A Multicenter, Double-blind, Phase 2b/3 Extension Study to Assess the Safety and Efficacy of ABP-671 in Participants With Gout Who Completed the Double-blind Treatment Period in Study ABP-671-301

The primary objectives of this study are to assess the safety, tolerability, and efficacy of ABP-671 in lowering serum uric acid (sUA) in participants with gout who roll over from Study ABP-671-301 after they complete the double-blind 28-week Treatment Period of Part 1 (Phase 2b) or Part 2 (Phase 3).

开始日期2024-04-22

申办/合作机构-

CTR20233710

/ Recruiting临床2/3期

一项多中心、随机、双盲、安慰剂/非布司他对照的IIb/III期临床研究以评价ABP-671片在痛风患者中降尿酸治疗的有效性和安全性

主要目的：评价不同剂量ABP-671片在痛风患者中降尿酸的有效性。

开始日期2023-12-19

申办/合作机构

杭州新元素药业股份有限公司

NCT05818085

/ Completed临床2/3期

A Multicenter, Randomized, Double-blind, Controlled, Phase 2b/3 Study to Assess the Efficacy and Safety of ABP-671 in Participants With Gout

This is a multicenter, randomized, double-blind, Phase 2b/3 study to evaluate the efficacy and safety of ABP-671. Part 1 of the study will compare the efficacy and safety of different doses and regimens of ABP-671 with placebo and allopurinol. Part 2 of the study will compare the dosing regimen(s) of ABP-671 selected from Part 1 with placebo in participants who have not been enrolled for Part 1.

开始日期2023-08-11

申办/合作机构

杭州新元素药业股份有限公司

100 项与 Lingdolinurad 相关的临床结果

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100 项与 Lingdolinurad 相关的转化医学

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100 项与 Lingdolinurad 相关的专利（医药）

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项与 Lingdolinurad 相关的文献（医药）

2025-03-24·JACS Au

Structural Basis for Inhibition of Urate Reabsorption in URAT1

Article

作者: Bai, Yingjie ; Guo, Nianxin ; Fan, Junping ; Lei, Xiaoguang ; Ke, Han ; Wang, Haijun ; Zhang, Jing ; Xie, Wenjun ; Wang, Jin

The urate transporter 1 (URAT1) is the primary urate transporter in the kidney responsible for urate reabsorption and, therefore, is crucial for urate homeostasis. Hyperuricemia causes the common human disease gout and other pathological consequences. Inhibition of urate reabsorption through URAT1 has been shown as a promising strategy in alleviating hyperuricemia, and clinical and preclinical drug candidates targeting URAT1 are emerging. However, how small molecules inhibit URAT1 remains undefined, and the lack of accurate URAT1 complex structures hinders the development of better therapeutics. Here, we present cryoelectron microscopy structures of a humanized rat URAT1 bound with benzbromarone, lingdolinurad, and verinurad, elucidating the structural basis for drug recognition and inhibition. The three small molecules reside in the URAT1 central cavity with different binding modes, locking URAT1 in an inward-facing conformation. This study provides mechanistic insights into the drug modulation of URAT1 and sheds light on the rational design of potential URAT1-specific therapeutics for treating hyperuricemia.

2021-12-01·Bioorganic chemistry2区 · 化学

Novel natural scaffold as hURAT1 inhibitor identified by 3D-shape-based, docking-based virtual screening approach and biological evaluation

2区 · 化学

Article

作者: Chang, Shan ; Chen, Xinhua ; Tian, Yuanxin ; Li, Zhonghuang ; Zhao, Zean ; Wan, Shanhe ; Zhang, Jiajie ; Shen, Yudong ; Wu, Ting ; Pang, Jianxin ; Luo, Jiajun

As a promising therapeutic target for gout, hURAT1 has attracted increasing attention. In this work, we identified a novel scaffold of hURAT1 inhibitors from a personal natural product database of verified herb-treated gout. First, we constructed more than 800 natural compounds from Chinese medicine that were verified to treat gout. Following the application of both shape-based and docking-based virtual screening (VS) methods, taking into account the shape similarity and flexibility of the target, we identified isopentenyl dihydroflavones that might inhibit hURAT1. Specifically, 9 compounds with commercial availability were tested with biochemical assays for the inhibition of ¹⁴C-uric acid uptake in high-expression hURAT1 cells (HEK293-hURAT1), and their structure-activity relationship was evaluated. As a result, 8-isopentenyl dihydroflavone was identified as a novel scaffold of hURAT1 inhibitors since isobavachin (DHF3) inhibited hURAT1 with an IC₅₀ value of 0.39 ± 0.17 μM, which was comparable to verinurad with an IC₅₀ value of 0.32 ± 0.23 μM. Remarkably, isobavachin also displayed an eminent effect in the decline of serum uric acid in vivo experiments. Taken together, isobavachin is a promising candidate for the treatment of hyperuricemia and gout.

