芬奈布鲁替尼(Fenebrutinib) - 药物靶点：BTK C481S_在研适应症：多发性硬化症，复发性多发性硬化，横纹肌肉瘤_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Fenebrutinib (USAN/INN)、G-0853、GDC-0853

+ [4]

靶点

BTK C481S

作用方式

抑制剂

作用机制

BTK C481S抑制剂(酪氨酸蛋白激酶BTK C481S抑制剂)

治疗领域

肿瘤免疫系统疾病神经系统疾病+ [1]

在研适应症

多发性硬化症复发性多发性硬化横纹肌肉瘤+ [1]

非在研适应症

难治性B细胞淋巴瘤慢性淋巴细胞白血病慢性荨麻疹+ [5]

原研机构

Genentech, Inc.

在研机构

Hoffmann-La Roche, Inc.F. Hoffmann-La Roche Ltd.

罗氏（中国）投资有限公司

非在研机构

Genentech, Inc.

Roche Holding AG

权益机构-

最高研发阶段临床3期

首次获批日期-

最高研发阶段(中国)临床3期

特殊审评-

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结构/序列

分子式C37H44N8O4

InChIKeyWNEODWDFDXWOLU-QHCPKHFHSA-N

CAS号1434048-34-6

关联

24

项与芬奈布鲁替尼相关的临床试验

NCT07161258

/ Recruiting临床2期

An Open-label, Single-arm Study to Evaluate Pharmacokinetics, Pharmacodynamic Effects, Safety and Tolerability of Fenebrutinib in Children and Adolescents With Relapsing Multiple Sclerosis

This open label, single arm study will evaluate the PK and PD effects of fenebrutinib in children and adolescents with RMS aged between 10 and < 18 years.
This study consists of a Dose Exploration Period and an Optional Extension Period. Eligible participants may choose to continue treatment with fenebrutinib in the optional extension period after completing the dose exploration period.

开始日期2025-10-06

申办/合作机构

Hoffmann-La Roche Ltd.

ISRCTN41455091

/ Recruiting临床1期

A phase I, open-label, single-dose study to evaluate the effect of severe renal impairment on the pharmacokinetics of fenebrutinib

开始日期2024-06-06

申办/合作机构

Genentech, Inc.

ISRCTN46432183

/ Recruiting临床1期

A phase I, open-Label, single-Dose study to evaluate the effect of mild or moderate hepatic impairment on the pharmacokinetics of fenebrutinib

开始日期2023-10-18

申办/合作机构

Genentech, Inc.

100 项与芬奈布鲁替尼相关的临床结果

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100 项与芬奈布鲁替尼相关的转化医学

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100 项与芬奈布鲁替尼相关的专利（医药）

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66

项与芬奈布鲁替尼相关的文献（医药）

2025-11-01·ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY

Emerging IgE and non-IgE targeted therapies for chronic urticaria

Review

作者: Chhiba, Krishan D ; Saini, Sarbjit S

Chronic urticaria affects a significant percent of the global population and carries a higher burden of unmet medical need. Current standard-of-care includes antihistamines and omalizumab, but omalizumab is not effective in all patients and has not been found to induce long-term disease remission. This review evaluates the diverse therapeutic pipeline spanning IgE-based and non-IgE-based mast cell targeting strategies, including recent clinical data. The therapeutic landscape has expanded rapidly with multiple mechanisms under investigation. IgE-targeted approaches include omalizumab biosimilars, with CT-P39 having received Food and Drug Administration (FDA) approval. Dupilumab received FDA approval for antihistamine-refractory chronic spontaneous urticaria supporting the targeting of type 2 cytokines, interleukin-4, and interleukin-13, in this disease. Bruton's tyrosine kinase inhibitors have promise, with remibrutinib receiving FDA approval and demonstrating significant reductions in UAS7 in phase 3 trials. c-Kit (c-Kit or KIT) inhibition with barzolvolimab demonstrates robust efficacy with sustained effects post-treatment. Finally, Janus kinase inhibitors, Mas-related G protein-coupled receptor X2 antagonists, and other novel mechanisms are advancing through clinical trials. Although some programs have been discontinued due to safety concerns or lack of efficacy such as fenebrutinib (Bruton's tyrosine kinase inhibitor), THB001 (c-Kit inhibitor), EP262 (Mas-related G protein-coupled receptor X2 antagonist), tezepelumab (anti-TSLP), and lirentelimab and AK006 (sialic acid binding immunoglobulin-like lectin-targeting agents), these studies have informed many of the other positive studies. In summary, in the last year, we have seen the chronic urticaria pipeline mature with multiple phase 3 programs and new approvals representing diverse mechanisms of action. Nevertheless, significant therapeutic gaps persist for omalizumab-refractory disease and chronic-inducible urticaria.

