구조모아 (StructureMoa)항암 chemical structure spider web
방문프로그램 상세에서 관심 등록 후 2개 이상 모으면 여기서 한 번에 비교할 수 있습니다.
표가 넓으면 좌우로 스크롤하세요. 핵심 비교 모드에서는 중요 항목만 표시됩니다.
| 항목 | lecanemab (Leqembi, BAN2401, lecanemab-irmb) Eisai / Biogen·Amyloid-beta protofibrils 37 trials·t½ ~5–7 days | donanemab (Kisunla, LY3002813, donanemab-azbt) Eli Lilly·N3pG amyloid-beta plaque 21 trials·t½ ~12 days |
|---|---|---|
Overview Program | Leqembi (lecanemab) | Kisunla (donanemab) |
Overview Company | Eisai / Biogen | Eli Lilly |
Overview Modality | ANTIBODY | ANTIBODY |
Overview Target | Amyloid-beta protofibrils | N3pG amyloid-beta plaque |
Overview Indication | Early symptomatic Alzheimer's disease (MCI or mild dementia) with confirmed amyloid pathology | Early symptomatic Alzheimer's disease with confirmed amyloid pathology |
Overview Phase | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED |
Overview Content status | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved |
Positioning Key differentiator | Protofibril selectivity targets the species most closely tied to synaptic toxicity, with lower ARIA-E rates than plaque-directed antibodies at comparable clearance. | Plaque-only specificity permits aggressive clearance and pre-specified treatment discontinuation once amyloid PET turns negative. |
Positioning Known limitation | Amyloid clearance does not fully arrest tau pathology, so clinical benefit is partial rather than disease-arresting. | High baseline tau burden limits clinical benefit despite full plaque clearance. |
Positioning Development positioning | Head-to-head with Kisunla; differs on titration, dosing interval, and stopping rules. | Monthly dosing and a finite course versus Leqembi's biweekly, open-ended schedule. |
MoA Mechanism | Binds soluble amyloid-beta protofibrils and promotes microglial clearance of aggregated amyloid, reducing plaque burden and downstream tau and neurodegeneration markers. | Binds the N3pG epitope present in deposited plaque and drives microglial phagocytic clearance, converting amyloid-PET-positive patients to negative within months. |
MoA Biomarker | Amyloid PET centiloid reduction, plasma p-tau181/217, CSF Aβ42/40 ratio. | Amyloid PET centiloid, plasma p-tau217; baseline tau PET stratifies benefit. |
PK/PD Half-life | ~5–7 days | ~12 days |
PK/PD Species | Amyloid PET SUVR, plasma p-tau217, CDR-SB and ADAS-Cog trajectory | Amyloid PET clearance rate, plasma p-tau217, iADRS/CDR-SB slope |
PK/PD Animal (cat.) | Human, In vitro | Human, In vitro |
PK/PD Experiment | pharmacodynamic | pharmacodynamic |
Toxicology Species | Mouse | Mouse |
Toxicology Major finding | Boxed warning for ARIA — amyloid-related imaging abnormalities with edema (ARIA-E) and microhemorrhage (ARIA-H). ApoE ε4 homozygotes carry the highest risk; concomitant anticoagulation raises hemorrhage concern. | Boxed warning for ARIA. Infusion-related reactions are common; the modified titration schedule was added to lower ARIA-E incidence. |
Toxicology CRS | N/A | N/A |
Clinical Safety signal | Boxed warning for ARIA — amyloid-related imaging abnormalities with edema (ARIA-E) and microhemorrhage (ARIA-H). ApoE ε4 homozygotes carry the highest risk; concomitant anticoagulation raises hemorrhage concern. | Boxed warning for ARIA. Infusion-related reactions are common; the modified titration schedule was added to lower ARIA-E incidence. |
Clinical Selected reported efficacy | 27% | 25.12% |
Clinical Result source | CLARITY AD (NCT03887455) | ClinicalTrials.gov NCT05738486 |
Clinical Program phase | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts |
Clinical Trial ref | NCT03887455 | NCT05738486 |
Preclinical Animal (cat.) | Mouse | Mouse |
프로그램 상세에서 관심 등록 후 2개 이상 모으면 여기서 한 번에 비교할 수 있습니다.
