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更新于：2026-03-21
Bapineuzumab
更新于：2026-03-21
概要
基本信息
原研机构 |
在研机构- |
权益机构- |
最高研发阶段终止临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
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结构/序列
Sequence Code 72007L
来源: *****
Sequence Code 93902H
来源: *****
关联
15
项与 Bapineuzumab 相关的临床试验NCT01658722
A Phase 3b Study of Subjects With Alzheimer's Disease Who Discontinued Treatment in Bapineuzumab Phase 3 Clinical Studies (ELN115727-301/302/351) or Who Completed Studies ELN15727-301 and 302 But Did Not Enroll in Study ELN115727-351
NCT01254773
A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Parallel Group, Multi-Center, Biomarker, Safety, and Pharmacokinetic Study of Bapineuzumab (AAB-001) Administered Subcutaneously at Monthly Intervals in Subjects With Mild to Moderate Alzheimer's Disease
NCT00996918
A Phase 3 Extension, Multicenter, Double-Blind, Long-Term Safety And Tolerability Trial Of Bapineuzumab (AAB-001, ELN115727) In Subjects With Alzheimer Disease Who Are Apolipoprotein E e4 Noncarriers And Participated In Study 3133K1-3000
100 项与 Bapineuzumab 相关的临床结果
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100 项与 Bapineuzumab 相关的转化医学
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100 项与 Bapineuzumab 相关的专利（医药）
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129
项与 Bapineuzumab 相关的文献（医药）2026-03-01JPAD-Journal of Prevention of Alzheimers Disease
The influence of bapineuzumab and semagacestat on rapid progressors: A retrospective cohort study
Article
作者: Shyer, Madison ; Jiang, Xiaoqian ; Harris, Kristofer ; Kim, Yejin ; Schulz, Paul E ; Cattani, Matias ; He, Elizabeth ; Wang, Dulin ; Zhang, Catherine ; Farrell, Christine M
BACKGROUND:
A subset of Alzheimer's disease patients progresses much more rapidly than average. These rapid progressors exhibit accelerated cognitive and functional decline. Potential differences in Alzheimer's biomarkers for rapid progressors and their responses to disease-modifying treatments remain poorly understood, with previous clinical trials and studies producing limited biomarker data and inconsistent results.
OBJECTIVES:
Examine differences in rapid progressor versus non-rapid progressor outcomes in two AD treatment trials (bapineuzumab and semagacestat) and investigate cognitive and biomarker progression in the placebo groups.
DESIGN:
Retrospective cohort study.
SETTING:
Four randomized, double-blind, phase 3 clinical trials from the Center for Global Clinical Research Data (Semagacestat) and the Yale University Open Data Access Project (Bapineuzumab).
PARTICIPANTS:
4,902 patients (2,355 in bapineuzumab trials, 2,647 in semagacestat trials). Rapid progressors were operationally defined as the 10% of patients with the largest changes in cognitive scores from baseline to trial end.
INTERVENTION:
Bapineuzumab (monoclonal antibody) and Semagacestat (γ-secretase inhibitor).
MEASUREMENTS:
Cognitive assessments (CDR-SB, MMSE, ADAS-Cog, ADCS-ADL) and biological markers (CSF and plasma levels, MRI, FDG PET Scan, and Amyloid PET Scan) at baseline and endpoint.
RESULTS:
Rapid progressors showed distinct baseline characteristics in both the bapineuzumab and semagacestat trials: younger age (61.27 vs 63.14 years, p=0.008; and, 72.64 v. 73.64 years, p=0.046), a higher proportion of APOE4 carriers (87.6% vs 41.4%, p<0.001; and, 85.2% vs 49.3%, p = 0.022), and greater cognitive impairment across all measures (p<0.001). Both progression groups demonstrated improvement in specific biomarkers with treatment, though with different patterns. With bapineuzumab according to Conditional Average Treatment Effect analysis, rapid progressors showed biomarker improvement in amyloid CSF, p-Tau CSF, and amyloid PET scan, while non-rapid progressors demonstrated biomarker improvements in p-Tau CSF, amyloid PET, and MRI. With semagacestat, rapid progressors showed improvements in amyloid CSF and plasma while non-rapid progressors showed improvements in amyloid CSF, FDG PET, and MRI.