2025-09-02·NATURAL PRODUCT RESEARCH

Molecular docking based comparative study of antiviral compounds on SARS-CoV-2 spike protein

Article

作者: Biswal, Pradyut K. ; Kumar, Jitendra ; Nagavarapu, Sowmya

The urgent need for effective therapeutic interventions against SARS-CoV-2 has prompted extensive exploration of potential drug candidates. Among the viral proteins, the spike (S) protein presents an attractive target due to its critical role in viral entry and infection. In this study, we employed molecular docking techniques to investigate the binding affinities and interaction profiles of a panel of active compounds against the SARS-CoV-2 spike protein. Utilising computational simulations, we assessed the binding properties of these compounds within the receptor-binding domain (RBD) and other key regions of the spike protein. Our comparative analysis elucidates the differential binding patterns and identifies promising lead compounds with high binding affinity and favourable interaction profiles. Furthermore, we discuss the implications of these findings for the development of potential therapeutics targeting the SARS-CoV-2 spike protein. Using molecular docking and the Lipinski five rule, this study illustrates possible compounds with strong binding affinities, their molecular interactions, for both naturally occurring and man-made drugs. Computational approach is applied, and it is concluded that, drugs like Withanolide, Dihydroergocristine, Fenebrutinib, and Ergotamine shows binding energies between -8.3 and -9.1 kcal/mol, and are possible candidate for anti covid drug.

2025-09-01·EUROPEAN JOURNAL OF PHARMACOLOGY

Next generation Bruton's tyrosine kinase inhibitors – characterization of in vitro potency and selectivity

Article

作者: Angst, Daniela ; Cenni, Bruno ; Pulz, Robert

Bruton's tyrosine kinase (BTK) mediates B cell receptor and Fc receptor signaling and is a key regulator of autoimmunity and allergy. A series of novel BTK inhibitors (BTKi) are currently in development for non-oncologic indications with covalent-irreversible (remibrutinib, evobrutinib, tolebrutinib, orelabrutinib), covalent-reversible (rilzabrutinib), and non-covalent reversible (fenebrutinib) binding modes. This study characterizes their in vitro potency and selectivity profiles under the same conditions to minimize assay differences across the different binding modes. Covalent BTKi showed human in vitro blood BTK binding in a time- and concentration-dependent manner with remibrutinib being the most potent and fastest in onset of action. Cellular BTK pathway inhibition was determined in human blood B cells and basophils, and for covalent BTKi correlated well with BTK binding. In contrast to the covalent-irreversible remibrutinib, the non-covalent reversible fenebrutinib showed rapid loss of cellular BTK inhibition after washout. Kinase selectivity was assessed in a binding screen across the human kinome, followed by quantification of binding affinities for a selection of kinases. BTKi ranked in their selectivity as follows (most selective to least): remibrutinib, fenebrutinib, evobrutinib, orelabrutinib, rilzabrutinib and tolebrutinib. These data suggest that next generation BTKi show important differences in their in vitro target binding and selectivity when compared under the same conditions.

