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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247

项与 Rocilinostat 相关的文献（医药）

2025-06-01·INTERNATIONAL IMMUNOPHARMACOLOGY

IDH1/MDH1 deacetylation activates the cGAS-STING pathway by promoting NETosis in acute liver failure

Article

作者: Zhang, Xiaoya ; Luo, Ke ; Guo, Jin ; Wang, Yukun ; Gong, Zuojiong ; Zhang, Danmei

BACKGROUND:

Acute liver failure (ALF) is a life-threatening disease caused by multiple factors. Our previous study shows that IDH1/MDH1 deacetylation aggravates ALF through NETosis (a new mode of cell death). However, the exact mechanism by which NETosis mediates ALF is still unclear.

METHODS:

The transcriptome sequencing data of hepatic tissues from ALF mice and healthy control mice were downloaded from the GEO database. Inflammation-related pathways of ALF were identified by differential expression analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. In vivo, a mouse ALF model was established with LPS/D-gal. In vitro, HepG2 cells were used to simulate hepatocyte injury. The cell death rate of HepG2 cells was detected by flow cytometry. The levels of inflammatory factors in mouse liver tissues were detected by enzyme-linked immunosorbent assay (ELISA). The formation of NETs and the levels of cGAS-STING pathway-related proteins were detected by Western blotting, immunohistochemistry and immunofluorescence.

RESULTS:

The cGAS-STING pathway was activated in LPS/D-gal-induced ALF. In the ALF mouse model, ACY1215, as a histone deacetylase 6 inhibitor, alleviated ALF by inhibiting cGAS-STING pathway. Deoxyribonuclease 1 (DNase 1) degraded NETs formed by IDH1/MDH1 deacetylation in mouse liver tissue. DNase 1 attenuated hepatic tissue injury, reduced serum ALT and AST levels and reduced the levels of TNF-α and IL-6 in liver tissues. IDH1/MDH1 deacetylation increased the levels of cGAS-STING pathway-related protein, which was reversed by DNase 1. Exogenous NETs enhanced LPS/D-gal-induced hepatocyte death and activation of the cGAS-STING pathway in vitro.

CONCLUSION:

IDH1/MDH1 deacetylation activates the cGAS-STING signaling pathway by NETs. The activation of STING promotes pro-inflammatory cytokine production and exacerbates the inflammatory response in LPS/D-gal-induced ALF.

2025-05-01·BIOCHEMICAL PHARMACOLOGY

HDAC6 is involved in diabetic nephropathy by regulating TGFβ/Smads and NF-κB signaling pathways

Article

作者: Li, Jialin ; Zhang, Jiawen ; Liu, Zhiping ; Huang, Xiaocui ; Wu, Suzhen ; Jin, Songzhi ; Yu, Zhaolong

Histone deacetylase 6 (HDAC6), a cytoplasmic member of the histone deacetylase family, plays an incompletely understood role in diabetic nephropathy (DN). While the TGF-β/Smads and NF-κB signaling pathways are established mediators of renal fibrosis and inflammation respectively, the potential regulatory effect of HDAC6 on these pathways in DN remains to be elucidated. Notably, Smad7 has been documented as a negative regulator of both TGF-β/Smads and NF-κB signaling pathways. This study utilized high glucose to establish a diabetic cell model and employed a high-fat diet combined with STZ injection to create a diabetic animal model to explore HDAC6's role in DN and its potential mechanism. Our research indicates that HDAC6 is upregulated in DN, and inhibiting HDAC6 activity with ACY1215 or downregulating HDAC6 expression with siRNA can suppress the TGF-β/Smads and NF-κB signaling pathways, thereby reducing renal fibrosis and inflammation. Moreover, further studies have shown that lentivirus-mediated overexpression of HDAC6 results in increased expression of FN and p-Smad2/3, decreased expression of Smad7 compared to their respective controls. ACY1215, an HDAC6 inhibitor, could alleviate DN by suppression of both the TGF-β/Smads and NF-κB signaling pathways. To sum up, this study reveals that HDAC6 is involved in the pathogenesis and progression of DN. Mechanistically, HDAC6 may participate in DN by regulating the TGF-β/Smads and NF-κB signaling pathways through Smad7.

