The purpose of this study is to learn more about a drug called Vorinostat (an experimental drug) in combination with chemoradiation. The intention of this study is to learn if this drug is safe for the participants and whether this drug with chemoradiation is able to further increase the clinical efficacy of chemoradiation, which is an approved therapy. The main question it aims to answer is: How may Vorinostat interact with standard chemotherapy and radiation therapy in head and neck cancer? Participants will receive the study drug (Vorinostat) as a pre-treatment, followed by standard chemoradiation.

开始日期2025-06-01

申办/合作机构

The Case Comprehensive Cancer Center

NCT04339751

/ Recruiting临床2期IIT

The Effect of Vorinostat on ACTH Producing Pituitary Adenomas in Cushing's Disease

Background:
Cushing s disease is caused by excess ACTH hormone release by a benign tumor of the pituitary gland. It can lead to decreased quality of life and early death. The current best treatment for Cushing s disease is surgery. If surgery does not work or if the tumor returns, there are no more good treatment options. Vorinostat, which is approved to treat a type of lymphoma, might be a treatment option.
Objective:
To test vorinostat to see if it can kill tumor cells and change the number of hormones released in people with Cushing s disease.
Eligibility:
People ages 18 and older who have Cushing s disease and are scheduled for surgery under protocol 03-N-0164 to remove a tumor in their pituitary gland
Design:
Participants will be screened under protocol 03-N-0164.
Participants will stay in the hospital for 8 days before their surgery.
On the first day, participants will have a physical exam and blood tests. They will have their urine collected for testing all day. They will have an ECG: For this, small metal disks or sticky electrode pads will be placed on their chest to record heart activity.
For the next 7 days, participants will have blood tests and all-day urine collection. They will drink at least 2 liters of fluid per day. They will take the study drug by mouth each morning.
On the eighth day, participants will have their surgery. Leftover tissue will be collected for research.
On the day they are discharged from the hospital, participants will have a physical exam and blood tests.

开始日期2025-04-09

申办/合作机构

National Institute of Neurological Disorders & Stroke

NCT06693284

/ Recruiting早期临床1期IIT

A Window of Opportunity Trial of Mirdametinib Plus Vorinostat for NF1 Associated, H3K27 Trimethylation Deficient Malignant Peripheral Nerve Sheath Tumor [MPNST]

This is a single center Phase 0 "window of opportunity" trial for the treatment of newly diagnosed, PRC2 deficient, primary malignant peripheral nerve sheath tumors (MPNSTs) with a short course of the combination of mirdametinib and vorinostat prior to the most appropriate standard of care treatment for their specific tumor (typically localized radiation followed by surgical resection). Four to eight patients, 12 years of age or older and meeting the study's biomarker inclusion criteria, would be enrolled onto this trial. After voluntary written consent (assent with parent consent for minors) the patient undergoes MRI and PET imaging of the tumor and a needle biopsy to collect tumor is performed. Patients with histone H3K27 trimethylation deficient MPNST, as confirmed by immunohistochemistry, receive a single 28-day course of mirdametinib and vorinostat at standard oral dosing for each. At day 26, 27, or 28 the patient returns to clinic for a research visit repeating the baseline MRI and PET imaging and the needle biopsy for tumor tissue.
This ends direct study participation. The patient goes on to the most appropriate standard of care treatment for their MPNST. Information about the subsequent standard of care treatment is collected for the purposes of this study.

开始日期2024-12-01

申办/合作机构

University of Minnesota

100 项与伏立诺他相关的临床结果

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100 项与伏立诺他相关的转化医学

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100 项与伏立诺他相关的专利（医药）

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项与伏立诺他相关的文献（医药）

2025-12-31·JOURNAL OF DERMATOLOGICAL TREATMENT

Insights into treatment of patients with mycosis fungoides or Sézary syndrome using mogamulizumab

Article

作者: Kim, Youn H. ; Akilov, Oleg ; Scarisbrick, Julia ; Bagot, Martine ; Ristuccia, Robert ; Wu, Wende ; Dwyer, Karen ; Foss, Francine

PURPOSE:

Mogamulizumab demonstrated improved outcomes vs. vorinostat across a range of disease and patient characteristics in patients with mycosis fungoides or Sézary syndrome in the MAVORIC trial.