Drug Design Development and Therapy

Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Food Effects of Single and Multiple Oral Doses of ABP-671 in Healthy and Hyperuricemic Subjects

Article

作者: Schwertschlag, Ullrich ; Wu, Roy J ; Jin, Adam W ; Shi, Dongfang ; Gurwith, Marc

Purpose:

To evaluate the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and food effects of single and multiple oral doses of ABP-671, a novel URAT1 inhibitor, in healthy and hyperuricemic subjects.

Patients and Methods:

This placebo-controlled study of ABP-671 was conducted in the United States, and contained three parts: a. single ascending dose (SAD); b. multiple ascending dose (MAD); c. food effect. The study doses of SAD part, 0.1, 0.5, and 1.0 mg, and placebo oral solutions were investigated in healthy volunteers. In the MAD study, hyperuricemic but otherwise healthy subjects received 0.2, 0.5, or 1.0 mg/d of ABP-671 or placebo oral solutions for 10 days. In the food effect study, healthy subjects received 1.0 mg ABP-671 tablet in the fasted or fed state in a crossover design.

Results:

A total of 24, 27, and 12 subjects were enrolled, with 5, 9, and 5 treatment-emergent adverse events (TEAEs) observed in the SAD, MAD, and food effect studies, respectively. There were no serious adverse events (SAEs) or TEAEs leading to discontinuation or death. In the SAD and MAD studies, the peak plasma concentration and areas under the curves increased with the increasing drug doses. The serum uric acid (sUA) levels started decreasing 3 hours after ABP-671 administration, and the percentage changes from baseline for sUA increased with the increasing drug doses. Fasting or postprandial state did not affect the PK of ABP-671.

Conclusion:

Single or multiple oral doses of ABP-671 are well tolerated at doses 0.1, 0.5 and 1.0 mg for the SAD, 0.2, 0.5, and 1.0 mg/d for the MAD, and 1.0 mg for the food effect study. A proportional relationship between dose and exposure was observed. ABP-671 reduced the sUA levels with a rapid (3 hours) onset and in a dose responsive manner.