2025-05-01·MOLECULAR PHARMACOLOGY

HDAC6 inhibition ameliorates sensory hypersensitivity and reduces immune cell signatures in the dorsal root ganglia in murine chronic pain models

Article

作者: Zimering, Jeffrey ; Giosan, Ilinca M ; Serafini, Randal A ; Shen, Li ; Tuffy, Madden J ; Zachariou, Venetia ; Babes, Alexandru ; Ramakrishnan, Aarthi

Histone deacetylase (HDAC)6 is a broadly expressed class IIb HDAC that regulates cytoskeletal dynamics and some nuclear processes. Previously research has shown that HDAC6 enzymatic inhibition has analgesic properties in models of chemotherapy-induced peripheral neuropathy. Here, we evaluated the effects of genetic and pharmacologic inhibition of HDAC6 on the development of sensory hypersensitivity in mouse models of peripheral nerve injury and peripheral inflammation. Daily administration of the peripherally restricted HDAC6 inhibitor, ACY1215 (Regenacy Pharmaceuticals, Inc), attenuated mechanical allodynia in the von Frey assay within 2 days of treatment initiation, with no signs of analgesic tolerance after 21 days of administration. We observed a similar antiallodynic effect across the implemented injury models after conditionally knocking down Hdac6 in the adult dorsal root ganglia (DRGs). Bioinformatic analysis of whole-transcriptome RNA-sequencing data predicted that ACY1215 treatment predominantly attenuated proinflammatory mechanisms, such as the suppression of immune cell infiltration into the DRG after injury. Accordingly, we demonstrated a reduction in the expression of various immune cell markers in the DRG after pharmacologic and genetic HDAC6 inhibition in both neuropathic and inflammatory pain models. We identified a direct relationship between Ccl5/Ccr5 and Hdac6 downregulation, as well as reduced hypersensitivity after hind paw CCL5 administration upon Hdac6 knockdown in the DRG. Our findings highlight that peripheral inhibition of HDAC6 ameliorates sensory hypersensitivity in models of postoperative inflammatory and neuropathic pain through mechanisms beyond reduction of tubulin deacetylation. SIGNIFICANCE STATEMENT: Recent studies highlight the role of histone deacetylase (HDAC)6 in chemotherapy-induced peripheral neuropathy, through mechanisms of action including tubulin acetylation and mitochondrial trafficking. In this study, various murine models of acute and chronic pain are applied to show that inhibition of HDAC6 activity in the periphery, using the clinically tested ACY1215 compound, and genetic inactivation of the Hdac6 gene in the dorsal root ganglia, alleviated mechanical hypersensitivity in male and in female mice through mechanisms that include targeting injury-induced inflammation.

项与 Rocilinostat 相关的新闻（医药）

2022-09-28

·BioSpace

Portfolio Highlights: Clinical and Financial Updates of ABM, F5, AceLink, HAYA, Regenacy, and Arthrosi