MATERIALS AND METHODS:

This post-hoc analysis further examined MAVORIC data to assess factors associated with long-term response (ORR >12 months), time to next treatment (TTNT), and impact of concomitant steroid use, lymphopenia, and mogamulizumab-associated rash (MAR) on patient response.

RESULTS:

A higher proportion of patients achieved ORR lasting ≥4, 6, 8, or 12 months in the mogamulizumab vs. vorinostat arm. Long-term response was also observed in mogamulizumab-treated patients with more advanced disease (stage IVA1 [17/20], B2 blood involvement [18/20], and SS [14/20]). PFS was significantly longer (9.4 vs. 3.1 months; p < 0.0001) in mogamulizumab vs. vorinostat-treated patients taking concomitant steroids. Mogamulizumab-treated patients experienced longer TTNT vs. vorinostat. Lymphopenia and MAR were associated with response to mogamulizumab.

CONCLUSIONS:

MAVORIC demonstrated greater efficacy with mogamulizumab vs. vorinostat in relapsed/refractory patients with CTCL, including those with more advanced disease. Concomitant steroid use improved ORR and PFS but did not impact vorinostat outcomes. Overall responses occurred more frequently in mogamulizumab-treated patients that developed lymphopenia than those that did not. A higher percentage of patients with MAR had an overall response than those without MAR.

2025-12-31·JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY

Discovery of novel biphenyl compounds bearing hydroxamic acid moiety as the first PD-L1/class I HDACs dual inhibitors

Article

作者: Huang, Yudan ; Liu, Jieqing ; Ding, Xueyan ; Ma, Junjie ; Yuan, Dandan ; Gao, Yali ; Liu, Han ; Li, Jin ; Xia, Lin ; Deng, Changchun ; Dai, Wenqi ; Wu, Xingye

Herein, we firstly reported a series of biphenyl compounds bearing hydroxamic acid moiety as PD-L1/class I HDACs dual inhibitors. Among them, compound 14 displayed the strongest inhibitory activity in vitro against HDAC2 and HDAC3 with IC₅₀ values of 27.98 nM and 14.47 nM, and had an IC₅₀ value of 88.10 nM for PD-1/PD-L1 interaction. Importantly, 14 could upregulate the expression of PD-L1 and CXCL10 in a PD-L1 low-expression cancer cell line (MCF-7), highlighting the potential to enhance efficacy by recruiting T-cell infiltration into TME and improving the response of PD-1/PD-L1 inhibitor associated with PD-L1 low-expression. Besides, we identified another compound, 22, which possessed the strongest inhibitory activity against PD-1/PD-L1 interaction with an IC₅₀ value of 12.47 nM, and effectively inhibited the proliferation of three cancer cell lines. Our results suggest that compounds 14 and 22 can be served as lead compounds of PD-L1/class I HDACs dual inhibitors for further optimisation.

2025-06-01·CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY

Efficacy and safety of targeted therapy and immunotherapy in advanced vulvar squamous cell carcinoma: A scoping review

Review

作者: Arenhardt, Martina Parenza ; de Andrade, Diocesio Alves Pinto ; Dos Santos, Marcela Bonalumi ; de Melo, Andréia Cristina ; Gomes, Larissa Müller ; da Silva, Jessé Lopes ; Giannecchini, Giovanna Vieira

INTRODUCTION:

Vulvar squamous cell carcinoma (VSCC) is a rare gynecological tumor with limited treatment options for advanced stages. Current chemotherapy, adapted from cervical cancer protocols, often results in poor outcomes. This scoping review evaluates the efficacy and safety of immunotherapy and targeted therapies in advanced VSCC.

MATERIAL AND METHODS:

After extensive assessment, examination, and curation of relevant literature data, eight trials focused on immunotherapy or targeted therapy for advanced, recurrent, or metastatic VSCCs were identified and selected. The findings have been compiled and synthesized into a narrative overview, adhering to the PRISMA-ScR guidelines.

RESULTS:

The study analyzed four unpublished and four published trials, evaluating the efficacy and safety of immunotherapy or targeted therapy for VSCCs. Pembrolizumab was assessed in the KEYNOTE-028 and KEYNOTE-158 trials, showing objective response rates (ORRs) of 6 % and 10.9 %, respectively, and median overall survival (OS) between 3.8 and 6.2 months. CheckMate 358 reported a 20 % ORR for nivolumab. Combination strategies (ipilimumab plus nivolumab and pembrolizumab plus vorinostat) demonstrated efficacy with median OS of 7.6 and 17.5 months, respectively. Toripalimab showed an ORR of 33.3 %. Safety profiles were generally manageable, with common adverse events like fatigue and gastrointestinal disorders. Serious adverse events included grade 5 immune-related hepatitis and chronic kidney disease.

