This is a randomized, double-blind, 2-arm, parallel group study of up to 274 evaluable patients designed to evaluate the safety and efficacy of the histone deacetylase 6 (HDAC6) inhibitor ricolinostat for painful DPN.

开始日期2020-12-07

申办/合作机构

Regenacy Pharmaceuticals LLC

100 项与 Rocilinostat 相关的临床结果

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100 项与 Rocilinostat 相关的转化医学

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100 项与 Rocilinostat 相关的专利（医药）

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241

项与 Rocilinostat 相关的文献（医药）

2027-01-01·BONE

Ricolinostat restrains osteoclastogenesis through HDAC6-associated regulation of p65 stability

Article

作者: Jialiang, Wang ; Junhao, Tu ; Shengbin, Huang ; Shufan, Zhao ; Fangdan, Hao ; Xinyi, Ma ; Suxin, Wu ; Qingzhou, Deng ; Shuomin, Chen ; Yifan, Ping ; Mengjia, Yi ; Bin, Li ; Wangzhi, Li ; Yongkai, Wang ; Yixin, Mao ; Yang, Chen ; Haofu, Jiang

Excessive osteoclast activity is a central driver of pathological bone loss in osteoporosis; however, the mechanisms governing osteoclast differentiation remain incompletely understood, and current therapeutic options remain limited in efficacy. Therefore, we performed high-throughput drug screening to identify candidate agents and further explored the molecular mechanisms underlying targeted osteoclastogenesis inhibition. Here, we identified ricolinostat (RICO), a selective histone deacetylase 6 (HDAC6) inhibitor, as a potent inhibitor of the receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis. RICO suppresses osteoclast differentiation and reduces osteoclast-associated gene and protein expression without compromising cell viability. RICO attenuates estrogen deficiency-induced bone loss and reduces osteoclast abundance in vivo. Mechanistically, transcriptomic profiling revealed that RICO broadly suppressed osteoclastogenic, inflammatory, and metabolic programs. Specifically, by inhibiting HDAC6, RICO promoted proteasomal degradation of p65 by increasing its acetylation and ubiquitination, thereby reducing p65 protein abundance in both cytoplasmic and nuclear fractions and suppressing canonical NF-κB signaling. Collectively, these findings identify RICO-as a phase II clinical stage investigational compound with repurposing potential as a promising anti-resorptive candidate for the treatment of osteoporosis and uncover a novel mechanism whereby HDAC6 governs p65 protein stability to inhibit osteoclastogenesis.

2026-11-01·BIOCHEMICAL PHARMACOLOGY

Targeting HDAC6 mitigates diabetic nephropathy through modulation of oxidative stress, inflammatory pathways, and apoptotic signaling

Article

作者: Kim, Ui Jin ; Lee, Eunah ; Kim, Hyung Sik ; Kwon, Oh Kwang ; Song, Yun Jeong ; Cho, Yeong Eun ; Kim, Ju Ri ; Park, Jae Hyeon

Histone deacetylase 6 (HDAC6), a key regulator of non-histone protein acetylation and inflammatory signaling, has emerged as a potential therapeutic target in renal diseases. This study investigated the renoprotective effects of selective HDAC6 inhibition in streptozotocin (STZ)-induced diabetic nephropathy (DN) in rats. Male Sprague-Dawley rats injected STZ (60 mg/kg, i.p.) to induce diabetes, followed by treatment with the selective HDAC6 inhibitors tubastatin A (TubA, 30 mg/kg/day, i.p.) or ACY-1215 (30 mg/kg/day, i.p.) for 3 weeks after confirmation of hyperglycemia. Diabetic rats exhibited significant increases in blood glucose, blood urea nitrogen (BUN), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total cholesterol, and triglycerides, along with severe renal histopathological alterations. Urinary biomarkers of kidney injury, including kidney injury molecule-1 (KIM-1), selenium-binding protein 1 (SBP1), and neutrophil gelatinase-associated lipocalin (NGAL), were significantly elevated in diabetic rats and were significantly reduced following treatment with HDAC6 inhibitors. Proteomic profiling identified 159 and 167 differentially expressed proteins in the TubA/STZ and ACY-1215/STZ groups, respectively, indicating partial restoration of diabetes-associated molecular dysregulation. Mechanistically, HDAC6 inhibition restored antioxidant defenses, as evidenced by increased expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), Heme oxygenase 1 (HO-1), sirtuin-3 (SIRT3), and MnSOD, reduced oxidative stress markers including advanced glycation end-products (AGEs), malondialdehyde (MDA), and 8-Hydroxy-2-deoxyguanosine (8-OHdG), suppressed Interleukin-1 beta (IL-1β) and Interleukin 6 (IL-6), attenuated apoptosis, and inhibited fibrosis and epithelial-mesenchymal transition by modulating the expression of transforming growth factor β1 (TGF-β1), vimentin, α-smooth muscle actin (α-SMA), and E-cadherin. Collectively, these findings demonstrate that HDAC6 inhibition exerts potent renoprotective effects and represents a promising therapeutic strategy for diabetic nephropathy.

2026-11-01·FREE RADICAL BIOLOGY AND MEDICINE

HDAC6 inhibition alleviates dexamethasone-induced skeletal muscle atrophy and enhances UCP3-associated redox homeostasis

Article

作者: Bian, Yiding ; Hou, Gang ; Deng, Mingming ; Wang, Kai ; Li, Chang ; Zheng, Ziwen

OBJECTIVE:

Long-term use of glucocorticoids, such as dexamethasone, often leads to glucocorticoid-induced muscle atrophy (GIMA), a condition associated with mitochondrial oxidative stress and abnormal activation of protein degradation pathways. Histone deacetylase 6 (HDAC6) is involved in cellular stress regulation, but its role in GIMA remains unclear. We investigated the protective effects of HDAC6 inhibition/loss-of-function against dexamethasone-induced muscle atrophy and its potential molecular mechanisms.

METHODS:

Using Hdac6 knockout (KO) mice and C2C12 myotube models, combined with the HDAC6-selective inhibitor ACY-1215, we evaluated the phenotype of dexamethasone-induced muscle atrophy. We performed transcriptomic sequencing, Western blotting, immunofluorescence assays, and measured oxidative stress markers including reactive oxygen species (ROS), malondialdehyde (MDA), and the reduced glutathione to oxidized glutathione disulfide ratio (GSH/GSSG). Mitochondria-specific parameters, including mitochondrial superoxide (MitoSOX), mitochondrial membrane potential (MT-1 and JC-1), mitochondrial biogenesis markers (PGC-1α and TFAM), and antioxidant enzymes (SOD2, GPx1, and GPx4), were assessed. To investigate the regulatory mechanism, we assessed Ucp3 mRNA abundance and UCP3 protein stability. We also performed UCP3 knockdown and overexpression experiments in C2C12 myotubes to determine the functional contribution of UCP3 to the protective effects of HDAC6 loss or inhibition.