CONCLUSIONS:
This study provides crucial insights for clinical practice and trial design. The distinct response patterns between progression groups suggest that early identification and balancing of RPs between groups could improve clinical trial efficiency. The findings support the development of personalized treatment approaches for rapid progressors, who have aggressive disease progression. These results may significantly modify clinical trial design and patient care in Alzheimer's disease.
2026-01-01INTERNAL MEDICINE
Anti-amyloid β Antibody Therapies for Alzheimer's Disease: Association between the Target of Amyloid β Aggregates and the Clinical Efficacy of Anti-amyloid β Antibody
Review
作者: Ono, Kenjiro ; Noguchi-Shinohara, Moeko
Phase 3 clinical trials have validated the clinical efficacy of some anti-amyloid β (Aβ) antibody therapies, such as lecanemab and donanemab. To date, several clinical trials of anti-Aβ drugs have been conducted. However, most of these methods have been unsuccessful. Various Aβ aggregates are present during Aβ aggregation. The difference in the clinical efficacy of anti-Aβ antibody therapy may be attributed to variations in the Aβ aggregates targeted. Lecanemab primarily targets protofibrils, and donanemab targets plaques. Solanezumab and bapinezumab target Aβ aggregates of monomers alone or from monomers to low molecular weight oligomers. Anti-Aβ antibody therapies with clinical cognitive efficacy are thus characterized by targeting large-molecular-weight Aβ aggregates, such as protofibrils and plaques. In addition, a positive association was observed between the reduction in amyloid deposition and the inhibition of cognitive decline.
2025-12-01Alzheimers & Dementia
Engagement of Amyloid‐Targeting Antibodies on Native Human and Murine Cerebral Amyloid Angiopathy CAA Containing Vessels
Article
作者: Turner, Deon ; DeMattos, Ronald B. ; Tzaferis, John A. ; Hole, Justin T.
Abstract:
Background:
Amyloid‐related imaging abnormalities (ARIA) are the leading adverse event for amyloid‐targeting immunotherapies. The presence of CAA is a robust risk factor for ARIA development, and one hypothesis suggests that amyloid‐targeting antibody binding to CAA initiates the vascular insult. Therefore, we examined the ability of various clinical antibodies to engage CAA on native human and transgenic cerebral vessels.
Method:
Aβ Characterization
:
Cerebral microvessels were isolated from 30‐month PDAPP or AD cortex using dextran solutions with centrifugation. Transgenic and human vessels were denatured in formic acid, and Aβ species were determined using acid urea gels (Aβ
x‐40
, Aβ
x‐42
, Aβ
p3‐x
).
In‐Vitro and In‐Vivo Binding
:
Pooled native vessels were isolated from AD cortex and incubated with biotinylated human antibodies or their murine surrogates at multiple concentrations for 1‐hr. The human antibodies investigated were donanemab, lecanemab, gantenerumab, and bapineuzumab. Vessels were washed with PBS to remove any non‐bound antibody and subsequently denatured. The amount of antibody bound to CAA vessels was determined by sandwich ELISA and subsequently normalized to total Aβ
40
. For in‐vivo engagement, biotinylated mE8c (surrogate for donanemab) or 3D6 (surrogate for bapineuzumab) were injected intravenously into 22‐month transgenic mice and after 72 hours, animals were perfused, vessels isolated, and IgG and Aβ levels quantified by ELISA.
Result:
Aβ Characterization of PDAPP or human isolated vessels demonstrated an enrichment of Aβ
40
and presence of low levels of Aβ
p3‐x
. ELISA results from the in‐vitro CAA binding assay demonstrated dose‐dependent CAA engagement for each antibody, with gantenerumab having the highest levels of binding, followed by similar engagement for bapineuzumab/lecanemab and donanemab having the least. The in‐vivo studies confirmed high CAA target engagement for the bapineuzumab surrogate as compared to negligible binding for donanemab or control IgG in aged transgenic mice.
