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타깃 · 모달리티 · 임상 근거 · 비임상 맥락으로 최대 5개 프로그램을 나란히 비교합니다. · 다음 갱신 D-5 · 마지막 9월 2일

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프로그램 상세에서 관심 등록 후 2개 이상 모으면 여기서 한 번에 비교할 수 있습니다.

API CSV30행 · 2개 프로그램

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항목
AntibodyCurated CoreFDAApproved
lecanemab (Leqembi, BAN2401, lecanemab-irmb)
Eisai / Biogen·Amyloid-beta protofibrils
37 trials·t½ ~5–7 days
AntibodyCurated CoreFDAApproved
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 / BiogenEli Lilly
Overview
Modality
ANTIBODYANTIBODY
Overview
Target
Amyloid-beta protofibrilsN3pG amyloid-beta plaque
Overview
Indication
Early symptomatic Alzheimer's disease (MCI or mild dementia) with confirmed amyloid pathologyEarly symptomatic Alzheimer's disease with confirmed amyloid pathology
Overview
Phase
APPROVEDAPPROVED
Overview
Status
APPROVEDAPPROVED
Overview
Content status
Curated CoreCurated Core
Overview
Data Confidence
Data Confidence · HighData Confidence · High
Overview
Development Signal
Development Signal · EstablishedDevelopment Signal · Established
Overview
Approval status
FDA approvedFDA 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 trajectoryAmyloid PET clearance rate, plasma p-tau217, iADRS/CDR-SB slope
PK/PD
Animal (cat.)
Human, In vitroHuman, In vitro
PK/PD
Experiment
pharmacodynamicpharmacodynamic
Toxicology
Species
MouseMouse
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/AN/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
APPROVEDAPPROVED
Clinical
Trial activity
No active/completed countsNo active/completed counts
Clinical
Trial ref
NCT03887455NCT05738486
Preclinical
Animal (cat.)
MouseMouse