RESULTS:

Hdac6 knockout or HDAC6 inhibition significantly attenuated dexamethasone-induced muscle atrophy, as evidenced by increased grip strength, restored muscle mass, enlarged muscle fiber diameter, and downregulated MuRF1/Atrogin-1 expression in mice. RNA-seq analysis identified DEX-responsive changes in redox-related pathways in Hdac6-deficient skeletal muscle, with Ucp3 among the DEX-responsive genes. Mechanistically, HDAC6 knockdown increased Ucp3 mRNA abundance without detectably altering UCP3 protein stability. This was accompanied by reduced mitochondrial superoxide, restored mitochondrial membrane potential, and increased expression of mitochondrial biogenesis markers and antioxidant enzymes. Importantly, UCP3 overexpression in C2C12 myotubes, without HDAC6 manipulation, was sufficient to attenuate dexamethasone-induced myotube atrophy. Functional rescue experiments showed that UCP3 knockdown reversed the antioxidant and anti-atrophic effects of HDAC6 knockdown. ACY-1215 attenuated dexamethasone-induced muscle atrophy in both mice and C2C12 myotubes. In C2C12 myotubes, UCP3 knockdown abolished the antioxidant and anti-atrophic effects of ACY-1215, demonstrating UCP3 dependence in the in vitro model.

CONCLUSION:

This study identifies UCP3-associated redox homeostasis as an important downstream mechanism linking HDAC6 inhibition to protection against dexamethasone-induced muscle atrophy. In C2C12 myotubes, UCP3 was required for the protective effects of HDAC6 knockdown and ACY-1215, whereas UCP3 overexpression was sufficient to attenuate dexamethasone-induced myotube atrophy. ACY-1215 also alleviated dexamethasone-induced muscle atrophy in mice, although the UCP3 dependence of this in vivo effect remains to be determined.