233

项与芬奈布鲁替尼相关的新闻（医药）

2026-02-24

·QQ浏览器

资讯 | 穿越血脑屏障！新型口服疗法3期临床研究结果积极

近期，罗氏（Roche）公布了3期FENtrepid研究的新数据。结果显示，相对于PPMS获批疗法Ocrevus（ocrelizumab），其在研布鲁顿酪氨酸激酶（BTK）抑制剂fenebrutinib在原发进展型多发性硬化（PPMS）患者中，在主要终点降低残疾进展方面达到非劣效性。罗氏预计在2026年上半年，另一项复发性多发性硬化（RMS）3期研究数据公布时，向监管机构递交所有相关3期试验结果。FENtrepid是一项多中心、随机、双盲、平行分组的3期研究，旨在评估fenebrutinib与ocrelizumab在985例PPMS成年患者中的疗效与安全性。符合条件的受试者按1：1随机分组，分别接受每日口服fenebrutinib（并联合与静脉输注ocrelizumab匹配的安慰剂）或静脉输注ocrelizumab（并联合与口服fenebrutinib匹配的安慰剂）治疗，治疗时间至少为120周。图片来源：123RF分析显示，以12周复合确认残疾进展（cCDP12）发生时间为评估指标，与PPMS获批疗法ocrelizumab相比，fenebrutinib使残疾进展风险降低了12%（HR=0.88；95% CI：0.75-1.03），且两组曲线最早在24周即出现分离。在整个治疗期间以及各患者亚组中，cCDP12均观察到一致的治疗效果。cCDP12这一主要终点包括基于扩展残疾状态量表（EDSS）评估的功能性残疾确认进展（CDP）、用于评估步行速度的25英尺计时步行测试（T25FW），以及用于评估上肢功能的九孔插钉测试（9HPT）。与ocrelizumab相比，fenebrutinib在9HPT恶化风险方面显示出最显著的治疗效果，风险降低26%（HR=0.74；95% CI：0.56-0.98）。在fenebrutinib组中常见（≥10%）的不良事件（AE）与ocrelizumab组总体相当，包括感染（67.0% vs 70.9%）、恶心（12.0% vs 7.1%）和出血（10.2% vs 8.1%）。Fenebrutinib组中一过性且可逆的肝酶升高发生率更高（13.3% vs 2.9%），且所有病例在停用研究药物后均得到缓解。严重不良事件发生于19.1%的fenebrutinib治疗患者（ocrelizumab组为18.9%），并导致4.3%的患者停药（ocrelizumab组为3.0%）。在FENtrepid研究中，fenebrutinib组的死亡病例比例为1.4%，ocrelizumab组为0.2%，研究者评估认为所有死亡事件均与研究治疗无关，且在发生时间或原因上未观察到一致性模式。Fenebrutinib是一种在研的口服、可穿越血脑屏障、可逆且非共价的BTK抑制剂，具有优化的药代动力学（PK）特征和较高效力。与目前大多数共价且不可逆、可与酶形成永久化学键的BTK抑制剂不同，fenebrutinib与酶结合后最终可解离，这些设计特征可能有助于降低脱靶效应。Fenebrutinib对BTK的选择性较其他激酶高出130倍，这意味着其可特异性结合BTK靶点而不干扰其他激酶。该药物可穿越血脑屏障进入中枢神经系统，在全身发挥作用，以靶向慢性炎症。参考资料：[1] Roche’s is the first investigational medicine in over a decade that reduces disability progression in primary progressive multiple sclerosis (PPMS). Retrieved February 9, 2026 from https://www.roche.com/media/releases/med-cor-2026-02-07免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

临床结果临床3期临床成功细胞疗法

2026-02-20

·Firstwordpharma

Biopharma bites: Blockbuster hopes for Brinsupri, Biogen stops MS study, plus mRNA patent fight heats up