项与 Lingdolinurad 相关的新闻（医药）

2025-12-16

·今日头条

新元素药业ABP-745启动全球多中心II期临床试验

药融圈获悉浙江杭州及美国消息 (2025年12月16日) - 杭州新元素药业股份有限公司 (新元素药业，Atom Therapeutics)是一家创新型生物医药企业，专注于代谢和炎症领域疾病的创新药研发，今天宣布抗炎症领域小分子创新药ABP-745用于治疗动脉粥样硬化II期临床试验申请已获得美国FDA批准，并已启动了包括美国、中国和澳大利亚在内的多中心II期临床试验，并由中国科学院院士，复旦大学附属中山医院的心脏病学专家葛均波院士担任Leading PI。动脉粥样硬化是一种常见的心血管疾病，是导致不良心血管事件 (MACE) 的关键因素，每年由动脉粥样硬化引发的心血管疾病可导致1800万人死亡。高血压、高血脂、高血糖和炎症等因素会损伤血管内皮，促使低密度脂蛋白、胆固醇沉积并氧化，引发炎症反应，形成泡沫细胞和脂质斑块，最终造成血管狭窄、硬化、弹性降低、变薄、甚至破裂，以及不稳定斑块的脱落而产生血栓，导致血管急性堵塞，可能引发心肌梗死、脑卒中、及死亡等严重后果。目前治疗动脉粥样硬化主要是通过降脂疗法，如使用他汀、依折麦布和PCSK9抑制剂等，但尚未实现对斑块形成相关炎症通路的精准靶向干预。慢性炎症反应贯穿于动脉粥样硬化形成的每个阶段，炎症介质的释放不仅进一步加重内皮损伤、促进脂质沉积和斑块不稳定，更会增加斑块破裂风险，是心血管事件的独立危险因素。秋水仙碱是FDA于2023年批准用于治疗心血管疾病的首款抗炎药物，在标准降脂治疗的基础上，通过调控炎症通路额外将主要MACE风险降低31%。最新的临床研究显示，秋水仙碱能够在标准降脂治疗基础上显著降低动脉粥样硬化斑块的进展。而冠脉斑块体积每额外降低1%，MACE发生率可降低25%。但秋水仙碱由于较低的安全窗口，限制了其使用剂量，以及秋水仙碱会产生药物-药物相互作用，如与一些他汀类药物联合使用会进一步增加横纹肌溶解风险，也限制了其临床的使用范围。公司创始人、董事会主席、执行董事兼CEO史东方博士表示：“ABP-745开启治疗动脉粥样硬化II期临床是继其用于治疗急性痛风后，进入治疗因长期炎症导致的疾病的又一重要里程碑，使新元素药业布局了治疗“代谢+心脑血管疾病”双赛道，有力地强化了公司在炎症治疗领域的核心竞争力。” 史博士进一步表示：“公司十分荣幸邀请到葛院士领导此次II期临床试验，这将为临床试验提供坚实的质量和时间保障。期待ABP-745在治疗动脉粥样硬化疾病上早日取得突破性成果，以造福全球广大患者。” ABP-745口服给药，不存在药物-药物相互作用风险。动物试验表明，与秋水仙碱相比较，其安全窗口远高于秋水仙碱。ABP-745可抑制NLRP3炎症小体活化，抑制炎性细胞向斑块部位的聚集，并强效抑制IL-1β、IL-6、IL-18、TNF-α等多种关键炎症因子，覆盖动脉粥样硬化从内皮损伤到斑块破裂的全周期炎症通路。且ABP-745良好的透脑率，对于脑部斑块可能有较佳的缩小效果，具有潜在的对脑卒中的预防和治疗。在小鼠研究中，与模型组相比，ABP-745单药治疗可使主动脉斑块面积降低56.1%；在另一相似的试验中，ABP-745与他汀类药物联用可使主动脉斑块面积下降超过75%，展现出良好的降低主动脉斑块的效果。 ABP-745已在美国及中国完成了I期临床，展现出良好的安全性、耐受性和药物代谢动力学。目前已经在美国、澳大利亚和中国推进治疗“急性痛风”国际多临床中心的II期临床试验。关于新元素药业新元素药业是一家创新型生物医药企业，专注于代谢和炎症领域疾病的创新药研发。公司的核心产品ABP-671正在关键性临床研发中，用于慢性痛风的治疗。重要管线ABP-745用于抗炎自免领域多个适应症，正在开展治疗急性痛风II期临床研究，点击查看原文：新元素药业治疗急性痛风药物ABP-745全球多中心II期临床试验完成首例患者入组。更多信息请访问: https://www.atomthera.com或https://atomthera.us。