CONCLUSION:

Immunotherapy may be considered an option for VSCCs in the second-line setting. Despite the limited research on targeted therapies for VSCCs, combination approaches with immunotherapy demonstrate promising potential. Prioritizing the identification of biomarkers that predict responses to immune checkpoint inhibitors is essential.

项与伏立诺他相关的新闻（医药）

2025-03-29

·学术经纬

Nature | 研究揭示髓母细胞瘤常见突变的致癌机制

撰文 | 吴大荣责编 | 周叶斌理解突变如何导致蛋白质-蛋白质相互作用的改变，以及这些改变如何驱动肿瘤的发生，仍癌症研究一个重要的未解决问题。KBTBD4是一种CULLIN3-RING E3泛素连接酶复合物的底物受体，其突变在髓母细胞瘤中频繁出现，而这些突变使KBTBD4 获得功能，从而诱导转录辅阻遏物CoREST5的异常降解。近日，Brian B. Liau 和合作伙伴们在 Nature 上发表题为 Converging mechanism of UM171 and KBTBD4 neomorphic cancer mutations 文章，揭示了功能获得性E3突变和分子胶降解剂UM171之间基于形状互补性的吻合机制，证明HDAC1/2抑制剂可以阻断突变型KBTBD4–HDAC1界面和KBTBD4突变型髓母细胞瘤细胞的增殖。在泛素-蛋白酶体系统中，人类疾病突变早已知道会损害几种E3泛素连接酶的功能。相比之下，促进底物蛋白异常降解的E3功能获得性突变最近被发现。尽管有通过改变连接酶稳定性或调节性导致非计划的底物泛素化的多形态（hypermorphic）E3突变病例，但直接诱导新底物参与和降解的E3突变，即“新降解”，是E3连接酶失调的新例子。KBTBD4（一种 CULLIN3-RING E3 连接酶的底物受体）的癌症突变主要发生在 KELCH 重复 β 螺旋桨 2b-2c 环的热点中，具有相当大的分子多样性，包括1-5 个氨基酸的插入或缺失（insertion or deletion）以及点替换。值得注意的是，KBTBD4 还参与了 UM171 的机制，后者是一种诱导 CoREST 降解的造血干细胞扩增小分子激动剂。为揭示UM171 和 KBTBD4 癌症突变之间惊人的相似机制，该团队做了几个关键实验：深度突变扫描：绘制了KBTBD4 癌症热点的突变图，揭示了插入和替换可以促进功能获得的不同偏好以及热点相互作用中有关的关键残基。KBTBD4的癌症突变通过直接靶向HDAC1/2，促进CoREST（一种控制染色质可及性和转录的复合物）的降解，这种降解会改变表观遗传程序，进而改变转录程序，促进癌细胞干细胞的增加，从而驱动肿瘤发生。冷冻电子显微镜分析：对与 LSD1–HDAC1–CoREST （LHC 综合体）结合的两个不同 KBTBD4 癌症突变体的低温电子显微镜分析表明，KBTBD4 同型二聚体与 HDAC1 不对称地结合，具有两个 KELCH 重复的β-螺旋结构域。髓母细胞瘤突变稳定了 HDAC1 和其中一个 KBTBD4 β-螺旋之间的界面，使一个庞大的侧链插入 HDAC1 活性位点。最近的研究表明，KBTBD4作用机制与UM171 相吻合， UM171 通过促进 CoREST 的泛素化和降解在表型上和髓母细胞瘤中KBTBD4突变相似。在相关的研究中，研究人员确定UM171的加入稳定了KBTBD4-LHC 复合物的结构，并证明了UM171充当分子胶以诱导 E3 和 HDAC1 之间的复合物形成。比较KBTBD4-UM171-LHC 复合物与两个和LHC 结合的 KBTBD4突变体之间的结构，明显看出两机制的吻合，如图1所示。通过该机制，分子胶和癌症突变可以补充和优化 E3 连接酶和 HDAC1 之间较差的蛋白质-蛋白质界面，从而驱动它们的结合。图1，左-UM171（黄色和蓝色棒）、突变型KBTBD4- Tyr312 侧链（青色和红色棒）以及另一突变型 KBTBD4- Arg312 侧链（绿色和蓝色棒）在 HDAC1 活性位点口袋处（粉色）的比较。深紫色棒显示了两个苯丙氨酸残基，勾勒出 HDAC1 活性位点通道的入口。右- UM171（黄色和蓝色棒状图）与突变型KBTBD4的 2b-2c 环状图的比较，其中 KBTBD4–UM171–HDAC1 结构通过 HDAC1 与突变型 KBTBD4–HDAC1 结构叠加，界面处关键残基的侧链以红色棒状标示。药物干预实验：结构和深度突变扫描结果表明KBTBD4 MB 突变体通过去乙酰化酶活性位点的热点相互作用直接与 HDAC1/2 结合，从而促进 CoREST 降解。这些观察结果意味着HDAC1/2 活性位点抑制剂可以在空间上阻断突变连接酶的结合，从而阻断其致癌功能。突变型KBTBD4-HDAC1 与与辛二酰苯胺羟肟酸 (SAHA) 结合的 HDAC2 的叠加分析支持这一观点，即 HDAC1/2 抑制剂和插入的精氨酸残基可能会发生位置冲突。用SAHA，CI-994（一种 2-氨基苯甲酰胺衍生的抑制剂）和RBC1HI（新型 HDAC1/HDAC2 抑制剂，Regenacy Brain I 类 HDAC 抑制剂）进行试验，证明了这三种抑制剂可以保全由两种突变KBTBD4-P 和 KBTBD4-PR 表达引起的 CoREST 降解，如图2所示。