项与 Rocilinostat 相关的新闻（医药）

2026-08-07

·劲帆生物

HDAC6/STAT3/CCL7轴：神经病理性疼痛治疗的全新靶点机制解析

导读神经病理性疼痛是由神经系统损伤或功能异常介导的难治性慢性疼痛，全球患病率达7-10%，临床以自发性疼痛、痛觉过敏、痛觉超敏为核心表现，严重损害患者生活质量。目前临床一线用药（抗癫痫药、抗抑郁药等）普遍疗效有限、不良反应突出，亟需挖掘新型治疗靶点与干预策略。近日，宁波大学与宁波市第二医院联合团队在《Journal of Neuroinflammation》发表研究“Inhibition of histone deacetylase 6 alleviates neuropathic pain via direct regulating posttranslation of spinal STAT3 and decreasing downstream C-C Motif Chemokine Ligand 7 synthesis”，以保留神经损伤（SNI）小鼠模型为核心，系统揭示了选择性HDAC6抑制剂ACY-1215通过调控脊髓STAT3翻译后修饰平衡、抑制下游CCL7介导的神经炎症，从而缓解神经病理性疼痛的完整机制。该研究首次明确了神经系统内HDAC6/STAT3/CCL7信号轴的疼痛调控功能，为HDAC6抑制剂向疼痛适应症的临床转化提供了坚实的实验依据。劲帆医药劲帆生物医药科技（武汉）有限公司（以下简称 “劲帆医药”），深耕临床前药理药效CRO服务领域，可提供一站式神经病理性疼痛（NP）模型构建及药效评价服务，覆盖从方案定制、模型构建、疼痛行为学评估、血清分子检测到标准化报告交付的完整流程。依托慢性坐骨神经压迫（CCI）、坐骨神经分支选择性损伤（SNI）、脊神经结扎（SNL）等经典外周神经损伤模型，以及糖尿病周围神经病变（DPN）、化疗诱导周围神经病变（CIPN）等疾病特异性模型的多元化技术体系，搭配体重变化趋势、机械痛缩爪阈值（Von Frey 法）、热痛潜伏期、血清炎症因子水平等全维度评价方法，可高效支撑神经病理性疼痛发病机制探究、创新镇痛靶点验证与临床前药物药效评价，一站式赋能镇痛领域新药研发管线高效突破。一临床痛点与待解科学问题组蛋白去乙酰化酶（HDAC）是表观遗传调控的核心分子，除组蛋白外，还可修饰微管蛋白、STAT3等非组蛋白底物，参与肿瘤、炎症、神经疾病等多种病理过程。其中Ⅱ类HDAC家族成员HDAC6特异性靶向非组蛋白底物，已有研究证实其抑制剂可缓解神经损伤与炎症诱导的疼痛，且可透过血脑屏障，但具体作用机制尚未完全阐明。 STAT3是调控神经炎症与疼痛敏化的关键转录因子，其激活依赖Tyr705位点磷酸化，进而发生核转位并启动下游促炎基因转录。既往研究多聚焦胶质细胞STAT3的作用，且仅发现HDAC抑制剂可影响STAT3的mRNA水平；神经系统内HDAC6与STAT3是否存在直接互作、是否通过翻译后修饰调控STAT3活性、其下游关键效应分子是什么，均是领域内尚未解决的核心问题。此研究围绕上述科学问题，从动物行为、组织定位、蛋白互作、细胞验证、分子筛选多个层面展开系统研究。二核心研究结果 1 ACY-1215显著缓解SNI模型小鼠的神经病理性疼痛研究首先构建SNI神经病理性疼痛小鼠模型，术后第1天起连续14天腹腔注射选择性HDAC6抑制剂ACY-1215（20mg/kg/天，该剂量按体重换算与人体临床试验剂量范围一致），并动态检测机械痛阈值。如图1所示，雌雄两性SNI小鼠均出现稳定的机械性痛觉超敏与痛觉过敏；ACY-1215给药后从术后第7天开始显著提升疼痛阈值，至第13天药效趋于稳定，在雌雄小鼠中均表现出明确的镇痛效果。图1 HDAC6抑制剂ACY-1215缓解SNI模型小鼠的机械性疼痛 2 ACY-1215调控脊髓STAT3翻译后修饰平衡为探究镇痛效应的分子机制，研究检测了小鼠L4-L6腰段脊髓内STAT3的修饰状态。如图2所示，SNI术后脊髓内Tyr705位点磷酸化STAT3（p-STAT3）水平显著升高，Lys685位点乙酰化STAT3（Ac-STAT3）无明显变化；ACY-1215处理后，p-STAT3表达显著下调，Ac-STAT3水平明显上调，总STAT3蛋白量无改变。同时研究证实，ACY-1215不影响HDAC6本身的表达水平，但可显著升高HDAC6经典底物乙酰化α-微管蛋白（Ac-α-Tubulin）的水平，证实药物有效抑制了HDAC6的去乙酰化酶活性。脊髓背角免疫荧光染色结果与蛋白印迹结论完全一致。图2 ACY-1215上调SNI小鼠脊髓STAT3乙酰化水平、降低其磷酸化水平 3 细胞定位：HDAC6与p-STAT3主要表达于脊髓背角伤害性神经元研究通过免疫荧光双标染色明确HDAC6与p-STAT3的细胞分布，如图3所示，在SNI小鼠脊髓背角中，HDAC6与p-STAT3均主要与神经元标志物NeuN共定位（HDAC6神经元阳性率43%，p-STAT3神经元阳性率54%），仅少量表达于星形胶质细胞与小胶质细胞。进一步分析发现，二者均与脊髓Ⅰ-Ⅱ板层的非肽能伤害性神经元标志物IB4、肽能伤害性神经元标志物CGRP存在共定位，证实其表达于直接参与伤害性信号传导的背角神经元中。图3 HDAC6与p-STAT3主要定位于脊髓背角神经元 4 神经病理性疼痛特异性促进p-STAT3发生核转位 STAT3作为转录因子，需转位至细胞核才能发挥基因调控功能。研究通过亚细胞组分分离实验验证不同修饰形式STAT3的核定位差异。如图4所示，SNI术后脊髓细胞核内p-STAT3水平显著升高，胞质内p-STAT3无明显变化；而Ac-STAT3在细胞核内仅维持极低水平，且SNI术后无明显升高。该结果提示：STAT3的磷酸化修饰促进其核转位与转录激活，而乙酰化修饰可能阻碍其入核过程。