SHANGHAI, Sept. 28, 2022 /PRNewswire/ -- As the investment division of Viva Biotech, Viva BioInnovator is committed to being a collaborative platform for Innovative Biotech companies from around the world. Over the past 2 months, our portfolio companies progressed greatly. ABM Therapeutics Announces First Patient Dosed in Phase I Clinical Trial of ABM-1310 in China On September 16, 2022, ABM Therapeutics, a clinical-stage biopharmaceutical company that is invested and incubated by Viva BioInnovator, announced that the first patient has been successfully dosed with ABM-1310 in a multi-center phase I clinical trial in China. ABM-1310, ABM Therapeutic's proprietary clinical candidate developed as a next-generation BRAF inhibitor, is a highly selective, highly water-soluble, orally administrated, and brain-penetrant small molecule BRAF inhibitor. ABM-1310 phase I trial, conducted in China, is a multi-center, open-label study to investigate the safety, tolerability, pharmacokinetics, and preliminary anti-tumor activity of ABM-1310 in Chinese patients with BRAF V600X mutated advanced solid tumors. F5 Therapeutics awarded First Servier FAST Discovery Award F5 Therapeutics, which invested and incubated by Viva BioInnovator, was recently awarded the first Servier FAST Discovery Award. Winning this award means F5 stood out from 23 applications, indicating the industry's recognition of F5's innovative treatment methods in the field of biomedicine. "Servier FAST Discovery Award" is co-sponsored by Servier and the California Life Sciences Association (CLSA) to support early-stage life science companies using innovative approaches in areas designated by the group: oncology, auto-immune diseases, genetically driven neurodegenerative, and movement disorders. F5 is transforming targeted protein degradation to advance drug discovery by utilizing the cell's normal protein regulation systems to remove disease-causing proteins that cannot be targeted by traditional approaches. The NExMods™ Platform (NEosubstrate Expression Modulators) represents a novel approach to "molecular glues" capable of delivering effective medicines to patients across diverse therapeutic areas: oncology, immuno-oncology, fibrosis, inflammation, and neurodegeneration. AceLink Therapeutics Receives Orphan Drug Designation for its Novel GCS inhibitor AL01211 for the Treatment of Fabry Disease AceLink Therapeutics, Inc. (AceLink), invested and incubated by Viva BioInnovator, is an innovative biopharmaceutical company developing transformative therapies for genetic diseases. On September 7, 2022, they announced that they received Orphan Drug Designation (ODD) from the U.S. Food and Drug Administration (FDA) for AL01211 as a treatment for Fabry Disease. AL01211 was selected based on its unique properties to effectively treat peripheral organs that Fabry disease affects by reducing the risk of off-target effects by preventing the crossing of the blood-brain barrier. HAYA Therapeutics won the "TOP 100 Swiss Startup Award 2022" and was successfully selected for the "Soonicorn Club 2022" On Sept. 7th, 2022, the "Top 100 Swiss Startup Award 2022," sponsored by Venturelab, was announced. HAYA Therapeutics, invested and incubated by Viva BioInnovator, was named TOP100 Swiss Startups' 8th Best Startup and came first in the Cardiovascular & Drug Discovery sectors. In addition, HAYA Therapeutics was recently included in the"SoonicornClub 2022", which names the top Swiss technology startups. The awards given demonstrate the industry's recognition of their potential in the field of biomedicine. Regenacy Pharmaceuticals Announces Completion of Enrollment for their Phase 2 Study in Diabetic Peripheral Neuropathy and $9.3 Million in Series B Financing Regenacy Pharmaceuticals Inc, invested and incubated by Viva BioInnovator, is a clinical-stage, biopharmaceutical company developing breakthrough treatments for diabetes and other peripheral neuropathies. On August 24, 2022, they announced completion of enrollment for the company's phase 2 study of ricolinostat, an oral selective deacetylase 6 (HDAC6) inhibitor for painful diabetic peripheral neuropathy (DPN). The company also announced the closing of a $9.3 million Series B financing led by Cobro Ventures. Arthrosi