图2，左-SAHA（黄色）与突变型KBTBD4 2b-2c 环（绿色）中央精氨酸残基之间的位置冲突。右-细胞增殖实验， DMSO，SAHA，CI-994或 RBC1HI与带有标示的KBTBD4 突变体之间的荧光素信号（纵轴），两次生物学重复了解突变是如何实现新蛋白质-蛋白质相互作用（PPI）的分子机制不仅对于理解疾病病因至关重要，而且对于指导治疗方法（例如分子胶和 PPI 抑制剂）用化学调节这些界面也至关重要。该研究表明，KBTBD4的癌症突变通过与HDAC1的相互作用促进CoREST的降解，且可以通过小分子药物进行调节，这为针对KBTBD4突变的治疗提供了新的思路。未来的研究应集中在扩展对其他相关突变的研究，探索其在不同类型癌症中的作用；开发针对KBTBD4突变的特异性治疗策略，例如分子胶UM171和HDAC1/2抑制剂；进一步研究KBTBD4与其他蛋白质的相互作用，以全面理解其在肿瘤发生中的角色。撰文责编制作排版 | 车洁校对 | uu延伸阅读*本文由深圳市拾玉儿童公益基金会“儿童肿瘤前沿”团队编译或约稿，文中图表均源引自文献原文。本文著作权归文章作者所有，欢迎个人转发分享，未经允许禁止转载，作者拥有所有法定权利，违者必究。如需转载，请留言或联系shiyu@curekids.cn。本文旨在分享儿童肿瘤科研前沿成果，不是治疗方案推荐。如需获得疾病治疗方案指导，请前往正规医院就诊。▼滑动查看更多▼原文摘要（Abstract）Cancer mutations can create neomorphic protein-protein interactions to drive aberrant function1,2. As a substrate receptor of the CULLIN3-RING E3 ubiquitin ligase complex, KBTBD4 is recurrently mutated in medulloblastoma3, the most common embryonal brain tumour in children4. These mutations impart gain-of-function to KBTBD4 to induce aberrant degradation of the transcriptional corepressor CoREST5. However, their mechanism remains unresolved. Here we establish that KBTBD4 mutations promote CoREST degradation through engaging HDAC1/2 as the direct target of the mutant substrate receptor. Using deep mutational scanning, we chart the mutational landscape of the KBTBD4 cancer hotspot, revealing distinct preferences by which insertions and substitutions can promote gain-of-function and the critical residues involved in the hotspot interaction. Cryo-electron microscopy analysis of two distinct KBTBD4 cancer mutants bound to LSD1-HDAC1-CoREST reveals that a KBTBD4 homodimer asymmetrically engages HDAC1 with two KELCH-repeat β-propeller domains. The interface between HDAC1 and one of the KBTBD4 β-propellers is stabilized by the medulloblastoma mutations, which insert a bulky side chain into the HDAC1 active site pocket. Our structural and mutational analyses inform how this hotspot E3-neosubstrate interface can be chemically modulated. First, we unveil a converging shape-complementarity-based mechanism between gain-of-function E3 mutations and a molecular glue degrader, UM171. Second, we demonstrate that HDAC1/2 inhibitors can block the mutant KBTBD4-HDAC1 interface and proliferation of KBTBD4-mutant medulloblastoma cells. Altogether, our work reveals the structural and mechanistic basis of cancer mutation-driven neomorphic protein-protein interactions.DOI: 10.1038/s41586-024-08533-3👇点击此处，直达原文