Insmed guides for $1B in Brinsupri salesBiogen bins mid-stage MS studyModerna's mNEXSPIKE faces patent suitInsmed guides for $1B in Brinsupri salesHaving been approved in the US last August, and subsequently authorised in the EU, as the first treatment for non-cystic fibrosis bronchiectasis (NCFB), Insmed now expects Brinsupri (brensocatib) to generate revenue of at least $1 billion in 2026. "Our US commercial launch…continues to exceed our expectations," said CEO Will Lewis.The oral, once-daily DPP1 inhibitor — designed to block the activation of neutrophil serine proteases in neutrophils that are responsible for the underlying inflammation in NCFB — generated sales of $144.6 million in the fourth quarter of 2025 and $172.7 million for the full year.Insmed expects regulatory decisions for Brinsupri for the treatment of NCFB in the UK and Japan in 2026. However, the company cautioned that it "continues to evaluate the potential effect of evolving US policies," which could impact the timing of potential international commercial launches.-Matthew DennisBiogen bins mid-stage MS study Biogen this week terminated the Phase II FUSION study evaluating BIIB091 in patients with relapsing multiple sclerosis (MS), according to an update on ClinicalTrials.gov. The candidate, a reversible, non-covalent BTK inhibitor, was being studied alone or in combination with diroximel fumarate; the trial had enrolled 127 patients. The study discontinuation comes as at least one BTK inhibitor seems to have found its footing in MS. While the drug class has shown tantalising promise in treating the disease, none have yet reached the finish line — though Roche's fenebrutinib may be nearing approval (see – Physician Views Results: Neurologists share cautious optimism for Roche's fenebrutinib in PPMS).However, Sanofi was recently hit with a controversial FDA rejection for its BTK inhibitor, tolebrutinib, to treat non-relapsing secondary progressive MS. For more on how BTK inhibitors may shake up the MS treatment landscape, see KOL Views Q&A: What Sanofi’s PERSEUS, Roche’s FENtrepid divergence says about BTK inhibitors in MS.-Elizabeth EatonModerna's mNEXSPIKE faces patent suit BioNTech has filed a patent infringement lawsuit alleging that Moderna's next-generation COVID-19 vaccine unlawfully infringes on a patent related to the German company's own mRNA shot, Comirnaty. The complaint, filed Thursday in US District Court for the District of Delaware, claims Moderna's mNEXSPIKE infringes US Patent No. 12,133,899, which covers a streamlined mRNA vaccine design that allows for lower dosing. The case intensifies a long-running legal battle between the companies behind two of the world's most successful COVID-19 vaccines. BioNTech developed Comirnaty with Pfizer, while Moderna brought its own shot, Spikevax, to market in late 2020. In 2022, Moderna sued BioNTech and Pfizer, claiming they "unlawfully copied" its mRNA inventions to make Comirnaty; that case remains ongoing. Moderna recently highlighted mNEXSPIKE, which was approved by the FDA in 2025, as a significant growth driver with expected approvals this year in Europe and Japan. According to BioNTech's complaint, mNEXSPIKE accounted for 55% of COVID-19 vaccines sold by Moderna in the 2025-2026 respiratory virus season. A spokesperson for Moderna said Thursday it would defend itself against the new allegations.-Anna Bratulic

上市批准临床2期疫苗信使RNA专利侵权

2026-02-18

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NEXT WORD | BTK战场的“幸存者游戏”：当罗氏开始颠覆自己的药王

