What is the Difference Between Aducanumab and Lecanemab?
🆚 Go to Comparative Table 🆚Aducanumab and lecanemab are both monoclonal antibodies used for the treatment of Alzheimer's disease, but they target different versions of amyloid beta and have distinct mechanisms of action.
Aducanumab targets beta-amyloid, a protein that accumulates in the brain and is associated with the development of Alzheimer's. It works by removing beta-amyloid from the brain. On the other hand, lecanemab targets a different structure of beta-amyloid called N3pG, which is believed to play a key role in the formation of amyloid plaques in the brain. Lecanemab works by blocking the formation of amyloid plaques in the brain.
The main differences between aducanumab and lecanemab include:
- Mechanism of Action: Aducanumab removes beta-amyloid from the brain, while lecanemab blocks the formation of amyloid plaques in the brain.
- Target: Aducanumab targets beta-amyloid, while lecanemab targets the N3pG structure of beta-amyloid.
- Clinical Trial Results: Lecanemab has shown a consistent effect in clinical trials, with a lower incidence of ARIA (amyloid-related imaging abnormalities) compared to aducanumab. Aducanumab's clinical trial results were mixed, with only one of two identically designed trials showing a significant slowing of cognitive decline.
Further research is needed to determine the long-term safety and efficacy of these medications, and it is essential to consult with a healthcare provider to determine the best course of action for an individual with Alzheimer's disease.
Comparative Table: Aducanumab vs Lecanemab
Aducanumab and Lecanemab are both monoclonal antibodies used for the treatment of Alzheimer's disease, but they have different mechanisms of action and binding profiles. Here is a table summarizing their differences:
Parameter | Aducanumab | Lecanemab |
---|---|---|
Mechanism of Action | Removes beta-amyloid from the brain | Blocks the formation of amyloid plaques in the brain |
Binding Profile | Selective towards fibrils over protofibrils | Stronger binding to protofibrils than to fibrils |
Dosing | Titration regimen up to the seventh infusion to target 10 mg/kg IV | 10 mg/kg once every 2 weeks |
Clinical Trial | EMERGE and ENGAGE trials (one met its primary endpoint, the other failed) | CLARITY-AD trial (met its primary endpoint) |
Side Effects | Amyloid-related imaging abnormalities (ARIA) | Amyloid-related imaging abnormalities (ARIA), lower incidence |
Aducanumab works by removing beta-amyloid from the brain, while Lecanemab works by blocking the formation of amyloid plaques in the brain. Aducanumab and Gantenerumab demonstrated selectivity towards fibrils over protofibrils, whereas Lecanemab showed stronger binding to protofibrils than to fibrils. The dosing for Lecanemab is 10 mg/kg once every 2 weeks, whereas Aducanumab allows for a titration regimen up to the seventh infusion to target 10 mg/kg IV. Both drugs have a mechanistic action directed at aggregated soluble and insoluble forms of amyloid. The most common adverse event seen in both trials was amyloid-related imaging abnormalities (ARIA).
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