蛋白降解靶向嵌合体

2025-03-29

·药事纵横

7500万美元！一家biotech在印度建立CGT工厂

声明：因水平有限，错误不可避免，或有些信息非最及时，欢迎留言指出。本文仅作医疗健康相关药物介绍，非治疗方案推荐（若涉及）;本文不构成任何投资建议。近日，印度药企Bharat Biotech 宣布：已在印度建立其首个细胞和基因治疗 (CGT) 工厂，并投资7500万美元。据悉，该公司正在研究两款细胞疗法和3款基因疗法，预计其新疗法将在未来3年内上市。该公司正将把重点从核心疫苗业务扩展到复杂的细胞和基因治疗，据市场研究公司 Precedence Research 的数据，该市场预计从 2024 年的 212.8亿美元增长五倍以上至 2034 年的 1174.6 亿美元。该 50,000 平方英尺的设施专门用于生产高滴度病毒载体，包括 AAV（腺相关病毒）、慢病毒和腺病毒，以支持基因治疗应用。该设施拥有最先进的能力，可在其平台上生产不同的产品，并为血癌、实体器官癌和遗传性疾病提供治疗选择。Bharat Biotech 首席开发官 Raches Ella 表示，其目标是使基因疗法普及化，就像疫苗一样，让所有人都能负担得起这些疗法。细胞疗法和基因疗法比传统疗法更贵，动辄几百万美元。Bharat Biotech 执行主席 Krishna Ella 博士表示：“与全球相比，印度仍处于CGT发展初级阶段，如果在印度市场售卖这些CGT疗法，售价约500万卢比（约57900美元），或许定价比这还低。”作为一家在开发抗病毒疫苗方面拥有数十年经验的公司，Bharat Biotech 具有独特的资质，可以进行大规模生产，从而加快临床产品的商业化。该公司还与威斯康星大学麦迪逊分校的 Krishanu Saha 教授合作开发下一代 CAR-T疗法。Bharat Biotech 是一家印度生物技术公司，在疫苗和生物治疗领域有突出表现，成立于1996 年，截至 2023 年有 1526 名员工，公司致力于开发价格亲民、安全且高质量的疫苗和生物治疗产品。其拥有 145 项全球专利，在生物信息学、分子流行病学、分子生物学、微生物学、细菌学、病毒学、免疫学、生物化学、临床研究、工业生物技术、制剂和产品开发等领域开展前沿研究。Bharat Biotech已开发出多种突破性的疫苗和生物治疗产品，包括世界上第一种伤寒结合疫苗 Typbar TCV、用于治疗糖尿病足溃疡的生长因子凝胶 Regen - D®，以及使 Revac - B mcf® 得以生产的专利技术 Himax®。Revac - B mcf® 是第一种重组乙型肝炎疫苗，与同类疫苗相比，具有最高水平的抗原回收率。其新冠疫苗 Covaxin4是印度本土开发的全病毒灭活新冠疫苗，与印度医学研究理事会（ICMR）和印度国家病毒研究所（NIV）合作研发。2021 年 1 月 3 日获得印度药品管理总局批准紧急使用。研究显示，Covaxin 对儿童具有良好的安全性和免疫原性。其结核病疫苗 MTBVAC与 Biofabri 密切合作进行临床试验。MTBVAC 是第一个从人类身上分离出来的结核分枝杆菌的减毒活疫苗，2024 年已开始在印度成年人中进行安全性和免疫原性试验，计划于 2025 年开始关键的安全性、免疫原性和有效性试验。它还与葛兰素史克公司建立产品转让合作伙伴关系，负责生产葛兰素史克公司开发的疟疾疫苗 RTS，S/AS01E 的 S 抗原成分。根据协议，巴拉特生物技术公司预计在 2029 年成为该疫苗的唯一供应商。研发管线参考资料：https://www.fiercepharma.com/manufacturing/bharat-biotech-enters-cell-and-gene-therapy-market-75m-production-investment