Completes AR882 Renal Impairment Study and its Phase 2b Study Enrollment Arthrosi Therapeutics, Inc., which invested and incubated by Viva BioInnovator, is a clinical-stage biotechnology company focused on the treatment and management of gout. On August 9, 2022, they announced the completion of their renal impairment study that utilizes the lead compound, AR882. AR882 is a potent and selective uricosuric agent which has shown effectiveness in lowering serum urate in patients with normal renal function and in patients with mild to severe renal impairment. On Aug. 23, 2022, Arthrosi announced the completion of enrollment for its global Phase 2b clinical study of AR882 for the treatment of chronic gout. The study, which exceeded the initial target enrollment of 120 patients, is designed to evaluate the safety and efficacy of AR882 in chronic gout patients who meet ACR/EULAR gout classification. About ABM Therapeutics ABM Therapeutics, a clinical-stage biopharmaceutical company with a mission to focus on the small molecule research and development of novel drugs for the treatment of cancer, and on brain cancer and cancer metastases. ABM has been building its broad and robust proprietary pipeline to construct a brain medicine R&D platform through collaboration with CROs. ABM's pipeline includes several programs in various stages of discovery and development, most of which have improved brain permeability to address the unmet needs of treating cancers and metastases in the brain. About F5 Therapeutics F5 is evolving targeted protein degradation to transform the landscape of drug discovery by utilizing the cell's normal protein regulation systems to remove disease causing proteins that cannot be targeted by traditional approaches. The NExMods™ Platform (NEosubstrate Expression Modulators) represents a novel approach to "molecular glues" capable of delivering impactful medicines to patients across diverse therapeutic areas: oncology, immuno-oncology, fibrosis, inflammation, and neurodegeneration. About AceLink Therapeutics Founded in 2018, AceLink Therapeutics is an innovative biopharma startup focusing on developing safe and effective medicines to address genetic diseases with high unmet needs. The company's initial focus is to develop novel therapeutics for Fabry disease. For more information, please visit . About HAYA Therapeutics HAYA Therapeutics is a precision therapeutics company that discovers and develops innovative tissue- and cell-selective genomic medicines for fibrotic diseases and other serious health conditions associated with aging, including cancer. The company's discovery engine focuses on long non-coding RNAs (lncRNAs) within the "dark matter" of the human genome -- key tissue and cell-specific drivers of fibrosis and other disease processes -- to identify novel targets and drug candidates with the potential for greater efficacy and safety than existing treatments. About Regenacy Regenacy Pharmaceuticals, Inc. is a clinical-stage biopharmaceutical company regenerating biological function by protein acetylation for the treatment of diabetic and other peripheral neuropathies and other chronic conditions. The company's selective inhibition technology provides superior safety profiles and potential enhanced efficacy compared to non-selective HDAC inhibitors. Regenacy selectively inhibits histone deacetylase 6 (HDAC6) to restore normal intracellular protein and organelle transport in peripheral neuropathies, and also has a portfolio of selective HDACs 1 and 2 inhibitors that have potential to treat major blood diseases such as leukemia, sickle cell disease, β-thalassemia, and cognitive dysfunction in neurological disorders. About Arthrosi Therapeutics Arthrosi Therapeutics, Inc. was founded in San Diego, CA, in 2018 with a mission to create a revolutionary treatment option to target uric acid levels and reduce joint damage for people living with gout. With its vast therapeutic and treatment knowledge, Arthrosi has accumulated a comprehensive and robust intellectual property portfolio and impressive Phase I and Phase II data showing industry leading efficacy rates and superior safety pro To learn more about Arthrosi, please visit View original content: SOURCE Viva Biotech Holdings

