A First-in-Human, Randomized, Placebo-Controlled, Phase 1 Single and Multiple Ascending Dose Study to Assess the Safety and Pharmacokinetics of RBN-3143 in Healthy Subjects and as Open-Label in Patients With Atopic Dermatitis Subjects

RBN-3143 Background: PARP proteins are members of a family of seventeen ADP-ribosyltransferase (ART) enzymes that regulate cellular processes including gene expression, protein degradation, and multiple cellular stress responses. RBN-3143 is a PARP-14 inhibitor. PARP14 is over-expressed in tissues with inflammatory diseases. RBN-3143 is a novel, orally administered PARP14 inhibitor that was developed to be evaluated as therapy for a range of inflammatory diseases, with an initial focus on Atopic Dermatitis.
Study Overview: The study consists of 2 parts. Part A: This part of the study is being conducted in a clinical research unit (CRU) and is enrolling healthy adult subjects to determine the safety of RBN-3143; its absorption, metabolism, and excretion (what the body does to this drug); and will assess its potential pharmacodynamic properties (what the drug does to the body).
There are 3 subsections to this part of the study. The first segment was conducted in a double-blind manner (neither the investigator nor subject knew if placebo or RBN-3143 was given) to assess dosing regimens of RBN-3143 when taken in a fasted state (before food). The last two segments are currently recruiting and are Open Label (all subjects will receive RBN-3143) and will assess RBN-3143 when taken with food, with pantoprazole, a medication that decreases the amount of acid in the stomach, and with midazolam.
Part B: In early 2023 the second part of the study will be conducted in patients with moderate to severe atopic dermatitis to measure the pharmacodynamic activity of RBN-3143 and evaluate preliminary efficacy of 28 days administration of the study drug. All patients will receive the same dose of RBN-3143.

开始日期2022-03-07

申办/合作机构

Ribon Therapeutics, Inc.

100 项与 PARP x PARP14 相关的临床结果

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100 项与 PARP x PARP14 相关的转化医学

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0 项与 PARP x PARP14 相关的专利（医药）

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157

项与 PARP x PARP14 相关的文献（医药）

2026-02-03·Microbiology Spectrum

Exacerbated salmonellosis in poly(ADP-ribose) polymerase 14-deficient mice

Article

作者: Vedantham, Madhukar ; Pulliainen, Arto Tapio ; Rissanen, Tiia ; Polari, Lauri

ABSTRACT:

Salmonella enterica subspecies enterica serovar Typhimurium is an enteropathogen annually causing millions of acute infections ranging from gastroenteritis to life-threatening systemic disease. Strong mucosal inflammation, a process with incomplete molecular understanding, is characteristic of S . Typhimurium gastroenteritis. Here, we investigated functions of the nucleocytoplasmic protein poly(ADP-ribose) polymerase (Parp14) in the mouse model of S . Typhimurium infection. Using a systemic Parp14 knockout approach, we found that infected Parp14-deficient mice suffered from exacerbated histopathology, in particular, in the large intestine, that is, increased immune cell infiltration, goblet cell loss, and epithelial erosion. A bulk tissue and single-cell RNA-Seq analysis supplemented with TaqMan qPCR assays was executed to obtain molecular-level functional approximations. We found evidence of a defective Th17 response in the infected Parp14-deficient mice. This parallels the known cell-intrinsic regulatory function of Parp14 in Th17 cell differentiation. However, based on immunohistochemistry, we found that Parp14 was also expressed by macrophages and, in particular, by epithelial cells across the mucosal tissues in small intestine, cecum, and large intestine. The bulk tissue and epithelial cell subtype single-cell RNA-Seq data comparison revealed a plausible epithelial cell-specific transcriptomic signature defective in the infected Parp14-deficient mice. Downregulation of ApoA1 , Spink1, and Sst , encoding apolipoprotein A1, serine protease inhibitor Kazal-type 1, and somatostatin, respectively, was characteristic of this defective transcriptomic signature. We conclude that Parp14 is an integral part of the physiological response to S . Typhimurium infection and that Parp14 acts as a multi-cell-type pleiotropic regulator of mucosal inflammation.

