预约演示
更新于：2026-09-07
Zigakibart
泽戈奇拜单抗
更新于：2026-09-07
概要
基本信息
非在研机构- |
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 |
特殊审评孤儿药 (欧盟) |
登录后查看时间轴
结构/序列
Sequence Code 10191220L
来源: *****
Sequence Code 10191228H
来源: *****
关联
9
项与 泽戈奇拜单抗 相关的临床试验NCT07146906
An Open-label, Multicenter Study to Assess the Effect of Zigakibart Treatment on Histologic, Circulating, and Excreted Markers of Kidney Disease and Dysfunction in Adult Patients With IgA Nephropathy.
NCT06858319
A Multicenter Open-label Extension Study to Evaluate the Long-term Safety and Tolerability of Zigakibart in Adults With Primary IgA Nephropathy.
ChiCTR2500096892
A Phase 3, Randomized, Double-blind, Placebo-controlled Study of BION-1301 in Adults with IgA Nephropathy(The BEYOND Study)
100 项与 泽戈奇拜单抗 相关的临床结果
登录后查看更多信息
100 项与 泽戈奇拜单抗 相关的转化医学
登录后查看更多信息
100 项与 泽戈奇拜单抗 相关的专利（医药）
登录后查看更多信息
5
项与 泽戈奇拜单抗 相关的文献（医药）2026-06-01Kidney International Reports
Zigakibart Potently Inhibits A Proliferation-Inducing Ligand-Mediated IgA Production, Addressing IgAN Pathogenesis Root Causes
Article
作者: Bakker, Jeroen ; Kreijtz, Joost ; van Eenennaam, Hans ; van Zandvoort, Peter ; Van Elsas, Andrea ; Dulos, John ; Kuo, Jay J ; Warncke, Max ; Cotton, Victoria ; Medema, Jan Paul ; Guadagnoli, Marco ; Barratt, Jonathan ; Jansen, Wout ; Driessen, Lilian ; Vink, Paul ; Lo, Jeannette
Introduction:
Zigakibart is a humanized IgG4 monoclonal antibody (mAb) binding A proliferation-inducing ligand (APRIL, TNFSF13), a critical factor in IgA nephropathy (IgAN) pathogenesis. Results from the ongoing phase 1/2 ADU-CL-19 study (NCT03945318) have shown clinically meaningful outcomes in patients with IgAN treated with zigakibart.
Methods:
We conducted a preclinical characterization of zigakibart using in vitro methods, including investigation of its binding to APRIL from various species, blocking of APRIL binding to transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) and B-cell maturation antigen (BCMA), investigation of the potency of zigakibart on BCMA- and TACI-reporter cells, and the assessment of the effect of APRIL blockade on human plasma cell survival and Ig production. In vivo methods were used to characterize zigakibart in human APRIL transgenic mice (hAPRIL-tg) and nonhuman primates.
Results:
Zigakibart potently blocked APRIL binding to TACI and BCMA and inhibited human plasma cell survival, which are key mediators in IgAN pathogenesis. Zigakibart selectively reduced circulating IgA and IgM to a greater extent than IgG and inhibited T-cell-independent antibody responses and IgA deposition in the kidney in vivo. Importantly, zigakibart inhibited IgA+ and IgM+ to a greater extent than IgG+ human plasma cells in vitro.
Conclusion:
In these preclinical studies, zigakibart demonstrated robust pharmacological activity and, by neutralizing APRIL, inhibited markers associated with the pathogenesis of IgAN. Zigakibart therefore provides a potentially disease-modifying approach for IgAN treatment. Evaluation of the effects of zigakibart on proteinuria and long-term kidney function in adults with IgAN is ongoing in the ADU-CL-19 study and the phase 3 BEYOND study (NCT05852938).
2025-09-01KIDNEY INTERNATIONAL
Zigakibart demonstrates clinical safety and efficacy in a Phase 1/2 trial of healthy volunteers and patients with IgA nephropathy
Article
作者: Kooienga, Laura ; Dulos, John ; Agha, Irfan ; Smith, William ; van Eenennaam, Hans ; Song, Yuanbo ; Van Elsas, Andrea ; Lo, Jeannette ; Kim, Sung Gyun ; Barratt, Jonathan ; Lee, Eun Young ; Thomas, Hannah ; Workeneh, Biruh
INTRODUCTION:
Zigakibart is a humanized IgG4 monoclonal antibody that binds the cytokine A Proliferation-Inducing Ligand (APRIL, also known as TNFSF13). APRIL is a critical factor in immunoglobulin (Ig) A nephropathy (IgAN) pathogenesis.
METHODS:
Here, we report healthy volunteers (63 overall) and 100-week data from an ongoing Phase 1/2 clinical trial in 40 patients with IgAN (NCT03945318) treated with zigakibart.