合作孤儿药小分子药物

2022-08-25

·BioSpace

Regenacy Pharmaceuticals Announces Completion of Enrollment for Phase 2 Study in Diabetic Peripheral Neuropathy & $9.3 Million Series B Financing

WALTHAM, Mass.--(BUSINESS WIRE)-- Regenacy Pharmaceuticals Inc, a clinical-stage biopharmaceutical company developing breakthrough treatments for diabetic and other peripheral neuropathies, announced completion of enrollment of the company’s phase 2 study of ricolinostat, an oral selective histone deacetylase 6 (HDAC6) inhibitor, in painful diabetic peripheral neuropathy (DPN). The company also announced the closing of a $9.3 million Series B financing led by Cobro Ventures with participation from Taiwania Capital Management Corporation, 3E Bioventures Capital, Yonjin Venture, and other undisclosed private investors. Painful DPN is characterized by debilitating symptoms that include pain, aberrant sensation, and loss of motor and sensory function. There is an important medical need for new treatments since available therapies do not address the full spectrum of signs and symptoms and offer only limited relief for many patients. Ricolinostat, and other HDAC6 inhibitors, have shown efficacy in animal models of DPN, chemotherapy-induced peripheral neuropathy (CIPN) and Type 2 Charcot Marie Tooth (CMT) disease, and have demonstrated a promising safety and tolerability profile. The ongoing double-blinded placebo-controlled clinical study, which recently completed enrollment, assesses the efficacy of ricolinostat in patients with painful DPN and other neuropathic symptoms. Initial results are expected to be available later this year. Regenacy plans to use the additional financing from this Series B to continue advancing the ricolinostat clinical development program. “Regenacy is committed to exploring ricolinostat’s unique and differentiating potential to address the underlying pathophysiology of small fiber neuropathies,” said David Michelson, M.D., Regenacy’s Chief Medical Officer. “The compelling data we have seen in preclinical studies indicate ricolinostat’s selective inhibition of HDAC6 may provide meaningful relief to patients suffering from painful DPN and other neuropathies, and we look forward to its continued progression in the clinic.” “We are energized by the ongoing support of our investors who share in our mission to address the underlying causes of peripheral neuropathy,” said John Rocha, Regenacy’s Chief Financial Officer. “This Series B positions Regenacy for continued progress as we uncover the potential of ricolinostat to restore peripheral nerve function.” “We at Regenacy believe that ricolinostat shows first-in-class potential to go beyond symptomatic treatment and instill lasting disease-modifying effects for patients with peripheral neuropathies,” said Simon Jones, Ph.D., Regenacy’s President and Chief Executive Officer. “This Series B financing comes at a pivotal stage in our clinical development, as we continue to evaluate ricolinostat in painful diabetic peripheral neuropathy while simultaneously advancing our joint venture Beijing 3E-Regenacy Pharmaceuticals Co., Ltd. to investigate ricolinostat in patients with chemotherapy-induced peripheral neuropathy (CIPN) in China.” Concurrent with the financing, Todd Kaloudis, Managing Director at Cobro Ventures, has joined Regenacy’s Board of Directors. Additionally, Regenacy announced the appointment of William W. Chin, M.D., SVP of Clinical and Translational Science at Frequency Therapeutics, as Executive Chairman of the Board and Michael Huang, Managing Partner at Taiwania Capital, as Vice-Chairman, effective immediately. Mr. Huang has served on Regenacy’s Board since 2020, and Dr. Chin has served since 2018 and is Chairman of Regenacy’s Scientific Advisory Board. About Ricolinostat Ricolinostat, an oral, selective histone deacetylase 6 (HDAC6) inhibitor, has the potential to become the first-in-class treatment that reverses the underlying peripheral neuropathy, thereby relieving pain, numbness, motor function loss, and all other symptoms of the disease. Ricolinostat restores nerve function by inhibiting HDAC6, which reestablishes the transport function of microtubules in the axon of the nerve cell. A functioning microtubule transport system is the key to restoring nerve function because nerves rely on this network to supply the energy and nutrients necessary to maintain the nerve signaling in the ends of the nerves in the skin and muscles of the feet and hands. When this transport is disrupted by a disease like diabetes or neurotoxic drugs used in chemotherapy, nerve cells can malfunction and send random signals (pain, tingling, muscle spasms) or no signal at all (numbness, paralysis). Multiple preclinical animal models have demonstrated that HDAC6 inhibition restores nerve fibers, leading to the reversal of both pain and numbness in peripheral and other neuropathies, such as diabetic peripheral neuropathy (DPN), chemotherapy-induced peripheral neuropathy (CIPN) and Charcot-Marie-Tooth disease Type 2, an orphan-designated disease. About Regenacy Regenacy Pharmaceuticals, Inc. is a clinical-stage biopharmaceutical company regenerating biological function by protein acetylation for the treatment of diabetic and other peripheral neuropathies and other chronic conditions. The company’s selective inhibition technology provides superior safety profiles and potential enhanced efficacy compared to non-selective HDAC inhibitors. Regenacy selectively inhibits histone deacetylase 6 (HDAC6) to restore normal intracellular protein and organelle transport in peripheral neuropathies, and also has a portfolio of selective HDACs 1 and 2 inhibitors that have potential to treat major blood diseases such as leukemia, sickle cell disease, β-thalassemia, and cognitive dysfunction in neurological disorders.