IMPORTANCE:

Eukaryotic cells rely on dynamic cell-signaling mechanisms to mount responses to external perturbations, such as an invading bacterial pathogen. The PARP protein family is a group of enzymes catalyzing a protein post-translational modification known as ADP-ribosylation. PARP1, the founding member, has received considerable research interest, in particular in cancer. However, recent data imply that PARP1 and, in particular, the other PARPs have regulatory functions in inflammatory responses. Yet, the mechanistic basis and, more importantly, the physiological relevance have largely remained elusive. Our study with the systemic Parp14-deficient mice provides compelling in vivo evidence that Parp14 is an integral part of the physiological response to S. Typhimurium infection.

2026-01-09·NAR cancer

The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells

Article

作者: Nicolae, Claudia M ; Moldovan, George-Lucian ; Dhoonmoon, Ashna ; Lynch, Katie A ; Hale, Anastasia

Abstract:

Degradation of reversed replication forks by nucleases has emerged as a major mechanism of chemosensitivity in BRCA-deficient cells. We previously showed that the mono-ADP-ribosyltransferase PARP14 regulates MRE11 recruitment to reversed replication forks to promote their degradation. This results in genomic instability in BRCA-deficient cells. While it has been shown that PARP14-mediated recruitment of MRE11 to reversed forks promotes their degradation and collapse, how PARP14 binds to nascent DNA is unknown. Here, we show that, in BRCA-deficient cells, PARP14 is recruited to nascent DNA at reversed replication forks via its RRM (RNA Recognition Motifs) domains. We reveal that the RRM domains are necessary for the recruitment of MRE11 to reversed forks to promote nascent strand degradation at stalled replication forks in BRCA2-deficient cells. We also show that these domains are essential for replication stress-induced double-strand break formation in these cells. Our work furthers the understanding of nuclease recruitment and engagement at stalled forks to regulate genomic stability.

2025-11-01·Clinical and Translational Medicine

Altered nicotinamide adenine dinucleotide metabolism drives cartilage degeneration and osteoarthritis

Article

作者: McCubbin, Tim ; Bertoldo, Michael J. ; Fan, Xiwei ; Wu, Xiaoxin ; Goss, Dale M. ; Wu, Lindsay E. ; Mao, Xinzhan ; Barrero, Roberto A. ; Stark, Terra ; Prasadam, Indira ; Plan, Manuel ; Marinova, Maria ; Crawford, Ross

Abstract:

Background:

We previously conducted a comprehensive survey of energy metabolism in osteoarthritis (OA), revealing significant reductions of nicotinamide adenine dinucleotide (NAD + ) levels in OA cartilage. This study aimed to test whether NAD + deficiency present in OA plays a mechanistic role in disease development.

Methods:

We conducted integrative analyses across human, murine, and rat OA models to examine NAD⁺ metabolism and its regulatory enzymes. The impact of pharmacological NAD⁺ augmentation (via nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR)) and genetic overexpression of the NAD⁺ biosynthetic enzyme NMN adenosyltransferase (NMNAT1) was tested in surgical and aging‐related OA models. Expression and function of the NAD⁺‐consuming enzyme poly (ADP‐ribose) polymerase 14 (PARP14) were examined via siRNA knockdown in chondrocytes under inflammatory conditions, coupled with metabolic assays and extracellular matrix gene profiling.

Results:

NAD + levels were decreased in human and murine OA, accompanied by upregulation of both the NAD + biosynthetic enzyme Nicotinamide phosphoribosyltransferase (NAMPT) and the NAD + consuming enzyme PARP14. While NAMPT expression was elevated, its effect on total NAD⁺ may be offset by increased NAD⁺ consumption or substrate limitation under inflammatory conditions. Treatment with NAD + precursors and transgenic overexpression of NMNAT1 suppressed cartilage disruption during in aging murine and surgical rat model of OA. Increased expression of PARP14 in OA cartilage contributed to NAD + decline and promoted cartilage degeneration.

Conclusions:

This study reveals that dysregulated NAD⁺ metabolism, driven by increased PARP14 consumption, constitutes a potential mechanism underlying OA pathogenesis. Our findings support the concept that enhancing NAD⁺ availability via precursors or biosynthetic pathway modulation may offer disease‐modifying effects at the molecular and histological level. Further investigation is needed to determine the functional and translational implications of targeting this pathway.