RESULTS:
In healthy volunteers, zigakibart was well tolerated following intravenous administration of single doses ranging from 10-1350 mg or multiple doses ranging from 50-450 mg every two weeks. Zigakibart exposure increased in a dose-proportional manner, with corresponding durable reductions in levels of free APRIL, IgA and IgM, and to a lesser extent, IgG. In patients with IgAN, zigakibart 600 mg, administered subcutaneously every two weeks, was well tolerated with no treatment-emergent adverse events leading to study drug discontinuation or death. A 60% reduction in proteinuria and sustained estimated glomerular filtration rate stabilization were observed at week 100. There was a notable decrease in hematuria, as well as rapid and durable reductions in IgA, galactose-deficient IgA (Gd-IgA1), and IgM levels, with a modest reduction in IgG.
CONCLUSIONS:
Overall, zigakibart demonstrated robust pharmacological activity, and clinical evidence shows an acceptable safety profile with clinically meaningful proteinuria reduction and sustained estimated glomerular filtration rate stabilization in patients with IgAN, providing a potentially disease-modifying approach for the treatment of IgAN. The effects of zigakibart on proteinuria and long-term kidney function in adults with IgAN are being evaluated in the ongoing phase 3 BEYOND study (NCT05852938).
2023-12-01Clinical rheumatology
A narrative review of potential drug treatments for nephritis in children with IgA vasculitis (HSP)
Review
作者: Lamond, Megan ; Chetwynd, Andrew J ; Marro, Julien ; Oni, Louise ; Williams, Chloe E C
Abstract:
Immunoglobulin A (IgA) vasculitis (IgAV, also known as Henoch-Schoenlein purpura, HSP) is the most common vasculitis of childhood. It usually presents with a simple, self-limiting disease course; however, a small subset of patients may develop kidney involvement (IgAV-N) which occurs 4–12 weeks after disease onset and is the biggest contributor to long-term morbidity. Treatment currently targets patients with established kidney involvement; however; there is a desire to work towards early prevention of inflammation during the window of opportunity between disease presentation and onset of significant nephritis. There are no clinical trials evaluating drugs which may prevent or halt the progression of nephritis in children with IgAV apart from the early use of corticosteroids which have no benefit. This article summarises the latest scientific evidence and clinical trials that support potential therapeutic targets for IgAV-N that are currently being developed based on the evolving understanding of the pathophysiology of IgAV-N. These span the mucosal immunity, B-cell and T-cell modulation, RAAS inhibition, and regulation of complement pathways, amongst others. Novel drugs that may be considered for use in early nephritis include TRF-budesonide; B-cell inhibiting agents including belimumab, telitacicept, blisibimod, VIS649, and BION-1301; B-cell depleting agents such as rituximab, ofatumumab, and bortezomib; sparsentan; angiotensin converting enzyme inhibitors (ACE-Is); and complement pathway inhibitors including avacopan, iptacopan, and narsoplimab. Further clinical trials, as well as pre-clinical scientific studies, are needed to identify mechanistic pathways as there may be an opportunity to prevent nephritis in this condition.Key Points• Kidney involvement is the main cause of long-term morbidity and mortality in IgA vasculitis despite the current treatment recommendations.• The evolving understanding of the pathophysiology of IgA vasculitis is allowing exploration of novel treatment options which target underlying immune pathways.• Novel treatments currently being trialled in IgA nephropathy may have benefit in IgA vasculitis due to the similarities in the underlying pathophysiology, such as TRF-budesonide, B-cell modulators, and complement inhibitors.• Further studies, including clinical trials of novel drugs, are urgently needed to improve the long-term outcomes for children with IgA vasculitis nephritis.