细胞疗法疫苗免疫疗法基因疗法上市批准

2025-03-23

·梅斯医学

18岁的他误以为腿痛是长高的代价，发烧是免疫力差……却没想到骨头内都是癌细胞！

14岁的初中生小浩（化名）半年前开始右大腿隐隐作痛，夜间尤其难熬，像是“骨头缝里插了根烧红的铁钉”。父母安慰他：“男孩子长个子都这样，多喝牛奶补钙。”校医也诊断为“生长痛”，开了钙片和止痛药。可疼痛非但没缓解，小浩还开始低烧，体温总在37.5℃-38℃之间徘徊，稍微运动就大汗淋漓。妈妈心疼：“这孩子免疫力太差，得炖点黄芪鸡汤补补。” 直到一次体育课跳远，小浩右腿突然“咔嚓”一声脆响，剧痛让他蜷缩在地。急诊X光片显示右股骨中段溶骨性破坏，内部布满“蜂窝状”空洞，周围骨膜如“洋葱皮”层层掀起。MRI更触目惊心——肿瘤组织如“灰白色岩浆”从骨髓腔喷涌而出，吞噬了周围肌肉。术中刮开股骨时，医生发现骨髓腔已被暗红色“腐肉”填满，血液像漏水的管道般不断渗出。病理报告显示弥漫分布的小圆细胞，免疫组化CD99膜阳性，基因检测EWSR1-FLI1融合阳性，确诊为尤文肉瘤(Ewing肉瘤，ES)。临床表现及分型 ES可分为“远端型”和“近端型”。远端型通常发生在四肢末端，常见于青少年，肿块质硬，可能伴随溃疡。近端型则发生在头颈、躯干等接近中线的部位，多见于中老年人，且更易侵犯深层组织如肌腱和筋膜。虽然局部生长较慢，但Ewing肉瘤具有较高的转移性，特别是近端型。最常见的转移部位为肺，肺转移的影像学表现多样，可能被误诊。即使初诊为M0（无转移），治疗后5年内仍有高达33%的转移发生率。因此，早期诊断和定期随访非常重要。诊断 Ewing肉瘤（ES）诊断依赖于病理检查。低倍镜下，肿瘤呈结节状生长，中央有坏死、出血和囊性变。高倍镜下可见嗜酸性上皮样细胞和梭形细胞。嗜酸性上皮样细胞异型性明显，梭形细胞呈涡纹状排列。免疫组化是区分ES与其他肿瘤（如血管肉瘤、恶性横纹肌样瘤）的关键。ES通常同时表达上皮和间叶标记（如CK、Vimentin），不表达CD68、CD31等。INI阴性是诊断ES的证据，ERG和SALL4联合检测可帮助区分ES和恶性横纹肌样瘤。此外，CA125标记物在ES中有一定诊断价值，升高与疾病进展相关，监测其水平有助于评估治疗效果和随访观察。治疗 Ewing肉瘤（ES）的治疗主要包括手术、化疗和分子靶向治疗。手术治疗：局限期ES首选手术切除，手术方式根据肿瘤的大小、部位和患者的意愿选择。截肢虽能提高治愈率，但不能完全避免复发或转移。孤立性肢体灌流结合化疗和皮瓣重建为替代方案。化疗：转移性ES主要通过化疗治疗。常用药物包括表阿霉素、多柔比星与异环磷酰胺联合治疗。吉西他滨联合多西他赛效果更佳，术后辅助化疗是否能降低复发仍有争议。分子靶向治疗：靶向治疗逐渐受到关注，主要针对PI3K/AKT/mTOR和c-MET信号通路，抑制药物（如依维莫司、INC280）可抑制ES细胞生长。组蛋白去乙酰化酶抑制药（如SAHA、FK228）在实验中显示抑制肿瘤效果，但临床应用仍有限。参考资料： [1]何建,周向东.上皮样肉瘤研究进展[J].武警医学,2017,28(12):1286-1288.DOI:10.14010/j.cnki.wjyx.2017.12.032. [2]王晶晶，许春伟,张俊,等.上皮样肉瘤临床病理特征并文献复习[J].临床与病理杂志,2015,35(3):523-528. [3]李莉，夏秋媛，饶秋，等.上皮样肉瘤免疫表型和INI1基因改变的研究[J].中华病理学杂志，2014,43（6)：389-393. 来源 | 梅斯医学编辑 | wanny 神经系统罕见病交流群 ↓点击下方“阅读原文”，下载梅斯医学APP吧！