图4 神经病理性疼痛增强p-STAT3的核转位 5 疼痛状态下HDAC6与STAT3直接结合增强，ACY-1215可阻断该互作为验证HDAC6是否直接调控STAT3，研究通过免疫共沉淀（Co-IP）检测二者的体内结合情况。如图5所示，SNI术后脊髓内HDAC6与STAT3的相互作用显著增强；给予ACY-1215后，二者的结合水平回落，同时STAT3乙酰化水平升高。该结果直接证实：病理状态下HDAC6与STAT3结合增强，介导STAT3去乙酰化并促进其激活；抑制HDAC6可阻断二者互作，逆转STAT3的异常活化。图5 神经病理性疼痛增强HDAC6-STAT3相互作用，ACY-1215可逆转该效应 6 神经元STAT3过表达足以诱发痛觉过敏，ACY-1215可逆转该效应既往研究多关注胶质细胞STAT3，本研究进一步验证神经元STAT3的功能。研究采用神经元特异性启动子hSyn驱动的AAV病毒，鞘内注射实现脊髓神经元STAT3特异性过表达。如图6所示，神经元STAT3过表达即可诱导小鼠出现机械性痛觉过敏，同时升高脊髓内p-STAT3水平，上调TNF-α、IL-1β等促炎因子的表达；给予ACY-1215后，可显著提升Ac-STAT3水平、降低p-STAT3/Ac-STAT3比值，并逆转痛觉过敏与促炎因子升高的表型。图6 神经元STAT3过表达诱发痛觉过敏与促炎反应，ACY-1215可逆转该效应 7 趋化因子筛选：CCL7是HDAC6/STAT3轴的关键下游效应分子为明确STAT3下游介导疼痛的关键效应分子，研究采用多重细胞因子芯片，对比假手术组、SNI组、SNI+ACY-1215组小鼠脊髓内27种细胞因子与趋化因子的表达水平。如图7所示，SNI术后IL-1β、IL-6、TNF-α、CCL7、CXCL13共5种分子显著上调，且均可被ACY-1215抑制；其中趋化因子CCL7的升高幅度最为显著，且其上调可被ACY-1215完全阻断，提示CCL7是HDAC6/STAT3轴最核心的下游效应分子。图7 ACY-1215逆转SNI诱导的趋化因子CCL7与CXCL13表达上调 8 体外验证：HDAC6-STAT3轴直接调控神经元CCL7生成研究在小鼠海马神经元细胞系HT22中开展体外验证，明确分子调控的上下游关系：如图8所示，敲低HDAC6可显著降低细胞内p-STAT3水平、升高Ac-STAT3水平，同时减少CCL7的生成；无论是否加入STAT3激活剂IL-6，该调控效应均稳定存在。反之，敲低STAT3可显著减少CCL7生成，但不影响HDAC6的表达水平。上述结果明确了信号轴的上下游关系：HDAC6是上游调控因子，通过修饰STAT3的翻译后状态调控其活性，最终介导下游CCL7的合成。图8 体外验证HDAC6/STAT3轴对CCL7的调控作用 9 在体验证：ACY-1215抑制SNI诱导的脊髓CCL7与促炎因子升高研究通过蛋白印迹与ELISA两种方法，再次在体验证ACY-1215对下游效应分子的调控作用。如图9所示，SNI术后小鼠脊髓内p-STAT3、CCL7、TNF-α、IL-1β水平均显著升高；ACY-1215给药可全面逆转上述分子的异常上调，从在体层面证实了ACY-1215对STAT3激活及其下游促炎信号的抑制效应。图9 ACY-1215抑制SNI术后小鼠脊髓内CCL7与促炎因子的生成三核心机制总结研究最终提出了HDAC6调控神经病理性疼痛的完整信号轴，机制如图10所示：病理状态：神经损伤后，脊髓内HDAC6与STAT3结合增强，介导STAT3去乙酰化，促进其磷酸化激活与核转位，进而启动下游CCL7、TNF-α、IL-1β等促炎介质的转录，加剧神经炎症与疼痛敏化。药物干预：HDAC6抑制剂ACY-1215可阻断HDAC6与STAT3的相互作用，提升STAT3乙酰化水平、降低其磷酸化水平，抑制STAT3核转位与促炎转录功能，减少下游炎症介质释放，最终缓解神经病理性疼痛。图10 HDAC6/STAT3信号调控神经病理性疼痛的机制示意图研究创新点与临床意义机制创新：首次证实神经系统内HDAC6与STAT3的直接互作，明确了“乙酰化-磷酸化修饰平衡”的全新调控模式，补充了STAT3激活调控的表观遗传机制。细胞层面拓展：揭示了神经元STAT3在疼痛发生中的直接作用，完善了既往仅聚焦胶质细胞STAT3的认知。转化价值明确：ACY-1215（Ricolinostat）已在淋巴瘤临床试验中证实良好的生物安全性，且可透过血脑屏障；本研究为其拓展至神经病理性疼痛、尤其是肿瘤相关神经痛的临床应用提供了核心理论支撑。同时研究也指出，目前结论仅基于SNI单模型验证，后续需在化疗痛、糖尿病痛、癌痛等更多疼痛模型中验证效应，且长期抑制HDAC6的神经系统安全性仍需进一步评估。 END 劲帆医药劲帆医药与国内外众多家药企、科研单位、医疗院所建立合作关系，已提供优质、高效、前沿的工具病毒和技术支持服务30000+。关于劲帆医药劲帆生物医药科技（武汉）有限公司简称“劲帆医药”，创立于2022年，提供一站式病毒载体、蛋白和疫苗CRO/CDMO服务，拥有全球领先的规模化AAV制备专利技术平台及病毒载体/cGMP级蛋白/疫苗生产车间，致力于推进基因治疗药物、蛋白药物、治疗性疫苗更有效，更安全，更经济，更可及，赋能客户，造福患者。联系我们电话：17720522078 官网：www.genevoyager.com 邮箱：marketing@genevoyager.com 地址：中国武汉东湖高新区光谷七路128号微信：Genevoyager2022 扫码进入官网扫码联系客服 1. 拆解CDE最新RCV指南《可复制型病毒风险控制研究与评价技术指导原则（征求意见稿）》：基因设计、生产管控、质量控制全链路要求梳理 2. 芳拓生物FT-003获FDA RMAT认定，系中国首个进入国际加速审评通道的nAMD AAV基因疗法 3. Sci Transl Med新发现：迷走神经刺激通过抑制SUMO化修饰缓解结肠炎，IBD治疗再添新靶点 4. 【产品与服务】炎症性肠病（IBD）模型构建及药效评价一站式服务