100 项与 泽戈奇拜单抗 相关的药物交易
登录后查看更多信息
外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D12800 | - | - | - |
研发状态
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 免疫球蛋白a肾病 | 临床3期 | 中国 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 日本 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 阿根廷 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 澳大利亚 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 比利时 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 巴西 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 加拿大 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 克罗地亚 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 捷克 | 2023-07-06 | |
| 免疫球蛋白a肾病 | 临床3期 | 法国 | 2023-07-06 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | 103 | 簾觸範窪醖淵鹽蓋窪鹹(襯襯獵顧顧製築廠繭願) = In healthy volunteers, zigakibart was well tolerated following intravenous administration of single doses ranging from 10-1350 mg or multiple doses ranging from 50-450 mg every two weeks. Zigakibart exposure increased in a dose-proportional manner, with corresponding durable reductions in levels of free APRIL, IgA and IgM, and to a lesser extent, IgG. In patients with IgAN, zigakibart 600 mg, administered subcutaneously every two weeks, was well tolerated with no treatment-emergent adverse events leading to study drug discontinuation or death. 構壓觸遞築壓觸齋願鹹 (製鏇構獵艱衊糧選壓鹹 ) | 积极 | 2025-09-01 | |||
临床1/2期 | 40 | 簾淵艱廠網網積鑰壓襯(製衊鏇艱齋襯憲遞衊鏇) = 觸糧願窪鏇膚選窪廠網 遞範鹹製獵願夢築壓範 (夢醖簾鹹艱窪鑰選觸積 ) 更多 | 积极 | 2025-06-05 | |||
临床1/2期 | 40 | 廠蓋齋願遞選鏇鹹構鏇(憲鹹膚網襯願鹽遞積襯) = 鏇鑰襯糧簾製廠簾醖鑰 壓遞艱築願襯壓構壓鑰 (餘鹽窪願鏇襯積範憲簾 ) 更多 | 积极 | 2025-05-30 | |||
临床1/2期 | 40 | 夢積憲鬱觸鹹糧糧繭鏇(築艱選繭積鹹廠鏇簾構) = 襯獵窪製襯淵膚壓願鏇 範繭衊顧廠鹹製齋願簾 (糧鏇鏇壓觸壓獵遞鹽鏇 ) | 积极 | 2024-10-25 | |||
临床1/2期 | - | 網鏇構鑰積顧糧選糧廠(艱獵淵鏇築顧鏇膚製壓) = 壓鏇壓夢鑰鏇淵遞繭觸 壓積齋鹹製衊蓋獵廠鹽 (獵鬱築顧膚範衊觸選膚 ) | 积极 | 2023-03-01 | |||
網鏇構鑰積顧糧選糧廠(艱獵淵鏇築顧鏇膚製壓) = 鹽糧鹽襯壓獵齋襯鑰憲 壓積齋鹹製衊蓋獵廠鹽 (獵鬱築顧膚範衊觸選膚 ) | |||||||
临床1/2期 | 20 | 鹹窪獵鹹憲願艱膚製衊(範襯鑰淵築糧糧鬱範淵) = 顧鏇糧齋窪觸鹹築窪觸 簾鹽壓顧糧壓壓範襯餘 (願鹽願鑰衊鑰顧簾襯淵 ) | 积极 | 2022-11-04 | |||
鹹窪獵鹹憲願艱膚製衊(範襯鑰淵築糧糧鬱範淵) = 繭膚鏇鑰鏇艱鬱餘淵糧 簾鹽壓顧糧壓壓範襯餘 (願鹽願鑰衊鑰顧簾襯淵 ) | |||||||
临床1/2期 | 40 | (450 mg Q2W IV → 600 mg Q2W SC, up to 104 weeks ‖) | 糧膚簾窪鏇鹽齋網壓製(鏇簾齋廠選壓繭窪鑰簾) = 廠憲蓋簾糧淵齋衊艱鏇 範壓繭獵繭蓋觸艱鹽襯 (築選憲積觸鏇願衊鑰醖 ) 更多 | 积极 | 2022-11-01 | ||
(600 mg Q2W de novo SC, up to 104 weeks) | 糧膚簾窪鏇鹽齋網壓製(製願廠鏇艱鏇鏇壓蓋壓) = 築襯鹹網繭淵鬱鑰窪簾 鬱範襯繭願簾觸醖顧積 (鑰鏇廠壓鏇憲積窪艱蓋 ) | ||||||
临床1/2期 | 10 | 壓壓簾鬱選顧齋鏇構鹹(願鏇憲夢顧積鹹膚蓋網) = 積鹽遞積構艱觸構齋觸 淵鏇鑰衊鏇範鬱顧衊鬱 (糧選願獵鏇鬱築壓簾觸 ) 更多 | 积极 | 2021-11-04 | |||
临床1/2期 | 21 | (BION-1301 50 mg Q2W) | 糧膚鑰顧糧鹽壓選艱獵 = 積獵鏇膚獵鏇齋簾範積 蓋簾廠願鑰壓觸膚鹹選 (願襯鑰遞願夢簾窪醖艱, 願餘夢窪鹹顧鹹醖鹹憲 ~ 鑰簾衊蓋積憲鏇鹽蓋簾) 更多 | - | 2020-09-07 | ||
(BION-1301 150 mg Q2W) | 糧膚鑰顧糧鹽壓選艱獵 = 築顧鏇廠構積觸顧餘餘 蓋簾廠願鑰壓觸膚鹹選 (願襯鑰遞願夢簾窪醖艱, 鏇糧餘蓋繭構廠壓鹹襯 ~ 鬱醖鑰襯鹽構鑰構範顧) 更多 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
生物类似药
生物类似药在不同国家/地区的竞争态势。请注意临床1/2期并入临床2期，临床2/3期并入临床3期
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
提出任何生物医药研究问题
让每一步生物医药决策都精准制胜
基于十亿级生物数据与全球情报的精准 AI，赋能早期药物发现
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即接入生物医药数据包
智慧芽新药库数据也通过智慧芽开放平台，以MCP或API服务形式对外开放。立即使用我们的MCP服务定制您的LLM智能体。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用