疫苗

100 项与伏立诺他相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D06320	伏立诺他	L01XX38	DB02546

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
皮肤T细胞淋巴瘤	美国	Merck Sharp & Dohme Corp.	2006-10-06

未上市

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
难治性多发性骨髓瘤	临床3期	-	Merck Sharp & Dohme Corp.	2008-12-01
非鳞状非小细胞肺癌	临床3期	-	Merck Sharp & Dohme Corp.	2007-05-01
恶性胸膜间皮瘤	临床3期	-	Merck Sharp & Dohme Corp.	2005-06-30
ER阳性乳腺癌	临床2期	美国	Merck Sharp & Dohme Corp.	2021-03-11
转移性乳腺癌	临床2期	美国	Merck Sharp & Dohme Corp.	2021-03-11
肛门肿瘤	临床2期	法国	Merck Sharp & Dohme Corp.	2020-10-28
阴茎肿瘤	临床2期	法国	Merck Sharp & Dohme Corp.	2020-10-28
转移性头颈部鳞状细胞癌	临床2期	法国	Merck Sharp & Dohme Corp.	2020-10-28
鳞状细胞癌，转移	临床2期	法国	Merck Sharp & Dohme Corp.	2020-10-28
鳞状细胞肺癌	临床2期	法国	Merck Sharp & Dohme Corp.	2020-10-28

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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