Buzz Words: 原发进展型多发性硬化症(PPMS)/Fenebrutinib 如果你在药物研发领域工作，特别是神经科学方向，你一定拥有一种特殊的韧性。你早已习惯了失败，习惯了那些精妙的假设在人体生物学的暗礁上撞得粉碎。而在所有这些“暗礁”中，神经退行性疾病的研发禁区无疑是最为险峻的。然而，我们正目睹多发性硬化症（MS）治疗史上的一个迷人转折点。几十年来，我们已经非常擅长应对“复发型”MS——那就像是一场场突发的丛林火灾，我们可以用大剂量的“水弹”（外周免疫抑制剂）将其扑灭。但对于原发进展型MS（PPMS），那种缓慢、持续、如同“暗火”般的病情恶化，我们曾长期束手无策。直到现在。驱动这一变革的关键词是 BTK抑制剂（布鲁顿酪氨酸激酶抑制剂）。而引爆本轮舆论的核心，则是罗氏（Roche）在2026年2月公布的 FENtrepid III期研究结果：其候选药物 fenebrutinib 在PPMS领域取得了历史性的成功。要理解这为何是一件足以载入史册的大事，我们需要跳过新闻稿的标题，去解构其背后的药物化学选择、此前该领域惨烈的失败史，以及那份堪称“豪赌”的临床设计方案。两种疾病的故事要理解任务之艰巨，必须先明白：虽然统称为“多发性硬化症”，但它实际上是披着同一诊断外壳的两种截然不同的生物学难题。超过85%的患者被诊断为复发缓解型MS (RRMS)。其特征是外周免疫细胞（T细胞和B细胞）被激活后穿过血脑屏障（BBB），进入中枢神经系统（CNS）引发急性攻击。这种入侵就像森林火灾，而现有的“药王”们——如罗氏自家的 Ocrevus（奥瑞珠单抗）——通过精准打击外周B细胞，能非常有效地“御敌于国门之外”。然而，原发进展型MS (PPMS) 完全是另一回事。它仅占患者总数的10-15%，没有明显的复发期，MRI上也往往看不见急性炎症引起的增强病灶。相反，从第一天起，患者就陷入了缓慢而不可逆的残疾加重。如果说RRMS是森林火灾，PPMS更像是深埋地下的煤矿暗火。血脑屏障（BBB）基本完好，这意味着巨大的单克隆抗体（如 Ocrevus）很难进入。这里的炎症不是由外来者驱动的，而是由已经潜伏在脑内的“内鬼”驱动的——即脑驻留小胶质细胞（Microglia）。在PPMS中，这些小胶质细胞处于持续激活状态，像是在大脑内部悄无声息地啃噬神经元。过去几十年的研发史证明：用治疗RRMS的方案去打PPMS，就像是往着火的煤矿地面上喷水——根本没用。雄心的“墓地”：那些惨烈的失败在庆祝成功之前，我们必须祭奠那些为前路探明方向的失败者。最令人扼腕的是诺华的 Gilenya（芬戈莫德）。作为首个口服MS药物，它在RRMS中堪称革命，但在PPMS的INFORMS研究中却遭遇了滑铁卢。数据证明：如果你的药物无法深入中枢神经系统（CNS），它对进展型病程毫无作用。即便是 Ocrevus 的成功，也带有一丝妥协。它是目前唯一获批的PPMS疗法，但作为一个庞大的单抗分子，仅有约0.1%的电荷能穿过血脑屏障。它能减缓恶化，但无法终结暗火。我们需要一种小到足以跨越血脑屏障，且能同时精准打击中枢B细胞和“发疯”的小胶质细胞的小分子。