临床2期申请上市

2025-12-16

·药闻康策

一品红下金蛋的鸡卖掉了

☝ 点击上方一键预约 ☝ 最新最热的医药健康新闻政策 ☝ ☝ 点击查看峰会活动议程 ☝ ☝ 恐怕一品红自己也没想到，原本好好的一桩BD，竟把自己送到20cm跌停板的地步。 14日晚，一品红公布了一起股权交易案。简单说就是一品红投资的美国Arthrosi公司卖掉了，首付款9.5亿美元，最高里程碑付款5.5亿美元。一品红通过子公司占股比例为13.45%，算一下光是首付部分就能收到1.28亿美元。买家Sobi公司看上的当然是Arthrosi手里的痛风药物AR882。这款药物基于痛风经典药物苯溴马隆进行氘代改造，已经拿到FDA快速通道认证，是同类URAT1抑制剂中目前进度最快的，这也是Sobi公司花15亿美元买下的原因。 AR882好在哪里此前已经有不少机构研究过，就不再赘述。问题是卖出去了，获益方一品红股价却大跌，这让很多人摸不着头脑，只留下一句笼统的 ▌“不及预期” 先来看看一品红的这笔交易是怎么不及预期的。 1 一品红非常看中AR882这个产品，2021年开始增资Arthrosi公司，并与Arthrosi公司在中国成立合资企业，拿到AR882在中国市场开发和商业化权益。一手投资，一手合作，是绑定对方产品的常见办法。一品红此前已经投入多轮，分别是： 2021年的C2轮，投资2500万美元； 2023年的C3轮，投入500万美元； 2023年的D轮，投入2100万美元。这三轮投完后，一品红通过子公司瑞腾生物持股Arthrosi公司达到22.52%。其中后两轮里，一品红的老板通过自己拥有的广润和Montesy两家企业参与了跟投。D轮时老板两家公司加起来持股约21%。（D轮后Arthrosi股权结构，红框为一品红及关联方持股）也就是说，上市公司和老板本人都投了钱，这应当是非常看好这个项目的。但是今年10月，Arthrosi公司又搞了个E轮，参与者包括弘晖基金、惠每创投等。E轮领投是一家叫做Prime Eight Capital的机构，这家机构2015年成立，总部在伦敦，有史可查的出手投资记录，就Arthrosi这一笔。一品红和老板的公司应该都没参与这一轮。在E轮之前，Arthrosi公司实际估值2.1亿美元。E轮一下融了1.53亿美元，把一品红的占股大幅拉低，从22.52%降到了13.45%。所以这次Arthrosi公司“卖身”的时候，一品红分到的钱自然也少了。这应当就是市场认为的“不及预期”。因为现在即使把15亿美元全算上，一品红投一家创新药企 ▌5年回报大约4倍左右这回报率其实还可以。但要命的是，AR882海外部分的收益从此就和一品红无关了。一品红股价从12元拉到80元的唯一支撑动力，就是AR882能在美国市场获批。毕竟这是全球第一个拿到FDA快速通道资格的痛风新药，比其他竞品更有希望。按照原本的计划，一品红每年靠收益分红也能有持续收入。如今下金蛋的鸡卖掉了，自己也没挣到多少钱，这是令市场最不满意的地方。至于E轮时候为何不带一品红玩，这就不得而知了。 2 尽管Arthrosi公司还与一品红在国内有合资企业，AR882的中国市场开发权益还握在手中，但这点撑不起200亿的市值。按照此前的预计，如果新股东Sobi公司延续合作协议，AR882最快可能在2026年下半年在中国获批。但是抢在一品红之前，日本卫材先下狠手了。卫材有一款多替诺雷，是目前全球在售的唯一新一代URAT1抑制剂，也是在苯溴马隆分子基础上改的。但卫材改的并不是太成功，没能彻底解决苯溴马隆的毒性问题，所以多替诺雷美国和欧盟一直没批准上市，目前只在日本和中国获批了。多替诺雷2024年底在中国上市，今年医保谈判中，卫材直接从28片一盒的药从原价3000多降到了198元，并顺利进入医保，明年1月1号开始报销， ▌摆明了是来抢市场的因为第一代的URAT1靶点痛风药苯溴马隆副作用比较明显，在国内销售并不好。米内网2024年统计过，原研+仿制最多也就年销售5亿元左右。多替诺雷进入医保后，明年能不能成功突袭，还有待观察。（苯溴马隆近年销售额，来自米内网） AR882一直以安全性为自己最大优势，虽然关键临床数据还没读出，但毒性问题肯定要比多替诺雷控制得好。不过卫材的医保定价直接为一品红设定好了价格上限，这是严重影响AR882估值的。一品红身后还有很多国内企业沿着URAT1这个思路在开发。进度比较快的，如恒瑞的鲁兹诺雷，国内上市申请今年6月已经受理；浙江新元素的ABP-671，全球III期临床已达主要终点，新元素还等着靠这个管线IPO。上海珊顿医药的SAP-001虽然刚完成II期临床，但今年7月获得FDA快速通道资格，实力不俗。这些竞品加一起，让一品红好不容易找到的冷门管线一下变成了热门。再加上卫材把原本年费用三四万的痛风新药打成了三四千，国产新药怎么冲击市场？看来不会太好办。一品红虽有AR882在中国市场的权益，也有全球供货的优先生产权，但Arthrosi公司如今易主，未来一切都不好说。只用老故事又怎么能说服现在的市场呢？一品红只能自求多福了。 (来源：拇指药略作者：西北哽）药闻康策新媒体矩阵微信公众号点击下方一键关注【免责声明】 1.“药闻康策”部分文章信息来源于网络转载是出于传递更多信息之目的，并不意味着赞同其观点或证实其内容的真实性。如对内容有疑议，请及时与我司联系。2.“药闻康策”致力于提供合理、准确、完整的资讯信息，但不保证信息的合理性、准确性和完整性，且不对因信息的不合理、不准确或遗漏导致的任何损失或损害承担责任。3.“药闻康策”所有信息仅供参考，不做任何商业交易或医疗服务的根据，如自行使用“药闻康策”内容发生偏差，我司不承担任何责任，包括但不限于法律责任，赔偿责任。欢迎转发分享、点赞、点在看