AACR2025	N/A	肺腺癌	-	Vorinostat	膚積蓋築獵艱鏇構膚願(蓋鹹膚襯網選夢憲膚糧) = 鹹艱鑰鏇憲鹽廠觸廠糧壓觸鹽鑰願顧構醖鏇願 (糧餘製淵鏇廠選艱遞夢 )	积极	2025-04-27
NCT00503971 (CTgov)	临床1/2期	非小细胞肺癌	33	Erlotinib+Vorinostat (Vorinostat Plus Erlotinib Phase II)	蓋蓋鬱築廠窪憲醖醖顧 = 鹹範鏇鬱築獵鬱壓夢夢願憲壓製夢衊遞憲選選 (獵糧遞繭繭壓餘繭鬱憲, 鏇蓋選築觸憲選糧醖淵 ~ 鹹醖襯鹹鹹網襯夢艱選) 更多	-	2025-03-25
				Erlotinib+Vorinostat (Vorinostat Plus Erlotinib Phase I)	築鏇鬱淵淵遞餘遞簾鬱 = 願鹹繭淵構壓積顧蓋鹽構醖憲願觸築鹽餘構鹹 (壓襯壓淵膚襯築獵顧鬱, 簾範憲憲窪網蓋廠願醖 ~ 鏇繭範衊窪窪遞窪鏇艱)
NCT02619253 (Phase I/IB, CTgov)	临床1期	晚期尿路上皮癌 \| 肾细胞癌 \| 膀胱癌	52	vorinostat+pembrolizumab (Expansion Cohort A)	築糧淵餘鹹艱醖築獵鹽 = 構簾築鑰顧蓋齋積窪願襯積簾蓋積鹹齋廠淵夢 (願簾顧鏇糧壓築簾蓋願, 膚鹹製膚醖製壓醖鏇鹹 ~ 繭蓋範膚遞糧築鬱選廠) 更多	-	2024-11-18
				vorinostat+pembrolizumab (Expansion Cohort B)	築糧淵餘鹹艱醖築獵鹽 = 遞鬱餘艱醖簾顧獵蓋鹽襯積簾蓋積鹹齋廠淵夢 (願簾顧鏇糧壓築簾蓋願, 膚憲範網選遞窪鏇製膚 ~ 膚構範壓鹽鑰醖鬱願糧) 更多
NCT04357873 (PEVOsq, AACR2024) 人工标引	临床2期	鳞状细胞癌 PD-L1 expression \| tumor-infiltrating lymphocytes quantification \| HPV typing ... 更多	112	Pembrolizumab anVorinostatVorinostat combination	-	积极	2024-03-22
				Pembrolizumab + Vorinostat (HPV+)	鬱選糧鏇艱醖餘積鑰廠(選醖鬱範蓋鹹糧憲願築) = 醖壓遞蓋製衊製醖艱選憲壓範獵衊構淵醖淵鏇 (鹹壓衊鑰製夢蓋襯觸淵 )
NCT03198559 (CTgov)	临床1/2期	HIV感染	5	Vorinostat, NDC 00006-0568-40+Disulfiram, (National Drug Code) NDC 0378-4141-01	淵鹽襯繭製廠窪鏇鹽遞 = 艱範鏇鹹膚製選糧網願鏇鹹顧願遞鏇網鏇餘願 (鑰鹹壓觸醖艱製醖選衊, 夢構衊糧壓壓艱築鑰蓋 ~ 獵遞構鹽蓋鹽蓋糧餘繭) 更多	-	2024-02-09
NCT02316340 (CTgov)	临床2期	转移性结直肠癌	42	Vorinostat+Hydroxychloroquine (Study Arm - VOR With HCQ)	蓋選窪淵餘簾選衊夢積(製願齋範窪簾遞觸簾鑰) = 獵窪構鹹遞繭簾願襯淵鹹願衊糧範積範獵構觸 (窪窪窪築範餘醖網廠選, 積蓋齋壓構齋窪襯繭淵 ~ 鏇顧網衊窪憲醖窪窪廠) 更多	-	2024-01-05
				Regorafenib (Control Arm - Regorafenib)	蓋選窪淵餘簾選衊夢積(製願齋範窪簾遞觸簾鑰) = 鏇顧窪鏇築糧觸膚齋襯鹹願衊糧範積範獵構觸 (窪窪窪築範餘醖網廠選, 繭廠餘製廠糧選鹹構製 ~ 鹹築襯膚窪簾網遞構網) 更多
NCT01802333 (S1203, Pubmed \| Leukemia) 人工标引	临床3期	急性髓性白血病 NPM1 \| FLT3	738	Daunorubicin and cytarabine (DA)	艱鬱顧齋蓋鏇齋鹹範範(網獵衊選膚壓衊獵壓積) = 網遞窪繭製鑰觸襯網顧繭顧選網鏇網獵淵鏇範 (願範淵襯製簾製願餘遞 ) 更多	不佳	2024-01-01
				Idarubicin with higher dose cytarabine (IA)	艱鬱顧齋蓋鏇齋鹹範範(網獵衊選膚壓衊獵壓積) = 壓範築鹽艱願窪築鏇鹽繭顧選網鏇網獵淵鏇範 (願範淵襯製簾製願餘遞 ) 更多
EUCTR2019-003839-33-FR \| NCT04357873 (PEVOsq, ESMO 12023 \| ESMO 22023) 人工标引	临床2期	外阴鳞状细胞癌	17	Pembrolizumab + Vorinostat	簾繭願築鏇選蓋築膚積(範簾範壓鏇構鏇憲顧衊) = 觸糧繭襯艱廠糧顧繭範糧鑰襯蓋憲夢憲觸淵獵 (築範憲膚遞齋觸範窪積 ) 更多	积极	2023-10-22
NCT04357873 (PEVOsq, ESMO 12023 \| ESMO 22023) 人工标引	临床2期	头颈部鳞状细胞癌	27	Pembrolizumab + Vorinostat	衊糧憲簾憲鹽簾遞鏇糧(壓醖窪獵鏇醖廠選鬱積) = 製觸簾淵蓋襯構艱醖憲鏇壓築鹽構艱襯願構鏇 (遞願壓鏇壓鏇鑰鹹觸窪, 6.6 ~ 39.4) 更多	积极	2023-10-22
EUCTR2019-003839-33-FR \| NCT04357873 (PEVOsq, ESMO 12023 \| ESMO 22023) 人工标引	临床2期	宫颈鳞状细胞癌	25	Pembrolizumab + Vorinostat	遞鹽築繭選繭網築鬱鬱(窪網壓繭遞餘淵窪遞廠) = 鏇蓋簾齋糧簾窪範糧膚積積襯觸憲簾遞膚淵範 (鹽餘蓋鹽範廠簾簾齋顧, 19.7 ~ 61.5) 更多	积极	2023-10-22