2026-08-03

·三六零零导航

【今日简报】2026年08月03日健康简报

1. 我国首例IgA肾病B细胞双靶点治疗药物泰它西普注射液正式进入临床应用，标志着IgA肾病治疗进入新时代。 2. 分子之心利用AI技术推进新药研发，通过从靶点发现到分子设计的全流程AI辅助，实现了从大规模筛选到可编程设计的转变，显著提高了研发效率和候选分子的质量。 3. 清华大学研究团队在《Science》杂志上发表了关于胶原蛋白结构的新发现，揭示了羟赖氨酸双糖修饰介导胶原纤维有序排布的分子原理，为胶原疾病诊疗及胶原生物材料开发奠定核心结构基础。 4. 南京大学研究团队在Nature杂志上发表了一项突破性研究，提出了一种名为瞬态孔分析物成环（tPAL）的纳米孔肽测序策略，通过工程化改造纳米孔和酶促切割，实现了对肽链氨基酸序列的连续读取，为单分子蛋白质测序领域带来了新的技术路线。 5. 复旦大学樊嘉团队在《Science》杂志发表研究，揭示了肿瘤细胞在肺转移过程中的时空动态和与微环境的相互作用机制，为恶性肿瘤抗转移治疗提供了新的研究方向。 6. 南方科技大学张明杰团队研究发现，桥尾蛋白是PX-RICS的主要突触锚定物，对于神经回路中兴奋-抑制平衡的精确调控至关重要，这一发现有助于理解自闭症谱系障碍和癫痫等神经发育障碍的分子基础。 7. 武汉大学于学杰团队研究发现，SFTSV病毒通过劫持CGAS-STING1依赖性自噬机制进行复制，这一发现揭示了新的抗RNA病毒策略，对预防和控制SFTSV等病毒性疾病具有重要意义。 8. 最新研究显示，在取栓再通后使用替罗非班辅助治疗，可显著提高患者功能独立的可能性，该成果已发表在《柳叶刀》杂志上。 9. 安迎锋团队在Nucleic Acids Research发表的研究突破性地在酿酒酵母中实现了光控CRISPR多层级精准基因转录调控，为构建动态基因回路和精准调控代谢通路提供了全新工具。这一成果在合成生物学、生物制造和微生物分子育种领域具有重大应用前景。 10. 科学家们开发出一种名为ADOC的人源子宫内膜芯片，能够实时捕获人囊胚的粘附和谱系重排过程，为研究胚胎着床机制提供了新的工具，对反复着床失败的患者和临床医生具有重要意义。 11. 研究发现，精氨酸缺乏会干扰免疫系统，增加结肠癌和病毒感染风险。适度补充精氨酸可能有助于恢复免疫系统功能，并可能用于治疗癌症和病毒感染。 12. 四川大学王永生和李丹团队研究发现，通过整合并行4-1BB共刺激信号，DLL3靶向CAR-T细胞在小细胞肺癌中表现出更长的持久性、更高的增殖能力和更慢的衰竭速度，为实体瘤治疗提供了新的策略。 13. 研究发现，CX3CR1⁺巨噬细胞通过CSF1R-PARP1-IL1B-线粒体自噬信号轴加剧多柔比星诱导的心肌病，为化疗药物的心脏毒性提供了新的治疗靶点。 14. 研究发现，每周进行至少2小时的抗阻运动，每天仅需10分钟，可显著降低心血管疾病风险，包括心肌梗死风险，同时对抗阻运动的好处还包括降低糖尿病风险、改善血压、抑制癌细胞生长和预防肌少症。提供五种居家可练的抗阻运动方法。 15. 南京医科大学团队在Science子刊发表研究，发现胆固醇25-羟化酶（CH25H）在帕金森病中调控α-突触核蛋白降解，为帕金森病治疗提供新思路。 16. 华东理工大学研究团队开发出新型硫酸化多糖26SCS，有效抑制破骨细胞骨吸收同时促进骨形成，为骨质疏松治疗提供新策略。 17. 最新研究揭示人类基因组中的两个未知古人类祖先，通过TRACE技术，研究人员确定了这些祖先的DNA区域，并建立了时间线。这一发现不仅揭示了人类演化过程中与古人类的杂交历史，也为理解人类遗传多样性提供了新的视角。 18. 研究发现蜱虫病毒WELV通过激活肝细胞焦亡和脂质代谢重编程导致肝损伤，关键蛋白GSDME在其中起关键作用。老药新用，通过抑制GSDME或FASN可能成为治疗新策略。 19. 习近平总书记强调到2035年建成健康中国，强调坚持中国特色卫生与健康发展道路，突出重点推进健康中国建设，并为此提供有力保障。 20. 我国第三批抗疫医疗专家组赴刚果（金）执行埃博拉疫情防控援助任务，将提供全面技术支持，并与当地卫生部门和国际组织合作，推动疫情防控和卫生人才培养。 21. ‘我是健康小达人’儿童青少年健康科普暑期专场活动在北京启动，旨在通过专业科普活动帮助儿童青少年了解健康知识，掌握健康生活技能，树立科学健康理念。 22. 最新2026版银屑病关节炎诊疗指南发布，权威专家解读为临床提供重要指导。 23. 新型药物Ricolinostat与BCR通路抑制剂联合治疗复发难治性CLL，临床前和临床研究显示显著疗效。 24. 中国科学技术大学朱小玉团队研究发现，使用老药维奈克拉预处理γδ T细胞，可显著提升其抗白血病疗效，为AML γδ T细胞疗法提供新策略。 25. 华中科技大学研究发现，帕金森病相关蛋白PARK7具有去乳酸化酶功能，能纠正RNA剪接错误、抗肿瘤纤维化，对肿瘤生长具有抑制作用，可能成为癌症治疗的新靶点。 26. 研究发现，蛛网膜上的微小开口允许脑脊液直接进入淋巴系统，这一发现为理解脑废物清除随年龄变化提供了新框架，并通过鼻内给药在老年小鼠中恢复了引流功能，为治疗神经退行性疾病提供了潜在的新靶点。 27. 研究发现，紫外光声显微镜可以无标记、无侵入地观察活体类脑器官中酒精的细胞毒性，为孕期饮酒的神经毒性评估提供了新的手段。该技术通过机器学习可以自动识别正常和受损的细胞核，为神经毒性筛查提供了新的可能性。 28. 杭州医学院张建宾团队研究发现，线粒体自噬依赖性将CD274招募至MERCs进行PRKN介导的泛素化，可激活抗肿瘤免疫并改善免疫治疗疗效，为宫颈癌治疗提供了新的策略性靶点。 29. 新型‘张力释放’共价弹头平台在癌症研究中取得突破，通过生物电子等排替换丙烯酰胺，实现精准靶向与高选择性，为共价疗法设计提供新框架。 30. 研究发现，正常衰老的细胞中也存在与罕见病相似的溶酶体残留物，揭示了正常衰老与特定少年型溶酶体贮积症之间的分子趋同性。这一发现为评估促进健康寿命的干预措施提供了新的框架。今日简报 · 每日资讯热点 | 生成精简日报为您提供以最少的时间获得最有价值的信息内容来源于互联网，仅供参考