First in Class

2022-08-05

·生物谷

Cell Stem Cell: 我国科学家在化学重编程获得巨核细胞及血小板研究领域取得重要突破

运用化学重编程技术实现了人成红细胞向巨核细胞及血小板的命运转换，并利用单细胞转录组和染色质开放性测序技术系统追踪了该过程中的细胞动态变化。血小板是由骨髓等造血组织中巨核细胞产生的具有生物活性的无核细胞，在机体止血、血栓形成、免疫调节、抗感染等生理和病理过程中发挥重要作用。临床上，血小板减少症常见于再生障碍性贫血、特发性血小板减少性紫癜等血液系统疾病。此外，病毒/细菌性感染、创伤、急性放射病、肿瘤放化疗等也易引发血小板减少。血小板输注是临床治疗血小板减少症、防治出血、挽救生命的主要手段之一。然而临床上血小板供应仅有健康志愿者捐献的唯一途径，而血小板贮存时间短且易被污染，遇到战争、重大自然灾害、突发公共卫生事件（如突发传染病）发生时，血小板短缺问题就会更加突出，因此亟需运用新技术解决血小板来源问题。基于干细胞技术、细胞重编程技术获取巨核细胞及血小板的研究一直是国际竞争的前沿与热点领域之一。体外仅通过化学小分子介导的重编程技术制备人巨核细胞（血小板的前体细胞）及血小板的研究成果鲜有报道。近日，军事医学研究院裴雪涛/李艳华团队联合天津大学医学部张健课题组运用化学重编程技术实现了人成红细胞向巨核细胞及血小板的命运转换，并利用单细胞转录组和染色质开放性测序技术系统追踪了该过程中的细胞动态变化。2022年8月4日，干细胞领域顶级期刊《Cell Stem Cell》（《细胞·干细胞》）在线发表了相关研究论文。在细胞重编程的研究中，种子细胞的选择对于能否成功而有效地启动细胞命运转换至关重要。前期研究表明，起始细胞和目的细胞在发育谱系上亲缘关系越近，越容易实现细胞类型转化。成红细胞是存在于骨髓、外周血和脐带血中的一种有核红细胞，成红细胞和巨核细胞在发育过程中来自共同的前体，即巨核-红系共祖细胞，它们之间紧密的谱系联系使成红细胞成为获得巨核细胞理想的候选种子细胞。研究人员通过从多个表观遗传调控和信号通路相关的小分子化合物中筛选出一个含有四个小分子的化合物组合，惊奇地发现该小分子化合物“鸡尾酒”能将人成红细胞高效地重编程为巨核细胞。研究人员进一步确定了两阶段的诱导及巨核细胞特化的体系，最终获得了与天然巨核细胞特性相似的诱导性巨核细胞（induced megakaryocytes, iMKs）。巨核细胞最重要的功能是能产生前血小板及血小板。研究人员首先通过体外实验分析iMKs是否具有生成血小板的能力。在体外特定诱导分化条件下，iMKs能够形成网状的具有多个分支延伸突起的前血小板并释放血小板。更为重要的是，研究人员发现iMKs来源的血小板表现出与天然血小板相似的凝血酶激活响应，并具有粘附、聚集等功能。为了确定iMKs是否具有体内生成功能性血小板的能力，研究人员将iMKs直接通过尾静脉注射到血小板减低症的免疫缺陷小鼠体内，他们在iMKs输注后的第1-3天检测到了人源性血小板，并通过微流控实验证实这些血小板具有参与血栓形成的能力。为了解析四个小分子“鸡尾酒”如何实现成红细胞向巨核细胞的谱系命运转变，研究人员运用单细胞测序技术、染色质开放性测序技术对重编程过程进行了系统追踪和深度剖析。他们发现起始细胞经历了一个红系/巨核共前体细胞的阶段，该阶段的细胞具有红细胞及巨核细胞的双向分化潜能。进一步分析发现，该化合物组合引发了广泛的染色质重塑变化，红系细胞发育关键性基因的染色质开放程度逐渐降低，造血及巨核发生相关的重要转录因子基因位点的染色质开放程度逐渐升高，从而逐渐启动了巨核细胞发育程序。值得注意的是，他们发现iMKs可以分为两个亚群，其中一个亚群为血小板生成偏向性强的巨核细胞，在iMKs总群体中的比例大于70%。另一个亚群是免疫偏向性的巨核系细胞，可能在免疫调节、炎症调节过程中发挥作用。四分子的重编程体系更有利于产生血小板生成偏向性强的巨核细胞。综上所述，该研究团队独辟蹊径，仅运用小分子化合物成功实现成红细胞向功能性巨核细胞及血小板的命运转变，为体外大规模人工制备巨核细胞和血小板开辟了新的路径。该化学重编程技术具有安全可控、高效便捷等优势，通过该技术获得的功能性巨核细胞及血小板有望为临床血小板短缺等问题的解决开辟全新的途径，在血液系统疾病、急性放射病、战创伤、病毒或细菌性传染病等多种疾病引发的血小板减少症、出血的防治等方面展现出潜在的临床应用价值。军事医学研究院裴雪涛研究员和李艳华研究员为该论文的共同通讯作者。军事医学研究院覃金华副研究员、天津大学医学部张健副教授以及军事医学研究院博士研究生姜佳楠是论文的并列第一作者。该研究得到国家重点研发计划和国家自然科学基金的支持和资助。

