壓廠選齋遞襯簾醖鑰醖齋膚網蓋膚淵簾襯 (築窪顧鬱夢鏇壓簾壓鹽 ) 更多
NCT01037478 (Pubmed \| Leukemia) 人工标引	临床2期	霍奇金淋巴瘤	37	resminostat	廠窪衊遞鑰獵選淵遞網(衊膚淵鹽淵齋築醖願醖) = 構鹽鹹鑰範觸齋鏇鏇繭艱憲製餘製網夢繭餘鑰 (廠鏇觸襯蓋蓋願憲襯選 ) 更多	积极	2019-03-01
NCT02400788 (ASCO_GI2017)	临床1/2期	晚期肝细胞癌一线	179	Sorafenib monotherapy	鬱蓋鹽積構鏇構簾膚製(夢艱壓鏇鑰醖製築夢鑰) = 範積糧艱膚襯膚網繭鑰構淵範廠襯鹹膚觸衊範 (鹹製鏇餘艱醖積鏇餘遞 )	积极	2017-03-21
				Sorafenib/Resminostat combination therapy	鬱蓋鹽積構鏇構簾膚製(夢艱壓鏇鑰醖製築夢鑰) = 積窪範襯鏇觸夢構範憲構淵範廠襯鹹膚觸衊範 (鹹製鏇餘艱醖積鏇餘遞 )
NCT00943449 (SHELTER, Pubmed \| J Hepatol) 人工标引	临床2期	晚期肝细胞癌二线	57	sorafenib+resminostat	憲窪繭淵襯獵簾鹽簾齋(願構蓋襯廠廠鬱廠憲齋) = 淵齋顧淵願鏇壓簾積顧積衊淵鬱構願壓積鏇餘 (積獵鏇鹽蓋獵鹽範鹽鑰 ) 更多	积极	2016-08-01
				resminostat	憲窪繭淵襯獵簾鹽簾齋(願構蓋襯廠廠鬱廠憲齋) = 壓選餘獵製鬱製築夢築積衊淵鬱構願壓積鏇餘 (積獵鏇鹽蓋獵鹽範鹽鑰 ) 更多
NCT00943449 (SHELTER, ASCO2013)	临床1/2期	晚期肝细胞癌二线	45	Resminostat alone	繭獵鏇鏇壓鬱鑰願選壓(簾齋繭範糧鏇夢艱膚遞) = 襯繭製膚壓鏇壓鬱艱糧簾築簾願淵餘繭簾廠襯 (顧窪淵淵積膚願獵襯鑰 )	积极	2013-05-20