2026-07-14

·研日新

研日新日报 ·8| 07月15日神经外科 | 骨科 | 耳鼻喉科

日报精选医学文献今日精选20篇医学文献，查看更多请点击阅读原文本文支持继续浏览摘要内容；完整摘要、收藏文章、订阅管理等完整功能，请前往小程序「医研日新」。前往小程序查看更多与订阅收藏 1. Pseudokinase-converting mutation in protein kinase C alpha drives chordoid glioma by pathway rewiring. [Brain Neoplasms] Proceedings of the National Academy of Sciences of the United States of America | 2026-07-13 | IF 9.4 AI脊索样胶质瘤中存在PKCα D463H突变，该突变使其丧失催化活性但获得脚手架功能，可作为疾病诊断的分子标志物及潜在治疗靶点。摘要Chordoid glioma (ChG) is a rare, low-grade brain tumor characterized by a novel recurrent point mutation, D463H, in the kinase domain of protein kinase C alpha (PKCα). The mutation is invariably an Asp to His substitution, suggesting a unique function beyond catalytic inactivation associated with other cancer-associated PKCα mutations. Here, we show that this mutation converts PKCα into a pseudoki...查看完整摘要 2. Targeting mitochondrial protease in diffuse gliomas. [Glioma] Molecular cancer therapeutics | 2026-07-13 | IF 5.3 AITR107作为新型ClpP激动剂，在IDH突变型胶质瘤中展现出优于现有药物ONC201的抗肿瘤活性，具有显著的临床转化价值。摘要Caseinolytic protease proteolytic subunit (ClpP) is part of the mitochondrial ClpXP protease responsible for degrading damaged proteins in the matrix, thus maintaining metabolic homeostasis. Small molecule activators of ClpP (ClpP agonists) have recently shown great promise against metabolically active cancers. TR107, a novel ClpP activator, demonstrates potent and selective cytotoxicity against g...查看完整摘要 3. Combating Inflammation and Promoting Anabolism in Osteoarthritic Cartilage Defect With an MMP13-Sensing Dual-Drug Scaffold. [Osteoarthritis] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AI该MMP13响应型双药物支架通过智能化按需释药机制，为早期OA提供了一种精准调控炎症与软骨修复的微创治疗新策略。摘要Osteoarthritis (OA) is a widespread degenerative joint condition marked by progressive cartilage breakdown, and a chronic inflammatory microenvironment, where conventional therapies largely fail to halt disease progression. To address this unmet need, an intra-articularly implantable, disease-responsive scaffold was developed for combinatorial treatment to simultaneously combat inflammation and pr...查看完整摘要 4. Hairyvein agrimony-derived nanovesicles in microneedles eradicate intracellular bacteria and reverse senescence to heal diabetic foot osteomyelitis. [Osteomyelitis] Journal of controlled release : official journal of the Controlled Release Society | 2026-07-13 | IF 10.5 AI该微针贴片为难治性DFO提供了一种无创、低毒的协同治疗方案，有望突破传统治疗的“三重瓶颈”，改善患者预后。摘要The refractory nature of diabetic foot osteomyelitis (DFO) wounds constitutes a primary cause of disability among diabetic patients. However, currently employed interventions fall short of clinical requirements because of undefined targeting mechanisms, suboptimal wound repair, and significant adverse effects, necessitating innovative therapeutic strategies that transcend traditional paradigms. By...查看完整摘要 5. Methotrexate for hand osteoarthritis. [Osteoarthritis] The Cochrane database of systematic reviews | 2026-07-13 | IF 8.8 AI该综述旨在明确甲氨蝶呤这一传统抗风湿药能否为手部骨关节炎提供新的治疗选择，为优化临床用药方案提供高质量证据支持。摘要This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To assess the benefits and harms of methotrexate for people with osteoarthritis of the hand. 6. Sensor-based measures of knee brace adherence have low agreement with self-report methods: a multi-measure study among knee osteoarthritis patients. [Osteoarthritis] Osteoarthritis and cartilage | 2026-07-13 | IF 7.2 AI在评估膝关节骨关节炎患者的支具依从性时，自我报告方法存在明显高估倾向，建议临床试验和实践中采用客观监测手段以获取更准确的治疗依从性数据。摘要To explore agreement between self-report and objectively measured adherence to brace wearing by patients with knee osteoarthritis. A single-arm observational analysis nested within the PROP OA randomised controlled trial (ISRCTN28555470). Of 237 adults with symptomatic knee osteoarthritis randomised to brace treatment, 60 were included in this sub-study investigating three different methods of ass...查看完整摘要 7. Developmental divergence in voice-reward circuitry differentiates autistic from typically developing children and adolescents. [Deafness] Proceedings of the National Academy of Sciences of the United States of America | 2026-07-13 | IF 9.4 AI自闭症青少年对社会声音处理的神经发育轨迹异常，表现为对母亲声音的依赖持续增强而非正常地向同伴声音转移，提示早期干预应关注社会声音处理网络的重塑。摘要Adolescence is a period of profound social change marked by a developmental shift in attention and motivation from parents toward nonfamilial peers. Autism is a neurodevelopmental condition characterized by lifelong challenges in social communication. However, the neurobiological signatures of adolescent social reorientation in autism are poorly understood. Human voice processing is a primary driv...查看完整摘要 8. Chronic Rhinosinusitis and Nasal Polyps in Eosinophilic Granulomatosis With Polyangiitis: A Scoping Review. [Sinusitis] 综述 | International forum of allergy & rhinology | 2026-07-13 | IF 7.2 AI对于表现为CRSwNP的患者，应警惕EGPA可能，即使鼻窦活检未提示血管炎，仍需长期随访以排除系统性血管炎。摘要Chronic rhinosinusitis (CRS) is one of the most common manifestations of eosinophilic granulomatosis with polyangiitis (EGPA), often preceding the diagnosis of systemic vasculitis by several years. The sinonasal presentation of EGPA typically resembles CRS with nasal polyps (CRSwNP), making it clinically indistinguishable from those without EGPA. This overlap frequently contributes to significant ...查看完整摘要 9. Detergent-like Toxicity Mechanism of Amyloid Cylindrins Revealed by Cross-Link Spin Labeling Electron Spin Resonance. [Neurodegenerative Diseases] Journal of the American Chemical Society | 2026-07-13 | IF 14.4 AI该研究揭示淀粉样蛋白寡聚体可能通过类洗涤剂机制破坏神经元膜，为理解神经退行性疾病发病机制及开发靶向膜损伤通路的新型治疗策略提供了重要理论基础。摘要Amyloid oligomers are considered to be the most toxic species in neurodegenerative diseases, such as Alzheimer's, and Parkinson's, among others. A major challenge in studying amyloid oligomers has been their heterogeneous character, coupled with a lack of methods that can probe targeted, localized structural information. In this paper, we show that in detergent micelles, the oligomeric state of am...查看完整摘要 10. Histone H3K18 Lactylation Promotes the Malignant Progression of Wilms Tumor via a PSRC1/AKT/HIF-1α Positive Feedback Loop. [Wilms Tumor] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AIH3K18la/PSRC1/AKT/HIF-1α正反馈环路可作为肾母细胞瘤精准分型和靶向干预的潜在生物标志物，为改善高危患儿预后提供新策略。摘要Nephroblastoma, also known as Wilms tumor (WT), is the most common pediatric renal malignancy. Current treatment regimens exhibit limited efficacy in high-risk patients and are associated with long-term adverse effects. Through gene set enrichment analysis (GSEA) and validation using clinical specimens, we identified aberrant glycolytic activity in WT, which drives lactate accumulation. Lactate is...