这就是BTK抑制剂的承诺。“BTK之战”：一场残酷的消耗战开发MS领域的BTK抑制剂是一场代价高昂、过程离奇的竞赛。为了攻克这一高地，赛诺菲、默克、罗氏和诺华纷纷下场。然而，近年来的战况却极其惨烈。默克的 Evobrutinib：在2023年末的III期研究中，它甚至没能击败老药奥巴捷（Aubagio），项目基本宣告流产。赛诺菲的 Tolebrutinib：这是最令业界心碎的案例。尽管该药物具有极强的中枢渗透力，但在2025年底公布的PERSEUS研究中，它未能在PPMS患者中显示出优于安慰剂的统计学差异，且伴随严重的肝毒性风险。到2026年初，BTK的赛道一片阴霾。许多人开始怀疑：“从小胶质细胞入手”这一药理假设是否从根本上就是错的？FENtrepid的“豪赌”：罗氏的化学与策略双重压制 2026年2月，罗氏在ACTRIMS论坛上公布了 FENtrepid 研究数据。罗氏做了两件完全不同的事，一件关乎化学，一件关乎战略。 1. 化学层面的“拨乱反正”：可逆性与赛诺菲采用的共价（永久结合）策略不同，罗氏的 fenebrutinib 是一种非共价、可逆的抑制剂。这意味着它在结合BTK后会适时释放。罗氏赌的是：在一种需要数十年每日服用的慢性病中，这种“柔性”结合能提供更高的肝脏安全性，从而允许更高的剂量和更持续的CNS渗透。 2. 战略层面的“同室操戈” 大多数PPMS试验选择安慰剂作为对照。但罗氏选择了一条最难的路：头对头挑战自家的“药王” Ocrevus。这在商业上是极其大胆的。如果 fenebrutinib 赢了，它将直接分食 Ocrevus 每年近80亿美元的市场。但如果输了，BTK这条路可能就彻底堵死了。结果分析：为何“非劣效性”实际上是“压倒性胜利”？数据揭晓：fenebrutinib 达到了主要终点。证明了一颗口服药片可以达到、甚至超越顶级输液疗法的临床效果。整体残疾恶化（cCDP12）：fenebrutinib 相比 Ocrevus 展现了 12% 的数值优势。在24周时，两条曲线就开始分道扬镳。上肢功能的突破（9-Hole Peg Test）：这是最令临床医生振奋的数据。在评估手部灵活性和上肢功能的测试中，fenebrutinib 将恶化风险降低了 26%。对患者的意义：对于PPMS患者来说，能走路固然重要，但能否自己扣纽扣、打字、进食（上肢功能），往往意味着作为一个人的独立尊严。fenebrutinib 这种深入脑组织的能力，似乎在保护这些复杂运动回路方面展现了独特的优势。结语在神经科学领域，我们通常对“突破”一词保持高度警惕。但 FENtrepid 的结果确实不同。它是一个理性药物设计的胜利：识别新靶点（小胶质细胞的BTK）、设计具备关键特性的分子（跨越BBB、可逆结合）、并执行了一场无畏的头对头试验。对于那些曾被告知“无药可救”的PPMS患者来说，一个能主动攻入大脑暗火中心的口服药物的到来，意义深远。 BTK战争旷日持久，尸横遍野。但看起来，罗氏通过押注可逆性和瞄准最难的目标，赢得了这场决定性的战役。PPMS这座曾经不可撼动的暗火城堡，终于被攻破了一道缝隙。