Key points:

PARP14 is upregulated in OA cartilage and contributes to NAD⁺ depletion.PARP14 silencing restores NAD⁺ levels and represses OA‐related metabolic and matrix‐degrading changes.NAD⁺ precursor treatment and NMNAT1 overexpression protect against cartilage degeneration in aging and post‐traumatic OA models.

项与 PARP x PARP14 相关的新闻（医药）

2026-03-17

·药化杂谈

海思科和思倍博的PARP14抑制剂是如何突破专利的

背景介绍（摘自专利WO2026051989A1）聚腺甘二磷酸核糖转移酶(PoIy(ADP-ribose)polymerase，简称PARP)是一种 DNA修复酶，共有17个成员，PARP1-PARP17，被认为在蛋白稳态、基因表达以及细胞应急反应中发挥重要作用。针对 PARP家族开发药物主要集中在癌症领域，然而近年来有研究发现其家族成员 PARP14在与 Th2型炎症密切相关的 STAT6 信号通路中发挥关键作用。STAT6作为转录调控因子,主要介导 Ⅱ-4/13等 Th2 型炎症因子的表达。PARP14抑制剂能够在细胞层面抑制 LPS 诱导的 STAT6 靶基因表达，提示针对 PARP14开发抑制剂在治疗Th2 型炎症相关疾病中还具有潜力，例如在过敏性气道疾病模型中，PARP14的遗传耗竭及其酶促活性导致肺部炎症和 IgE 水平降低，这是该模型中哮喘过程的关键指标。因此，抑制 PARP14催化活性还可以是 Th2型炎症疾病，包括过敏性气道疾病的潜在新疗法。目前该靶点只有一个化合物RBN-3134处于临床研发阶段，思倍博的专利WO2026051989A1通过螺环化进行了专利突破，代表性化合物如下。海思科专利WO2024251205A1也是对RBN-3134进行的专利突破，代表性化合物如下。

2026-03-10

·发发生信

IF 8.0！恭喜暨南大学借“孟德尔随机化+单细胞+虚拟敲除”拿下双一区TOP!

