Kinsula treatment

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You might want to consider joining the closed Facebook group "Leqembi and Kisunla Support Group". There are people taking both drugs in the group. Over time, we have compiled our own document which compares / contrasts Leqembi & Kisunla in great detail, from a patient perspective. It is "closed" FB group as it requires answering some questions about why you want to join (to prevent scammers from participating).
I'm on Leqembi, the other anti-amyloid medication approved by the FDA. I have had zippo reactions to the drug or to the infusions themselves.
Both drugs seem to have very similar results in terms of amyloid removal, and generally similar outcomes for reducing the cognitive decline associated with AD. The current dosing strategy for Kisunla results in slightly higher ARIA rates compared to Leqembi (Amyloid-Related Imaging Anomalies, in simple terms, bleeding and swelling in the brain). However, Eli Lily (drug company that developed Kisunla) recently completed testing showing that modifying the dosing strategy (slowing increasing the number of vials over the first few treatments) resulted in significant reductions in ARIA. One presumes that dosing modification could be quickly approved by the FDA, resulting in new patients on Kisunla soon using the new initial dosing strategy.
The other big differences are that infusions are bi-weekly for Leqembi and monthly for Kisunla, and the duration of treatment. Kisunla treatment lasts until the amyloid plaque has been removed, as determined by PET scans. The drug manufacturer for Leqembi recommends continuing treatment. Specifically for Leqembi, after the initial 18 months of bi-weekly dosing, the recommendation is to continue a maintenance dosing at a once a month interval. The rationale is twofold. First, Eisai (drug company primarily responsible for Leqembi) has published data showing the rebound effect if the drug is terminated, meaning that the amyloid begins to reaccumulate in the brain. Second, Eisai likes to note that Leqembi is dual-acting: targeting both amyloid plaque and "highly toxic amyloid protofibrils" (to use the Eisai term). Eisai notes the protofibrils contribute to neurodegeneration. This is distinct from Kisunla, which only targets amyloid plaque. It is unclear to non-professionals (like me) how important amyloid protofibrils are in the grand scheme of AD. I'm just reporting the facts.0
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