查看完整摘要 11. LRRC4 Orchestrates AP2A1-Containing Clathrin-Coated Vesicles to Disrupt Mitochondrial Cristae and Restrict Glioblastoma Progression. [Glioblastoma] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AILRRC4-AP2A1-Mic60轴的发现为GBM提供了新的线粒体脆弱性靶点，靶向高尔基体-线粒体互作可能成为胶质母细胞瘤的创新治疗策略。摘要Mitochondrial dynamics and metabolic homeostasis are pivotal for the aggressive progression of glioblastoma (GBM); however, how membrane-bound organelles modulate mitochondrial remodeling remains unclear. In this study, we identified LRRC4 as a Golgi-anchored tumor suppressor that coordinates a novel vesicle-to-mitochondrial axis to inhibit tumor growth. Using single-sample gene set enrichment ana...查看完整摘要 12. Cyclic Mechanical Loading of Cardiomyocytes via Pressure-Driven Non-Planar Membrane Deformation in a Bioreactor System. [Heart Failure] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AI该研究建立的生物反应器平台可模拟不同压力条件下心肌细胞的力学响应，为理解心肌肥厚和心力衰竭的发病机制提供了体外研究工具。摘要We introduce a novel bioreactor system that applies cyclic strain through controlled non-planar membrane deformation. The membrane deformation is driven by tunable pressure profiles spanning clinically reported end-diastolic pressure ranges observed in physiological and disease-associated conditions. Applied pressure was quantitatively related to spatial membrane strain through three-dimensional m...查看完整摘要 13. A Spatially Directed Microneedle Patch Enables Intratumoral Co-Delivery of FOLFIRINOX, Surufatinib, and Anti-PD-1 for Chemo-Immunotherapy of Pancreatic Ductal Adenocarcinoma. [Adenocarcinoma] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AI微针贴片局部共递送FOLFIRINOX、靶向药及免疫检查点抑制剂，可突破PDAC纤维化屏障，在降低全身毒性的同时重塑免疫微环境，为晚期胰腺癌提供新型联合治疗平台。摘要Pancreatic ductal adenocarcinoma (PDAC), a lethal malignancy with a 5-year survival of 13%, faces limited therapeutic efficacy due to fibrotic barriers that block drug access to the therapeutic site, systemic toxicity of conventional chemotherapy, and an immunosuppressive tumor microenvironment (TME). Therapeutic agents with different functions, including FOLFIRINOX (FFX), surufatinib (SUR), and a...查看完整摘要 14. Microenvironment-Responsive Nanomedicine Enables Vertical Modulation of Mitochondrial Pathological Networks in Myocardial Ischemia-Reperfusion Injury. [Myocardial Infarction] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AIBIM纳米制剂通过三重机制协同干预MIRI病理网络，为急性心肌梗死再灌注治疗后心肌保护提供了一种具有临床转化潜力的精准治疗新策略。摘要Myocardial ischemia-reperfusion injury (MIRI) is a severe and largely unavoidable complication of reperfusion therapy and remains a major determinant of poor outcomes after acute myocardial infarction. Here, we developed a mitochondria-targeted, ischemic microenvironment-responsive nanotherapeutic, termed Berberine/Isoliensinine-loaded Melanin Nanocomposite (BIM), by co-encapsulating the anti-infl...查看完整摘要 15. Versatile Detection of Cellular Protein via Fluorescence Anisotropy. [Neurodegenerative Diseases] Advanced science (Weinheim, Baden-Wurttemberg, Germany) | 2026-07-13 | IF 14.3 AICFAST技术为药物研发提供了一种快速、经济且高通量的蛋白检测工具，可加速靶点验证和先导化合物筛选。摘要Protein detection is a cornerstone of life science research. Here, we present Cell Lysate Fluorescence Anisotropy (CFAST), a versatile and accessible alternative cellular protein detection method. CFAST measures cellular protein levels through changes in fluorescence anisotropy of a long lifetime triangulenium dye-labeled nanobody probe. The minimal steps of centrifugation and nuclease incubation ...查看完整摘要 16. Neural checkpoint therapy in lung cancer. [Adenocarcinoma] Trends in cancer | 2026-07-13 | IF 14.3 AINav1.8+神经元-CGRP轴可能成为肺癌免疫治疗的新靶点，通过神经检查点阻断有望将免疫冷肿瘤转化为热肿瘤，从而增强免疫检查点抑制剂疗效。摘要Sensory nerves are emerging as regulators of tumor immunity. A newly identified Nav1.8+ neuron-calcitonin gene-related peptide axis in lung adenocarcinoma links nociceptive signaling to impaired tertiary lymphoid structure formation and immune escape, suggesting that neural checkpoint blockade may help remodel immune-cold tumors and improve immunotherapy responses (Ho et al.). 17. Preclinical and clinical efficacy of the HDAC6 inhibitor ricolinostat in combination with BCR pathway inhibitors in relapsed/refractory chronic lymphocytic leukemia. [Leukemia] 信函 | Blood cancer journal | 2026-07-13 | IF 12.9 AIHDAC6抑制剂ricolinostat与BCR通路抑制剂联用对复发/难治性CLL显示出协同抗肿瘤活性，可能成为改善疗效的潜在治疗方案。 18. Deep learning-based CD8+ T cell model for predicting prognosis and‌ targeted immunotherapy benefit in ccRCC. [Carcinoma] NPJ digital medicine | 2026-07-13 | IF 12.4 AIDL-CD8T模型可从常规H&E染色病理图像无创预测ccRCC患者免疫治疗获益，为精准选择靶向联合免疫治疗方案提供新工具。摘要Deep learning holds significant promise for improving clear cell renal cell carcinoma (ccRCC) diagnosis and treatment. However, studies concerning tumor microenvironment (TME) based on pathological images and artificial intelligence are very limited. In this multi-center cohort study, we developed a deep learning-based CD8+ T cell inflammation signature (DL-CD8T) for ccRCC from hematoxy...查看完整摘要 19. Impact of an AI algorithm for multi-day prediction of incident atrial fibrillation on clinical decision-making: PROVISION-AF study. [Atrial Fibrillation] NPJ digital medicine | 2026-07-13 | IF 12.4 AIAI风险评估工具能显著提升非专科医生的房颤识别能力，尤其在排除低风险患者方面表现优异，有望成为基层医疗和门诊场景中的实用辅助决策工具。摘要Atrial fibrillation (AF) is frequently asymptomatic and often remains undetected until complications arise. Although artificial intelligence (AI)-enabled electrocardiography (ECG) can predict incident AF from sinus rhythm ECGs, its influence on physician risk assessment in simulated clinical settings remains uncertain. We developed a deep learning model to predict multi-day AF risk using non-AF 12...查看完整摘要 20. Portable RF brain scanner enables stroke type detection using deep learning. [Stroke] NPJ digital medicine | 2026-07-13 | IF 12.4 AI该便携式射频脑扫描系统可帮助急诊医生快速区分中风类型，为及时精准治疗决策提供辅助工具，有望改善患者预后。摘要Stroke remains a leading cause of mortality worldwide, demanding rapid, accurate diagnosis; distinguishing stroke types matters because treatments differ significantly. Using a recently developed, non-invasive brain scanner integrating a 16-antenna radio-frequency array, we present a deep-learning model that distinguishes the two main stroke types. We employ masked autoencoder-based self-supervise...查看完整摘要在小程序获取完整功能收藏文章、管理订阅、查看本期完整摘要与个性化内容，请前往小程序「医研日新」。前往小程序查看更多内容免责声明：仅供学术交流参考，不构成任何医学建议或诊疗指导