📍暨南大学团队发表《Npj Precision Oncology》，借力虚拟敲除技术成功解码CD4+ T细胞活化基因在结直肠癌中的调控机制，为“虚拟细胞”从概念走向应用再添力证！ 🎉首次解锁「CD4+ T细胞活化动态基因→免疫治疗耐药→代谢介导」多维调控网络，突破靶点识别瓶颈😎！ ✨核心突破： ✅ 精准锁定：整合孟德尔随机化+单细胞eQTL，锁定28个CD4⁺ T细胞免疫靶点。 ✅ 高效验证：虚拟敲除证实ORMDL3/PARP14调控免疫耐药通路，大幅降低实验成本。 ✅ 临床转化：筛选16种候选药物，为CRC精准分层与联合治疗提供新策略。无需实验即可完成靶点验证，为文章补充关键机制证据——想做虚拟敲除的朋友，快来找发发生信帮您设计！分析框架 📌三大维度的研究分析框架已整理，点击图片查看。（10分钟获取核心要点） 1. 研究概况 I 2. 机制详解 I 3. 国自然关联分析你还在观望什么？【发发生信】定制思路，全面数据分析，下一篇高分SCI就是你！文献解读标题：全转录组孟德尔随机化与单细胞分析揭示结直肠癌CD4+ T细胞活化过程中的免疫治疗靶点发表期刊：Npj Precision Oncology 发表时间：2025年12月29日影响因子：8.0/Q1 科学验证因果，方法决定高度。完整生信方案，助力您的研究登上更高学术舞台。研究背景结直肠癌（CRC）是全球第二大癌症死亡原因，尽管免疫治疗（如CAR-T）在血液肿瘤中效果显著，但在实体瘤中疗效受限，主要由于肿瘤微环境的免疫抑制作用。CD4+ T细胞作用关键但其激活过程中的动态基因表达与结直肠癌的因果关系尚不明确。研究方法整合动态CD4+ T细胞eQTL与结直肠癌GWAS数据，通过孟德尔随机化、共定位、SMR分析筛选因果基因，并结合单细胞测序、虚拟敲除、药物筛选及中介分析进行多维度验证。图1.Mr分析框架网络示意图研究结果 01 绘制免疫图谱：研究采用孟德尔随机化技术分析CD4+ T细胞激活过程中基因表达与结直肠癌（CRC）风险的因果关联，从8587个遗传变异中锁定28个关键候选基因【图2A-C】。图2.动态CD4+ T细胞表达数量性状位点（eQTLs）对结直肠癌（CRC）因果效应的Mr结果其中75%的基因（21个）仅在T细胞激活后才显现出与CRC的因果关联，提示免疫激活状态是挖掘有效药靶的核心前提【图2F】。调控效应存在典型时序特征：NDUFA12对CRC的保护作用在T细胞激活40小时达峰，DCTN5则在多个时间点持续发挥作用，展现出免疫应答的动态复杂性【图2G】。 02 锁定核心目标：结合3套单细胞测序数据集对比CRC患者与健康人群的CD4+ T细胞表达谱，发现PARP14和ORMDL3在患者细胞中特异性高表达【表1】。表1.GEO数据库中CD4+T细胞的差异表达基因后续通过TCGA肿瘤数据库和CPTAC蛋白数据库多组学验证，两个基因在CRC组织的mRNA和蛋白水平均显著升高，且表达量与CD4+ T细胞肿瘤浸润程度正相关。图4.靶向ORMDL3和PARP14的潜在结直肠癌治疗药物 PARP14：激活上皮-间质转化（EMT）、炎症反应、干扰素-γ应答等促癌通路； ORMDL3：驱动EMT、血管新生、炎症反应等促癌程序激活。 ⏩基于多重证据链，PARP14和ORMDL3被确立为CRC免疫治疗的一级核心靶点【图4A】。 03 洞察治疗失效：分析免疫治疗前后患者CD4+ T细胞的表达动态，发现核心靶点直接参与耐药发生：图3.CD4+ T细胞对已识别靶点的时空差异分析治疗无效（疾病稳定，SD）患者的PARP14、ORMDL3、KCNA3在治疗后表达显著上升【图3C-E，表2】；治疗有效（完全/部分缓解，CR/PR）患者的PARP14表达则明显下降【图3F，表2】。表2.基于CD4+ T细胞单细胞RNA测序分析的免疫治疗前后差异表达基因功能验证显示，高表达上述基因的CD4+ T细胞功能受损更显著，T细胞耗竭评分更高，同时高表达PD-1、CTLA4等免疫抑制检查点【图3H】，提示PARP14和ORMDL3可能通过诱导T细胞耗竭介导免疫治疗耐药。 04 发掘老药新用：借助CMap数据库筛选可逆转PARP14和ORMDL3诱导的异常表达谱的小分子化合物，通过分子对接验证结合亲和力【表3】：表3.CMap数据库中的药物识别靶向ORMDL3：司骨化醇（维生素D受体激动剂）、强的松（糖皮质激素受体激动剂）；靶向PARP14：伊贝沙坦（血管紧张素受体拮抗剂）、氟哌啶醇（多巴胺受体拮抗剂）。 ⏩ 其中伊贝沙坦、APD-668等8种药物与靶点结合能低于-7 kcal/mol，亲和力极高【图4B-F】，为后续药物研发提供了优先候选方向。 05 探索代谢桥梁：通过两步骤孟德尔随机化分析，首次明确两条“基因-代谢物-肿瘤”调控轴：图5.免疫靶点ORMDL3、PARP14、代谢物与结直肠癌（CRC）之间的因果相互作用 PARP14的促癌效应部分通过吲哚乙酰肉碱介导，该通路解释约10.95%的因果效应； ORMDL3的促癌效应部分通过胆红素降解产物（C₁₇H₁₈N₂O₄）介导，该通路解释约5.81%的因果效应【图5】。 ⏩ 该发现为理解免疫基因通过重塑肿瘤代谢微环境调控肿瘤进展提供了全新视角。 06 评估安全风险：通过“虚拟基因敲除”模拟抑制靶点后的细胞转录组变化，发现扰动基因显著富集于TNF-α信号、低氧反应、Wnt/β-连环蛋白等CRC经典通路，与前期机制分析相互印证【图6A-B】。图6.ORMDL3、PARP14与FinnGen 数据库中多类表型的因果关联全表型组孟德尔随机化分析提示潜在安全风险：抑制ORMDL3可能升高儿童哮喘发病风险；抑制PARP14可能升高银屑病发病风险【图6C】。 ⏩ 上述结果为后续靶向药物临床应用提前预警了潜在不良反应。首次系统揭示CD4+ T细胞激活相关基因与结直肠癌的因果关系，鉴定28个潜在免疫治疗靶点，其中PARP14和ORMDL3与免疫治疗抵抗显著相关，为结直肠癌免疫治疗提供了新靶点。想学习如何复刻这类高分研究的同学，欢迎联系发发生信！ End 发发生信选题设计丨数据分析丨思路建议从零突破到SCI发表往期推荐 1 IF 48.5！恭喜浙江大学副院长拿下马年首篇《Nature》！破解GPCR药物研发半世纪难题! 2 IF48.5! 打破校史! 恭喜贵州中医药大学副教授一作首篇《Nature》! 获奖百万并晋升教授！ 3 IF30.9！恭喜南京大学鼓楼医院副院长“国自然”拿下《Cell》子刊！提出肥胖治疗新思路！求点赞求分享求喜欢

