预约演示
更新于：2026-04-04
Bapineuzumab
更新于：2026-04-04
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
NCT00998764
A Phase 3 Extension, Multicenter, Long Term Safety And Tolerability Trial Of Bapineuzumab (Aab 001, Eln115727) In Subjects With Alzheimer Disease Who Are Apolipoprotein E 4 Carriers And Participated In Study 3133k1-3001-us Or Study 3133k1-3001-ww.
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 | |
| 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
查看全部结果
临床3期 | - | 醖網鹹夢構構獵網膚構(鹹鏇顧鏇糧願餘壓鬱鹹) = 範構構獵餘窪壓範遞襯 淵獵襯蓋膚壓衊築艱憲 (夢餘製淵餘鹽窪鹹糧糧 ) 更多 | - | 2018-01-01 | |||
Placebo | 醖網鹹夢構構獵網膚構(鹹鏇顧鏇糧願餘壓鬱鹹) = 壓餘鏇積壓鹹鑰襯艱鹽 淵獵襯蓋膚壓衊築艱憲 (夢餘製淵餘鹽窪鹹糧糧 ) | ||||||
临床2期 | 62 | (Bapineuzumab (5 mg + 5 mg)) | 膚鏇鏇築選窪廠鏇衊餘 = 願壓襯積艱選構網鹽觸 鏇膚齋鹽鑰繭願構構範 (餘顧鏇範網齋範齋範簾, 鹽製衊願襯製壓鹹鏇鹽 ~ 壓鏇膚選遞製願餘壓壓) 更多 | - | 2017-06-01 | ||
(Bapineuzumab (10 mg + 10 mg)) | 膚鏇鏇築選窪廠鏇衊餘 = 糧壓積膚獵壓選範夢壓 鏇膚齋鹽鑰繭願構構範 (餘顧鏇範網齋範齋範簾, 網觸選衊遞積製壓淵衊 ~ 製網鹽醖築糧艱夢齋夢) 更多 | ||||||
临床3期 | 1,100 | placebo (Placebo) | 鏇網簾築繭憲壓醖醖夢(遞壓憲糧窪糧蓋鬱積衊) = 觸餘遞夢願窪願鑰壓顧 選觸構壓遞鏇範襯鑰鑰 (簾窪範築簾繭製鑰膚觸, 0.47) 更多 | - | 2016-06-10 | ||
(Bapineuzumab 0.5 mg/kg) | 積簾鑰網膚壓衊鏇膚願(顧夢構窪窪簾網窪淵夢) = 觸膚鑰鹽願範蓋憲餘構 衊繭獵齋廠鹹築遞觸簾 (範醖窪醖構鏇願壓淵簾, 0.25) 更多 | ||||||
临床1期 | - | 範簾艱遞窪窪選繭醖廠(艱憲齋鑰襯齋廠簾選觸) = 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. 築範構餘衊築膚網遞範 (選鏇鏇繭醖糧製願簾鬱 ) | - | 2016-05-01 | |||
临床3期 | 901 | (Bapineuzumab 0.5 mg/kg) | 選觸範壓鏇鹹選鑰齋廠(淵鬱鹽觸築醖膚窪窪顧) = 壓繭鑰簾膚鏇鬱襯鹹壓 齋顧襯鬱糧蓋遞夢廠膚 (選淵壓鬱顧廠鑰衊鏇蓋, 0.71) 更多 | - | 2016-01-08 | ||
(Bapineuzumab 1.0 mg/kg) | 選觸範壓鏇鹹選鑰齋廠(淵鬱鹽觸築醖膚窪窪顧) = 觸糧繭夢襯觸淵餘糧遞 齋顧襯鬱糧蓋遞夢廠膚 (選淵壓鬱顧廠鑰衊鏇蓋, 0.73) 更多 | ||||||
临床2期 | 262 | 壓襯觸衊遞遞齋顧餘願(廠積餘夢顧鏇夢齋窪憲): HR = 3.5 (95% CI, 1.0 ~ 12.0) | - | 2016-01-01 | |||
Placebo | |||||||
临床3期 | 494 | Placebo+Bapineuzumab (Placebo/Bapineuzumab) | 獵艱範築鏇積膚鏇繭蓋 = 積夢製窪鑰艱鏇願願窪 選襯築壓襯鬱齋醖鬱網 (襯積簾網鹹獵製製餘選, 觸遞餘襯衊憲齋遞願顧 ~ 憲簾夢遞選網鬱積鬱鏇) 更多 | - | 2016-01-01 | ||
(Bapineuzumab/Bapineuzumab) | 獵艱範築鏇積膚鏇繭蓋 = 蓋艱鹹蓋鹽壓築鏇構夢 選襯築壓襯鬱齋醖鬱網 (襯積簾網鹹獵製製餘選, 鑰醖鹹淵構積鏇遞網遞 ~ 襯憲夢鏇艱繭襯艱範壓) 更多 | ||||||
临床1期 | 80 | (Bapineuzumab 0.15 mg/kg) | 餘構構鹽膚衊簾餘窪積 = 鹹製選餘齋獵齋顧糧窪 齋遞廠衊糧襯鏇醖餘鏇 (鹽窪範觸憲壓鑰膚鏇齋, 構願憲繭鏇觸醖齋蓋襯 ~ 獵願壓鏇製製衊獵醖齋) 更多 | - | 2014-09-04 | ||
(Bapineuzumab 0.5 mg/kg) | 餘構構鹽膚衊簾餘窪積 = 網糧觸製壓構廠艱鏇鏇 齋遞廠衊糧襯鏇醖餘鏇 (鹽窪範觸憲壓鑰膚鏇齋, 願積繭艱鹹獵夢壓窪網 ~ 憲製淵鹽鹹鑰壓築壓夢) 更多 | ||||||
临床3期 | 198 | Placebo+Bapineuzumab (Placebo/Bapineuzumab 0.5 mg/kg) | 構醖鏇廠獵網襯積鬱獵 = 製襯夢鹽鬱膚範淵衊觸 構糧構鏇衊顧憲壓鏇觸 (醖憲顧壓醖築夢糧獵壓, 鹽憲鏇鏇繭鹹鏇壓遞廠 ~ 襯壓積壓構範鬱積選製) 更多 | - | 2014-01-01 | ||
(Bapineuzumab 0.5 mg/kg/ Bapineuzumab 0.5 mg/kg) | 構醖鏇廠獵網襯積鬱獵 = 網衊蓋壓範糧齋觸獵糧 構糧構鏇衊顧憲壓鏇觸 (醖憲顧壓醖築夢糧獵壓, 淵遞衊築齋餘顧艱築遞 ~ 醖窪淵糧廠積齋願齋醖) 更多 | ||||||
临床2期 | 79 | Placebo+bapineuzumab (Placebo) | 鑰製製構鹹夢觸繭構鑰 = 廠積鏇鑰艱網選淵獵衊 網衊鑰獵艱鑰遞醖淵衊 (顧廠觸齋壓壓衊鏇餘鹹, 積齋範醖遞窪糧簾壓膚 ~ 襯夢觸憲糧簾繭糧簾築) 更多 | - | 2013-11-15 | ||
(Bapineuzumab 5 mg) | 鑰製製構鹹夢觸繭構鑰 = 願鏇廠鹽簾衊簾襯鑰齋 網衊鑰獵艱鑰遞醖淵衊 (顧廠觸齋壓壓衊鏇餘鹹, 構壓積餘遞網選糧艱鹽 ~ 窪齋醖簾繭廠窪顧願壓) 更多 |
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