快速通道引进/卖出

2025-12-15

·FierceBiotech

Sobi pays $950M upfront to snap up phase 3 gout specialist Arthrosi Therapeutics

Under a new deal, Sobi gets its hands on Arthrosi Therapeutics’ pozdeutinurad, a next-gen, once-daily oral URAT1 inhibitor.\n Fresh off a $153 million series E round, Arthrosi Therapeutics is skipping an IPO route and is instead being bought up for a potential value of $1.5 billion from Swedish biopharma Sobi. Under the deal, San Diego-based Arthrosi will secure $950 million upfront as well as a contingent consideration of up to $550 million. For its part, Sobi gets its hands on Arthrosi’s pozdeutinurad, a next-gen, once-daily oral URAT1 inhibitor.This med is being assessed in several phase 3 tests for progressive and tophaceous gout, with initial readouts slated for next year.“The acquisition of Arthrosi allows us to expand our gout pipeline with a highly differentiated new asset,” Guido Oelkers, president and CEO of Sobi, said in a statement.“Pozdeutinurad has the potential to become the therapy of choice for patients who have progressive gout with persistent and unresolved symptoms despite first-line therapy,” the CEO added.Gout is a type of arthritis that causes sudden, severe joint pain. Common drug treatment includes simple pain relief, but pharma has been working on potential curative treatments for decades, though with mixed results.Arthrosi’s leading drug candidate is an inhibitor of URAT1, a transporter that has been a target for gout drugs going back to the approval of probenecid in 1951. Probenecid and other early gout drugs hit multiple targets but also caused a range of side effects. Seeking to avoid the adverse events, developers of subsequent waves of gout drugs tried to create more potent and specific URAT1 inhibitors.AstraZeneca acquired a URAT1 inhibitor in its $1.3 billion takeover of Ardea Biosciences in 2012 and won FDA approval for the drug in 2015. By 2020, the product, Zurampic, had, however, landed on the scrap heap.The commercial struggles of Zurampic, which carried a boxed warning, didn\'t deter others from trying to launch URAT1 inhibitors.A team behind Zurampic has reformed at Crystalys Therapeutics to advance dotinurad, a URAT1 inhibitor that is approved in Asian markets including Japan. And China’s Atom Therapeutic recently reported a phase 2b/3 win for its own URAT1 inhibitor, lingdolinurad.

上市批准临床3期并购IPO

100 项与 Lingdolinurad 相关的药物交易

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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
痛风	临床3期	美国	杭州新元素药业股份有限公司	2023-08-11
痛风	临床3期	澳大利亚	杭州新元素药业股份有限公司	2023-08-11
痛风	临床3期	危地马拉	杭州新元素药业股份有限公司	2023-08-11
痛风	临床3期	中国台湾	杭州新元素药业股份有限公司	2023-08-11
高尿酸血症	临床3期	中国	杭州新元素药业股份有限公司	-
慢性肾病	临床1期	中国	杭州新元素药业股份有限公司	-

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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


ACR2025	临床2期	高尿酸血症 \| 痛风	45	ABP-671 1 mg	觸衊齋顧鑰鏇艱餘餘簾(壓膚顧鑰選獵製艱築鏇) = 鬱醖築構鹹鹽窪積醖鏇顧齋鹹鏇廠憲鏇餘鏇淵 (製獵製壓範蓋膚衊醖鑰 ) 更多	积极	2025-10-24
				ABP-671 2 mg	觸衊齋顧鑰鏇艱餘餘簾(壓膚顧鑰選獵製艱築鏇) = 範壓鬱鹹齋鑰廠獵醖築顧齋鹹鏇廠憲鏇餘鏇淵 (製獵製壓範蓋膚衊醖鑰 ) 更多
NCT05818085 (ABP-671-301, NEWS) 人工标引	临床2/3期	高尿酸血症	-	lingdolinurad	鹹齋鹽網築範淵鏇鹽願(獵鬱製觸築鏇糧積鬱鹽) = patients receiving ABP-671 were more likely to see 衊鏇糧鏇構觸網憲築窪 (蓋膚夢齋遞淵淵窪壓選 ) 达到更多	积极	2025-09-08
				Allopurinol
Company_Website \| NEWS 人工标引	临床2/3期	痛风	-	ABP-671	積鹹鏇構窪壓壓遞積遞(襯顧廠繭衊觸夢壓襯獵) = 繭醖鹽襯廠製網醖選衊鬱糧製淵顧鏇齋醖衊遞 (廠淵壓簾襯襯衊夢壓構 )	积极	2025-09-08
				别嘌醇	積鹹鏇構窪壓壓遞積遞(襯顧廠繭衊觸夢壓襯獵) = 廠蓋觸遞醖鬱艱艱鬱遞鬱糧製淵顧鏇齋醖衊遞 (廠淵壓簾襯襯衊夢壓構 ) 更多