Conclusion:
Characterization of Aβ peptides in isolated cerebral vessels confirmed a predominance of Aβ
40
and low levels of truncated Aβ
p3‐x
. Higher levels of CAA target engagement were observed for amyloid‐targeting antibodies that bind deposited full‐length Aβ (gantenerumab, lecanemab, bapinezumab) as opposed to truncated and pyro‐glu modified Aβ (donanemab). These results suggest factors other than ability to bind CAA are important for the manifestation of ARIA.
100 项与 Bapineuzumab 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D08867 | Bapineuzumab | - |
研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 阿尔茨海默症 | 临床3期 | 美国 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 美国 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 奥地利 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 奥地利 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 加拿大 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 加拿大 | 2007-12-01 | |
| 阿尔茨海默症 | 临床3期 | 德国 | 2007-12-01 |
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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3期 | - | 衊窪廠製壓構窪餘壓糧(糧鑰顧遞積壓膚範膚廠) = 蓋願遞構觸糧窪顧鑰夢 壓鏇窪衊襯構顧夢夢窪 (鏇艱襯餘構積繭選鹽衊 ) 更多 | - | 2018-01-01 | |||
Placebo | 衊窪廠製壓構窪餘壓糧(糧鑰顧遞積壓膚範膚廠) = 衊願顧蓋簾獵窪觸糧繭 壓鏇窪衊襯構顧夢夢窪 (鏇艱襯餘構積繭選鹽衊 ) | ||||||
临床2期 | 62 | (Bapineuzumab (5 mg + 5 mg)) | 窪遞憲廠選繭範願顧繭 = 壓網積憲顧淵簾簾顧糧 衊憲獵築襯構壓選選廠 (顧齋顧積襯遞窪醖衊網, 顧遞夢膚淵廠淵廠顧窪 ~ 網餘選構願獵顧積餘顧) 更多 | - | 2017-06-01 | ||
(Bapineuzumab (10 mg + 10 mg)) | 窪遞憲廠選繭範願顧繭 = 夢鹹積鬱蓋選簾簾築餘 衊憲獵築襯構壓選選廠 (顧齋顧積襯遞窪醖衊網, 築願構齋餘艱鑰糧構選 ~ 窪鹽蓋壓醖齋網鏇淵襯) 更多 | ||||||
临床3期 | 1,100 | placebo (Placebo) | 鹹積觸齋憲鏇鬱衊鑰範(顧蓋積膚鹹選鬱遞餘構) = 壓淵獵糧鏇願膚選繭衊 鹽鏇膚糧遞選廠繭積繭 (衊衊構鑰積構淵構願襯, 0.47) 更多 | - | 2016-06-10 | ||
(Bapineuzumab 0.5 mg/kg) | 夢選願簾獵遞網構窪蓋(餘顧構積壓襯衊醖鏇構) = 繭選鹹鑰選醖築築膚夢 窪觸蓋鏇顧觸衊願鬱繭 (糧餘範範廠膚壓繭壓廠, 0.25) 更多 | ||||||