100 项与 Rocilinostat 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10661	-	-	DB12376

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
糖尿病周围神经性疼痛	临床2期	美国	Regenacy Pharmaceuticals LLC	2020-12-07
霍奇金淋巴瘤	临床2期	美国	Acetylon Pharmaceuticals, Inc.	2014-04-02
套细胞淋巴瘤	临床2期	美国	Acetylon Pharmaceuticals, Inc.	2014-04-02
多发性骨髓瘤	临床2期	美国	Acetylon Pharmaceuticals, Inc.	2014-04-02
难治性非霍奇金淋巴瘤	临床2期	美国	Acetylon Pharmaceuticals, Inc.	2014-04-02
难治性多发性骨髓瘤	临床2期	美国	Celgene Corp.	2014-03-01
复发性多发性骨髓瘤	临床2期	美国	Celgene Corp.	2014-03-01
乳腺癌	临床1期	中国	北京本草瑞生醫藥科技香港有限公司	2022-11-17
神经炎	临床1期	中国	北京本草瑞生醫藥科技香港有限公司	2022-11-17
卵巢癌	临床1期	美国	Celgene Corp.	2016-06-15

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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


NCT01997840 (CTgov)	临床1/2期	复发性多发性骨髓瘤 \| 难治性多发性骨髓瘤	103	pomalidomide+dexamethasone+ACY-1215 (Phase 1b - ACY-1215)	壓製餘網壓鹹構觸夢構 = 醖壓艱願築繭淵壓襯願顧糧繭衊齋鏇廠鹽選衊 (齋壓範鬱淵憲遞鑰選鹹, 鬱鏇淵鏇範鏇觸淵鬱醖 ~ 鏇繭衊構顧齋鏇遞艱觸)	-	2025-03-04
NCT01997840 (CTgov)	临床1/2期	复发性多发性骨髓瘤 \| 难治性多发性骨髓瘤	103	ACY-1215 (Phase 2 - ACY-1215 Dose Level 1)	餘憲積齋窪範艱範齋齋 = 襯壓壓鹹鏇範鬱衊膚獵構蓋襯鬱壓築構構鹹夢 (壓構選繭築夢窪範觸願, 製鹹廠夢積廠構獵鹽窪 ~ 淵選夢憲窪積糧餘糧餘) 更多	-	2025-03-04
NCT02091063 (CTgov)	临床1/2期	霍奇金淋巴瘤 \| 套细胞淋巴瘤 \| 难治性非霍奇金淋巴瘤 ... 更多	23	ACY-1215	襯醖壓構構齋廠鬱構夢(糧觸積鬱遞壓鹹願鏇憲) = 顧選願構餘窪醖壓憲齋繭壓網鹹選遞廠壓構簾 (鹹廠鑰鹹膚蓋糧糧構齋, 選觸積蓋願網餘築築鑰 ~ 範壓築顧鑰襯膚製鹹鹽) 更多	-	2024-08-06
NCT03176472 (CTgov)	临床2期	糖尿病周围神经性疼痛	282	ricolinostat (Ricolinostat)	艱艱膚齋觸製選艱壓觸(糧窪襯蓋醖憲壓襯構鑰) = 憲鏇顧鏇築觸廠醖鬱築簾鹹窪鏇夢壓襯顧蓋淵 (鹽鏇製鏇獵艱鹹壓艱廠, 1.4) 更多	-	2023-09-21
NCT03176472 (CTgov)	临床2期	糖尿病周围神经性疼痛	282	Placebo (Placebo)	艱艱膚齋觸製選艱壓觸(糧窪襯蓋醖憲壓襯構鑰) = 鏇網淵淵構構獵鹹積築簾鹹窪鏇夢壓襯顧蓋淵 (鹽鏇製鏇獵艱鹹壓艱廠, 1.4) 更多	-	2023-09-21
AACR2020	临床1/2期	转移性乳腺癌	16	Ricolinostat 240 mg qd + nab-paclitaxel	鏇夢淵製壓觸鹽膚積願(築膚選構製夢遞網鹹鑰) = 鏇膚憲選願廠鑰鑰醖積製簾選壓範顧網醖網顧 (鹽襯蓋鬱齋構壓製鑰蓋, 4.45 ~ 11.0)	积极	2020-08-15
P1-19-27 (SABCS2020)	临床1期	转移性乳腺癌 HDAC6 score	17	ACY-1215 240 mg qd + nab-paclitaxel 100 mg/m2	蓋鹽願遞繭顧餘鏇繭憲(網製憲憲憲艱繭觸鹹憲) = neutropenia (n=1), peripheral neuropathy (n=1), and 1 grade IV neutropenia 構積齋糧積積簾鹽糧壓 (鏇簾鹽膚鏇襯艱壓鑰憲 ) 更多	积极	2020-02-15
NCT02661815 (CTgov)	临床1期	原发性腹膜癌 \| 卵巢癌 \| 复发性铂耐药性输卵管癌	6	Paclitaxel+Ricolinostat (Phase 1 Escalation Cohort)	蓋遞遞鏇齋構製憲願衊 = 廠衊夢廠築鑰餘選築壓淵簾鑰鏇醖醖觸願餘膚 (齋鏇觸製繭願遞積襯醖, 糧憲夢鏇築衊範壓廠網 ~ 遞獵築鏇範選鹽製襯餘) 更多	-	2019-11-08
NCT02661815 (CTgov)	临床1期	原发性腹膜癌 \| 卵巢癌 \| 复发性铂耐药性输卵管癌	6	Paclitaxel+Ricolinostat (Phase 1 Expansion Cohort A)	遞憲顧獵構憲淵糧蓋積(醖齋範夢繭顧膚築網餘) = 廠獵獵鏇鏇襯構淵獵鏇鏇鹹顧壓遞窪夢襯齋遞 (範顧襯廠鏇餘鹹襯選鹽, 遞鏇範蓋糧襯範襯壓壓 ~ 顧鹹願構齋網鹽鹽獵衊) 更多	-	2019-11-08
NCT02661815 (Pubmed) 人工标引	临床1期	复发性卵巢癌 \| 铂类耐药性原发性腹膜癌 \| 输卵管癌二线	6	paclitaxel+ricolinostat	顧夢顧憲齋夢製築選繭(鬱淵積網簾醖鏇夢艱網) = 鹽遞觸衊繭衊艱膚餘糧鬱憲遞廠壓觸鹹積簾壓 (網醖夢顧鬱築製鏇膚願 ) 更多	积极	2019-08-10
NCT02632071 (ASCO 12018 \| ASCO 22018) 人工标引	临床1期	转移性乳腺癌	17	ACY-1215+nab-paclitaxel	膚築鑰齋鑰構鹹範醖糧(壓淵獵觸壓淵築餘淵網) = none 願餘願餘夢製構壓鹹壓 (襯願鏇鹹艱構簾淵繭積 ) 更多	积极	2018-06-02
NCT01583283 (Pubmed \| Lancet Oncol) 人工标引	临床1期	多发性骨髓瘤	38	lenalidomide+dexamethasone+ricolinostat	糧觸簾憲鑰繭鏇蓋廠壓(窪範餘膚鏇鑰簾鏇淵艱) = icolinostat（160 mg once daily on days 1-21 of a 28 day cycle）+ lenalidomide（25 mg）+dexamethasone（40 mg）壓鹹構夢簾蓋網襯範鏇 (遞淵構鏇餘醖鏇淵繭齋 ) 更多	积极	2016-11-01