小分子药物

100 项与 Rocilinostat 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB12376

研发状态

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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	北京本草瑞生医药科技香港有限公司	2022-11-17
神经炎	临床1期	中国	北京本草瑞生医药科技香港有限公司	2022-11-17
卵巢癌	临床1期	美国	Celgene Corp.	2016-06-15

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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)	壓窪觸製襯艱壓鹽蓋蓋 = 鹽鬱餘積壓廠遞繭遞鑰醖憲艱鹹獵鏇糧鏇遞顧 (鹹顧醖獵淵蓋範鹹鹽鏇, 衊廠構夢鏇廠鑰觸繭膚 ~ 膚醖衊簾蓋壓膚窪鬱襯)	-	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)	憲襯簾鑰鹽製壓簾醖製 = 簾鑰餘廠顧繭構製簾齋鬱鏇糧觸遞築願艱繭衊 (淵餘齋獵艱餘簾淵淵淵, 淵淵糧艱構壓鏇網鑰繭 ~ 壓顧淵製淵淵膚糧淵膚) 更多	-	2025-03-04
NCT03176472 (CTgov)	临床2期	糖尿病周围神经性疼痛	282	ricolinostat (Ricolinostat)	願淵壓觸夢夢夢襯鬱艱(簾鏇鹹淵簾膚艱鑰積壓) = 願淵遞廠憲衊膚衊網繭窪觸鹹窪築齋觸築鏇鹽 (淵憲壓鏇蓋鬱積獵餘遞, 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)	願淵壓觸夢夢夢襯鬱艱(簾鏇鹹淵簾膚艱鑰積壓) = 窪憲築鏇鑰觸鹽餘網淵窪觸鹹窪築齋觸築鏇鹽 (淵憲壓鏇蓋鬱積獵餘遞, 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	願範憲顧鬱獵醖餘鬱網(築襯餘鹽遞憲鹹築遞鹽) = 艱製築積選遞願蓋鹹膚遞鹹廠醖築製廠艱淵襯 (蓋廠構壓築構窪鏇願衊, 4.45 ~ 11.0)	积极	2020-08-15
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)	襯積窪廠獵鏇築鑰艱鑰 = 鑰鑰憲積餘繭構簾廠觸窪鹽鹹鑰鏇壓顧願壓鏇 (蓋網範壓構築觸願糧蓋, 範襯築願鑰糧衊構憲顧 ~ 淵積窪齋觸糧構憲齋憲) 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)	觸鏇醖夢觸窪選壓範憲(鏇網襯齋糧夢構艱艱淵) = 網窪廠廠獵鹽選獵襯衊簾艱襯鑰夢餘壓製築鏇 (醖築糧廠築淵築鹽顧選, 蓋艱獵蓋糧糧襯遞構膚 ~ 鹹築築醖廠築顧繭壓膚) 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	簾願選餘鬱襯壓襯選構(壓窪憲獵選鏇醖衊鏇壓) = 衊構膚範鬱淵艱鹽醖顧壓顧觸鹽憲顧鑰齋鑰艱 (簾顧鑰夢艱願選夢襯製 ) 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	鑰選齋憲築艱糧膚構醖(範範簾鑰膚繭鹹糧餘繭) = none 膚齋鏇積鹹顧網範憲餘 (襯繭夢憲糧夢夢鏇鏇鹹 ) 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	蓋積壓襯願鹽襯鑰廠壓(顧餘構鬱鹹願蓋廠網範) = icolinostat（160 mg once daily on days 1-21 of a 28 day cycle）+ lenalidomide（25 mg）+dexamethasone（40 mg）淵鑰獵範鹹製憲顧範衊 (膚簾膚鏇構膚鏇夢壓壓 ) 更多	积极	2016-11-01