引进/卖出

100 项与芬奈布鲁替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11457	-	-	DB14785

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
复发性多发性硬化	临床3期	荷兰	-	2020-11-16
横纹肌肉瘤	临床3期	荷兰	-	2020-11-16
原发性进行性多发性硬化	临床3期	美国	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	阿根廷	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	澳大利亚	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	奥地利	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	巴西	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	保加利亚	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	加拿大	Hoffmann-La Roche, Inc.	2020-10-26
原发性进行性多发性硬化	临床3期	智利	Hoffmann-La Roche, Inc.	2020-10-26

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临床结果

适应症

分期

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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


NCT04586023 (FENhance 2, GlobeNewswire) 人工标引	临床3期	多发性硬化症	1,497	fenebrutinib	壓齋獵顧製鹹艱憲網鑰(鬱網積範簾範簾糧選餘) = Fenebrutinib, an investigational Bruton’s tyrosine kinase (BTK) inhibitor, significantly reduced the annualised relapse rate (ARR) compared to teriflunomide over a period of at least 96 weeks of treatment. 鹹窪艱鹹蓋選蓋憲繭鹽 (選鑰壓積選廠淵築淵製 ) 达到	积极	2025-11-10
				teriflunomide
NCT04544449 (FENtrepid, GlobeNewswire) 人工标引	临床3期	多发性硬化症	985	OCREVUS	艱餘糧鬱構廠艱構願願(範糧壓遞夢淵壓網鑰蓋) = The results showed that fenebrutinib was non-inferior compared to ocrelizumab, the only approved therapy in PPMS, as measured by a delay in the onset of composite confirmed disability progression over a period of at least 120 weeks of treatment. 醖觸夢網構網餘鹹鏇廠 (遞築獵齋網鏇膚醖憲範 ) 达到	非劣	2025-11-10
				fenebrutinib
NCT05119569 (FENopta, Company_Website) 人工标引	临床2期	复发性多发性硬化	99	fenebrutinib	蓋網鏇鏇襯積鬱願繭窪(壓範襯鹽製網壓積鹹餘) = 鑰製夢衊夢製簾鏇顧艱齋網築積鏇鹹繭醖醖繭 (獵夢餘壓鑰憲構壓糧夢 )	积极	2025-05-30
NCT05119569 (FENopta, AAN2025)	临床2期	复发性多发性硬化	99	Fenebrutinib 200 mg	構鬱繭網願窪襯壓鬱窪(遞夢製鏇簾遞遞鹹築壓) = An asymptomatic alanine transaminase elevation occurred newly in one OLE participant (1%) that resolved 鬱糧艱廠觸獵鹹範蓋廠 (願鬱襯窪顧構鏇膚餘範 ) 更多	积极	2025-04-07
				Placebo
NCT05119569 (FENopta-OLE, GlobeNewswire) 人工标引	临床2期	复发性多发性硬化	109	Fenebrutinib	簾製築製製淵鏇齋艱鹹(鹹壓遞窪製簾齋構餘鏇) = 選鏇鬱積鬱壓廠遞廠艱網鏇糧艱選網網壓窪鑰 (積餘願蓋蓋襯餘淵鏇壓 ) 更多	积极	2024-09-04
NCT05119569 (["FENopta"] \| FENopta-OLE \| FENopta, CTgov)	临床2期	复发性多发性硬化	109	Fenebrutinib (DBT Phase: Fenebrutinib)	鹹觸膚餘觸淵淵積餘襯(窪範鑰憲夢顧積鹹襯窪) = 夢膚夢構範膚餘製鹹構積製淵積糧淵鏇顧築襯 (範選衊遞鹹鹹鹹餘構鬱, 廠構膚蓋簾醖淵夢選鏇 ~ 鑰蓋遞鬱願範繭壓壓鑰) 更多	-	2024-06-12
				placebo+fenebrutinib (DBT Phase: Placebo)	鹹觸膚餘觸淵淵積餘襯(窪範鑰憲夢顧積鹹襯窪) = 鹹鹹膚衊廠餘淵鑰蓋蓋積製淵積糧淵鏇顧築襯 (範選衊遞鹹鹹鹹餘構鬱, 選鬱壓醖築製衊淵構製 ~ 獵繭鏇鏇艱壓鑰製憲願) 更多
AAN2024	临床1期	-	-	Fenebrutinib 400 mg	壓製獵觸築願糧選築憲(廠顧簾醖餘遞範觸淵糧) = Both doses were well tolerated, and no serious adverse events (AEs), AEs of special interest or Grade ≥2 AEs were reported 鹹築蓋積蓋願鹽憲蓋餘 (艱網衊衊觸網築窪顧蓋 )	积极	2024-04-09
				Fenebrutinib 700 mg
NCT04586010 (FENhance, Biospace) 人工标引	临床3期	复发性多发性硬化	-	fenebrutinib	繭鹽鏇衊遞選鹽鬱壓遞(糧構顧構獵餘築窪糧憲) = 壓繭遞遞網獵鹹壓糧選鏇餘製選選衊願壓醖簾 (糧願遞餘鬱夢夢憲鏇願 )	不佳	2023-12-05
NCT05119569 (FENopta, ECTRIMS2023) 人工标引	临床2期	多发性硬化症	106	Fenebrutinib 200 mg	襯窪蓋衊糧獵糧淵觸製(鬱糧簾鑰鏇蓋網構簾糧) = 觸網窪獵糧淵膚築構鏇憲選餘顧蓋廠糧遞壓鹽 (夢膚遞願醖夢衊壓積顧 ) 更多	积极	2023-10-17
				Placebo	襯窪蓋衊糧獵糧淵觸製(鬱糧簾鑰鏇蓋網構簾糧) = 襯壓願網艱鹹繭遞製獵憲選餘顧蓋廠糧遞壓鹽 (夢膚遞願醖夢衊壓積顧 ) 更多
Fenebrutinib (EULAR2021)	临床2期	系统性红斑狼疮 C3 \| C4 \| ANA ... 更多	260	Fenebrutinib	艱夢糧繭艱壓壓範網選(構淵鬱夢夢積遞網鹹願) = 繭壓淵衊衊夢糧積範襯糧繭遞選糧選觸簾糧鹹 (鑰顧窪夢選繭廠鑰遞淵 )	-	2021-06-02