표가 넓으면 좌우로 스크롤하세요. 핵심 비교 모드에서는 중요 항목만 표시됩니다.
| 항목 | lecanemab (Leqembi, BAN2401, lecanemab-irmb) Eisai / Biogen·Amyloid-beta protofibrils 37 trials·t½ ~5–7 days | donanemab (Kisunla, LY3002813, donanemab-azbt) Eli Lilly·N3pG amyloid-beta plaque 21 trials·t½ ~12 days |
|---|---|---|
Overview Program | Leqembi (lecanemab) | Kisunla (donanemab) |
Overview Company | Eisai / Biogen | Eli Lilly |
Overview Modality | ANTIBODY | ANTIBODY |
Overview Target | Amyloid-beta protofibrils | N3pG amyloid-beta plaque |
Overview Indication | Early symptomatic Alzheimer's disease (MCI or mild dementia) with confirmed amyloid pathology | Early symptomatic Alzheimer's disease with confirmed amyloid pathology |
Overview Phase | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED |
Overview Content status | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved |
Positioning Key differentiator | Protofibril selectivity targets the species most closely tied to synaptic toxicity, with lower ARIA-E rates than plaque-directed antibodies at comparable clearance. | Plaque-only specificity permits aggressive clearance and pre-specified treatment discontinuation once amyloid PET turns negative. |
Positioning Known limitation | Amyloid clearance does not fully arrest tau pathology, so clinical benefit is partial rather than disease-arresting. | High baseline tau burden limits clinical benefit despite full plaque clearance. |
Positioning Development positioning | Head-to-head with Kisunla; differs on titration, dosing interval, and stopping rules. | Monthly dosing and a finite course versus Leqembi's biweekly, open-ended schedule. |
MoA Mechanism | Binds soluble amyloid-beta protofibrils and promotes microglial clearance of aggregated amyloid, reducing plaque burden and downstream tau and neurodegeneration markers. | Binds the N3pG epitope present in deposited plaque and drives microglial phagocytic clearance, converting amyloid-PET-positive patients to negative within months. |
MoA Biomarker | Amyloid PET centiloid reduction, plasma p-tau181/217, CSF Aβ42/40 ratio. | Amyloid PET centiloid, plasma p-tau217; baseline tau PET stratifies benefit. |
PK/PD Half-life | ~5–7 days | ~12 days |
PK/PD Species | Amyloid PET SUVR, plasma p-tau217, CDR-SB and ADAS-Cog trajectory | Amyloid PET clearance rate, plasma p-tau217, iADRS/CDR-SB slope |
PK/PD Animal (cat.) | Human, In vitro | Human, In vitro |
PK/PD Experiment | pharmacodynamic | pharmacodynamic |
Toxicology Species | Mouse | Mouse |
Toxicology Major finding | Boxed warning for ARIA — amyloid-related imaging abnormalities with edema (ARIA-E) and microhemorrhage (ARIA-H). ApoE ε4 homozygotes carry the highest risk; concomitant anticoagulation raises hemorrhage concern. | Boxed warning for ARIA. Infusion-related reactions are common; the modified titration schedule was added to lower ARIA-E incidence. |
Toxicology CRS | N/A | N/A |
Clinical Safety signal | Boxed warning for ARIA — amyloid-related imaging abnormalities with edema (ARIA-E) and microhemorrhage (ARIA-H). ApoE ε4 homozygotes carry the highest risk; concomitant anticoagulation raises hemorrhage concern. | Boxed warning for ARIA. Infusion-related reactions are common; the modified titration schedule was added to lower ARIA-E incidence. |
Clinical Selected reported efficacy | 27% | 25.12% |
Clinical Result source | CLARITY AD (NCT03887455) | ClinicalTrials.gov NCT05738486 |
Clinical Program phase | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts |
Clinical Trial ref | NCT03887455 | NCT05738486 |
Preclinical Animal (cat.) | Mouse | Mouse |
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