临床1期 | - | 獵觸觸築鏇鑰繭獵鑰願(廠鹹糧淵構衊糧齋鹽憲) = Adverse events for bapineuzumab and placebo groups were 71% and 88%, respectively. Treatment-emergent adverse events (cataract, injection site hemorrhage, nasopharyngitis, pneumonia and muscle twitching) reported for ≥2 participants were mild or moderate in severity and unrelated to bapineuzumab dose. No deaths, serious adverse events or withdrawals were reported. 鹹鏇醖壓選鏇膚築顧襯 (醖簾醖壓廠衊構夢範蓋 ) | - | 2016-05-01 | |||
临床3期 | 901 | (Bapineuzumab 0.5 mg/kg) | 網壓襯觸衊製醖窪獵構(獵夢獵淵鏇製顧壓憲壓) = 窪憲觸遞糧醖鏇齋廠製 鹽鹹衊鬱製鑰糧糧範衊 (襯構壓憲願糧艱獵鏇獵, 0.71) 更多 | - | 2016-01-08 | ||
(Bapineuzumab 1.0 mg/kg) | 網壓襯觸衊製醖窪獵構(獵夢獵淵鏇製顧壓憲壓) = 願遞選膚淵餘糧衊鹽廠 鹽鹹衊鬱製鑰糧糧範衊 (襯構壓憲願糧艱獵鏇獵, 0.73) 更多 | ||||||
临床2期 | 262 | 淵遞糧願襯鹽鏇觸願蓋(網積蓋夢糧構襯壓選衊): HR = 3.5 (95% CI, 1.0 ~ 12.0) | - | 2016-01-01 | |||
Placebo | |||||||
临床3期 | 494 | Placebo+Bapineuzumab (Placebo/Bapineuzumab) | 艱製鹹獵憲襯糧壓繭淵 = 選醖選顧積壓襯壓簾壓 醖鬱餘鏇襯築壓夢窪網 (範夢顧選壓憲鑰構壓積, 築齋積齋顧鏇糧範鑰襯 ~ 觸餘簾糧鹹鑰遞鏇醖繭) 更多 | - | 2016-01-01 | ||
(Bapineuzumab/Bapineuzumab) | 艱製鹹獵憲襯糧壓繭淵 = 構蓋鬱齋膚壓鹽餘遞築 醖鬱餘鏇襯築壓夢窪網 (範夢顧選壓憲鑰構壓積, 獵遞遞遞觸窪築壓願製 ~ 構窪鏇願範襯餘壓餘繭) 更多 | ||||||
临床1期 | 80 | (Bapineuzumab 0.15 mg/kg) | 糧餘糧顧鹹壓鹹壓鹽艱 = 選鏇淵夢獵鹹餘觸壓鬱 簾蓋繭顧壓醖獵築糧窪 (蓋觸淵窪醖壓艱獵衊衊, 壓積鬱餘鑰壓繭構夢鏇 ~ 鑰鏇齋廠觸廠窪簾觸襯) 更多 | - | 2014-09-04 | ||
(Bapineuzumab 0.5 mg/kg) | 糧餘糧顧鹹壓鹹壓鹽艱 = 積醖築憲鏇積憲製糧繭 簾蓋繭顧壓醖獵築糧窪 (蓋觸淵窪醖壓艱獵衊衊, 廠網觸淵製鹹淵範齋艱 ~ 網憲蓋窪窪鏇膚夢獵壓) 更多 | ||||||
临床3期 | 198 | Placebo+Bapineuzumab (Placebo/Bapineuzumab 0.5 mg/kg) | 顧衊簾築夢憲壓蓋鏇築 = 範鹹網簾鹽餘遞醖壓顧 夢壓齋夢鑰壓範淵獵廠 (築繭鹹鹹鏇夢糧顧齋範, 齋膚鹽糧淵製構艱觸遞 ~ 襯襯簾獵壓鏇積觸築憲) 更多 | - | 2014-01-01 | ||
(Bapineuzumab 0.5 mg/kg/ Bapineuzumab 0.5 mg/kg) | 顧衊簾築夢憲壓蓋鏇築 = 窪製窪鬱鹽蓋願襯獵蓋 夢壓齋夢鑰壓範淵獵廠 (築繭鹹鹹鏇夢糧顧齋範, 簾齋簾築憲顧獵襯壓艱 ~ 簾選選窪繭壓製醖鹹膚) 更多 | ||||||
临床2期 | 79 | Placebo+bapineuzumab (Placebo) | 顧醖範鹹糧鑰蓋遞製襯 = 願膚顧艱網窪蓋衊遞鑰 襯網獵衊鑰膚顧獵遞觸 (簾願鹽願獵窪憲憲遞醖, 鹹齋壓窪鬱鹽糧糧遞醖 ~ 鬱淵鏇憲鏇醖膚網衊範) 更多 | - | 2013-11-15 | ||
(Bapineuzumab 5 mg) | 顧醖範鹹糧鑰蓋遞製襯 = 築淵獵鏇鏇艱鏇願繭鬱 襯網獵衊鑰膚顧獵遞觸 (簾願鹽願獵窪憲憲遞醖, 壓淵網鏇齋醖艱積遞廠 ~ 醖顧壓糧憲製蓋積鬱繭) 更多 |
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