2026-02-28

·生物通

GENEVA平台：建模肿瘤遗传异质性以揭示KRASG12C抑制剂反应差异并优化联合疗法

在癌症治疗领域，靶向疗法通过精准打击驱动肿瘤生长的分子靶点，为患者带来了新的希望。然而，即使是针对同一靶点的药物，在不同患者甚至同一肿瘤的不同细胞中，疗效也可能天差地别。这种“同药不同效”的困境，很大程度上源于肿瘤本身惊人的遗传多样性——即肿瘤异质性。传统的临床前药物测试模型，如小鼠异种移植，虽然被视为“金标准”，但成本高昂、通量低下，难以在进入临床试验前，系统性地评估药物在大量、多样化的肿瘤模型中的效果。这导致一些在有限模型中表现优异的药物，最终在涵盖广泛遗传背景患者的临床试验中折戟沉沙。能否开发一种既高效又能深度解析药物作用机制的新平台，成为连接实验室发现与临床成功的关键桥梁。为此，研究团队在《Nature Cancer》上发表了他们的研究成果，介绍了GENEVA平台。该研究旨在解决传统模型的可扩展性瓶颈，通过在单个实验中对数十种遗传背景的癌细胞进行混合培养或移植，结合单细胞转录组学技术，实现了对药物反应异质性的高通量、高分辨率分析。为开展此项研究，作者主要应用了以下几项关键技术：1) GENEVA平台构建：将多种患者来源细胞系（PDX）或癌细胞系混合，形成“马赛克”式的三维（3D）培养物或小鼠异种移植模型，作为观察单元；2) 单细胞RNA测序（scRNA-seq）与多重样本标记：利用MULTI-seq等技术对混合样本进行标记和合并测序，随后通过单核苷酸多态性（SNP）分析和标签解复用，确定每个测序细胞的基因型归属和处理条件；3) 体内外药效与机制验证：包括细胞活力检测（如CellTiter-Glo）、线粒体功能分析（如Seahorse呼吸测定仪）、流式细胞术检测线粒体膜电位与活性氧（ROS），以及基于CRISPR干扰（CRISPRi）的体内功能基因筛选。研究结果多路复用表型分析以确定药物反应和耐受性的决定因素研究人员首先将11个携带不同突变（如BRAFV600E和KRASG12C）的细胞系混合，并分别用对应抑制剂（维莫非尼和ARS-1620）处理。通过scRNA-seq分析，他们不仅准确识别出各细胞系对特定药物的敏感性差异，还观察到了细胞系内部对药物反应的异质性。这验证了GENEVA平台在捕获药物敏感性和反应异质性等表型特征方面的有效性。用于异种移植模型多路复用高内涵表型分析的体内GENEVA 研究将GENEVA应用于体内环境，创建了包含不同KRASG12*突变细胞系的混合肿瘤模型。用ARS-1620治疗后，通过scRNA-seq分析发现，KRASG12C突变细胞显著减少，并且出现了细胞周期G1期阻滞的增加。在患者来源类器官（PDO）和患者来源异种移植（PDX）模型中进行的验证实验，进一步证实了KRASG12C抑制会导致G1期阻滞和凋亡细胞增加。 KRASG12C抑制增加线粒体电子传递链活性通过对GENEVA数据的深入挖掘，研究人员发现，在ARS-1620处理后存活的KRASG12C突变细胞中，线粒体相关转录本显著减少。进一步的基因集富集分析、已发表的CRISPRi筛选数据验证以及线粒体功能实验表明，抑制线粒体功能或降低线粒体含量会增加细胞对ARS-1620的耐受性。机制上，KRASG12C抑制剂（如索托拉西布sotorasib）会急性诱导线粒体呼吸活性增强、膜电位升高，随后导致caspase-3/7切割和细胞死亡。使用电子传递链复合体III抑制剂抗霉素A1（antimycin A1）可以挽救KRAS抑制剂在G12C细胞中诱导的死亡，证实了线粒体呼吸活性是KRASG12C抑制剂致死的关键机制。发现并靶向体内外KRASG12C抑制的耐受与耐药机制通过比较经ARS-1620处理的G12C与非G12C细胞之间的差异表达基因，研究人员发现多个与耐药相关的潜在可成药靶点基因（如JAK1、RPTOR、PARP14等）。体外联合用药实验显示，mTOR抑制剂INK128、IDH2抑制剂enasidenib等与KRASG12C抑制剂具有协同作用。其中，INK128与ARS-1620的体内联合治疗显著抑制了肿瘤生长。此外，通过比较体内外GENEVA数据，研究团队发现上皮-间质转化（EMT）相关基因在体内环境下被特异性上调，提示EMT是体内耐药的重要机制。使用TGFβ受体抑制剂galunisertib靶向EMT通路，与ARS-1620联用后，在体内同样显示出协同抗肿瘤效果。利用GENEVA指导的体内遗传筛选验证耐受与耐药机制为了进一步验证GENEVA平台所预测的靶点，研究团队在多种KRASG12*突变细胞系中进行了基于CRISPRi的体内功能筛选。结果显示，GENEVA预测的“保护性”基因（如线粒体核糖体成分相关基因）的敲低，在敏感的G12C细胞系中确实能增加对索托拉西布的耐受性；而“致敏性”基因（如EMT和mTOR通路效应基因）的敲低则使G12C细胞对药物更敏感。这些结果在遗传学水平上正交验证了GENEVA发现的有效性。利用GENEVA对联合疗法进行丰富表型分析最后，研究展示了GENEVA平台在分析联合疗法方面的强大能力。通过在混合肿瘤模型中测试ARS-1620分别与galunisertib、INK128或抗霉素A1的联合用药，并利用scRNA-seq进行分子表型分析，研究人员不仅定量评估了联合用药在诱导G1期阻滞等方面的协同效应，还通过构建基因表达线性模型，识别出在联合治疗中偏离加性效应的关键基因（如线粒体基因），从而在分子层面揭示了药物协同作用的驱动因素。结论与讨论本研究成功开发并验证了GENEVA这一可扩展的单细胞分辨率平台，它能够通过建模肿瘤遗传多样性，在体内外环境下高通量、高分辨率地剖析药物反应异质性。应用该平台研究KRASG12C抑制剂，获得了多项重要发现：首先，揭示了线粒体呼吸激活是该类药物诱导细胞死亡的一个先前未被重视的全新作用机制。其次，发现了EMT是体内特异性出现的重要耐药机制，而mTOR等通路则普遍参与耐受过程。这些机制通过体外联合用药实验和体内CRISPRi筛选得到了验证。该研究的重大意义在于，GENEVA平台有望重塑药物发现和评估的范式。它将传统上基于有限模型的“深度”靶点验证，与基于多样化模型的“广度”疗效和机制探索相结合，使得在药物研发早期就能系统性地捕获药物反应的异质性，并识别出具有广谱潜力的候选药物或联合疗法策略。尽管当前版本的体内GENEVA使用的是免疫缺陷小鼠，未能涵盖免疫相关机制，但其在揭示细胞自主性耐药机制方面已展现出强大能力。总之，这项工作为在临床前阶段更准确地预测药物临床效果、实现真正的精准医疗提供了强有力的新工具和新见解。

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