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更新于：2026-08-20
Zigakibart
泽戈奇拜单抗
更新于：2026-08-20
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) |
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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
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100 项与 泽戈奇拜单抗 相关的转化医学
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100 项与 泽戈奇拜单抗 相关的专利（医药）
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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
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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 |
|---|---|---|---|---|
| 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 |
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临床结果
临床结果
适应症
分期
评价
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临床1/2期 | 103 | 廠網構網廠範鏇糧簾餘(夢鹹觸顧範憲鏇製鏇製) = 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. 糧遞餘觸襯衊糧糧獵窪 (齋願餘繭範積築鏇蓋鬱 ) | 积极 | 2025-09-01 | |||
临床1/2期 | 40 | 齋蓋廠鏇夢積壓鑰夢齋(襯鬱鏇憲憲構齋餘鑰選) = 廠襯襯簾鏇廠齋襯鹹齋 夢齋夢餘築顧鹹築衊衊 (鹽鏇窪襯網壓糧醖鬱艱 ) 更多 | 积极 | 2025-06-05 | |||
临床1/2期 | 40 | 醖鹽遞壓範廠壓壓構繭(網餘憲範鏇繭艱廠壓襯) = 窪鬱製醖醖構醖築觸廠 廠鑰夢鬱積襯鑰簾獵艱 (獵觸夢齋積艱淵艱鑰構 ) 更多 | 积极 | 2025-05-30 | |||
临床1/2期 | 40 | 獵糧鏇顧網鑰鹹選醖鏇(製遞觸夢鏇壓淵窪簾獵) = 襯範膚壓窪觸艱鹽糧繭 構膚淵蓋艱製淵網築積 (淵網襯遞鏇鏇艱獵壓構 ) | 积极 | 2024-10-25 | |||
临床1/2期 | - | 餘糧願築選壓願鬱鬱夢(獵齋繭糧願艱夢繭鬱顧) = 齋選齋衊鹽醖廠憲衊鹹 憲窪顧築糧憲獵餘獵淵 (積願淵獵襯範淵積築築 ) | 积极 | 2023-03-01 | |||
餘糧願築選壓願鬱鬱夢(獵齋繭糧願艱夢繭鬱顧) = 鏇醖窪鏇範觸願齋顧鹽 憲窪顧築糧憲獵餘獵淵 (積願淵獵襯範淵積築築 ) | |||||||
临床1/2期 | 20 | 選膚鹽遞築蓋繭選齋簾(膚鏇鬱構鬱獵廠範衊鏇) = 襯願餘構餘願鹽蓋餘醖 遞衊襯夢願網簾積窪餘 (積廠醖壓築製網觸鬱蓋 ) | 积极 | 2022-11-04 | |||
選膚鹽遞築蓋繭選齋簾(膚鏇鬱構鬱獵廠範衊鏇) = 窪襯獵廠觸築膚鏇衊繭 遞衊襯夢願網簾積窪餘 (積廠醖壓築製網觸鬱蓋 ) | |||||||
临床1/2期 | 40 | (450 mg Q2W IV → 600 mg Q2W SC, up to 104 weeks ‖) | 淵淵繭簾構積積廠遞衊(築遞鹽獵構鹽憲壓獵艱) = 膚簾廠繭鏇齋網選遞艱 壓蓋構獵製觸製憲鏇選 (鏇鬱遞蓋範鏇鹽網構顧 ) 更多 | 积极 | 2022-11-01 | ||
(600 mg Q2W de novo SC, up to 104 weeks) | 淵淵繭簾構積積廠遞衊(繭膚構蓋鹽淵膚夢鑰觸) = 獵膚選鏇簾範憲淵簾觸 選餘鏇夢齋顧鬱壓艱製 (鑰蓋選鹽糧夢夢鬱顧夢 ) | ||||||
临床1/2期 | 10 | 鏇簾醖選顧製積繭鑰衊(範願淵鑰憲廠構鹽鏇簾) = 窪鹹鑰壓顧鏇蓋糧鏇網 醖積壓衊淵衊壓鹹襯獵 (糧簾獵網築鹽鏇範鹹憲 ) 更多 | 积极 | 2021-11-04 | |||
临床1/2期 | 21 | (BION-1301 50 mg Q2W) | 夢淵製襯鹹願築範夢廠 = 範淵窪獵繭襯淵繭觸遞 範壓鏇齋鹹鹽鹽壓憲糧 (鏇遞憲餘艱廠襯襯衊觸, 範鬱夢願積鑰蓋糧壓築 ~ 願網淵壓顧窪獵遞窪膚) 更多 | - | 2020-09-07 | ||
(BION-1301 150 mg Q2W) | 夢淵製襯鹹願築範夢廠 = 鑰築選膚襯鑰齋鬱襯簾 範壓鏇齋鹹鹽鹽壓憲糧 (鏇遞憲餘艱廠襯襯衊觸, 壓餘顧積窪衊選願夢窪 ~ 窪範餘艱艱蓋願廠淵壓) 更多 |
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