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Biotech / Medical : 2022 Biotech Charity Contest -- Ignore unavailable to you. Want to Upgrade?

To: technetium who wrote (195)	10/4/2022 12:42:44 PM
From: software salesperson	1 Recommendation Recommended By Lance Bredvold Respond to of 267

comments that caught my eye from alzforum.org re: lecanemab : CEO Haruo Naito recollected their ~25 years’ journey that led to the first success of disease-modifying therapy in a confirmatory trial, now proving the amyloid target hypothesis in human AD. - - Takeshi Iwatsubo University of Tokyo Specific concerns relate to how analyses were done and if they preserved the randomization (e.g., if randomization was stratified, analyses must reflect that stratification) and evidence that unblinding of participants (i.e., knowledge of treatment status) did not contribute to findings. - - Maria Glymour University of California, San Francisco We need to see the data to fully understand how clinically relevant the stabilization is, but theoretically the difference with placebo should grow over time. Furthermore, treating earlier (e.g. biomarker-positive, clinically normal) might give even an better benefit ( Karran and De Strooper, 2022). Another question is whether patients need to be continuously treated or not. In the latter case, these antibody treatments might be great, but dosing chronically will make this drug much too expensive. I hope that the price setting remains reasonable and not $50,000, as Aducanumab initially. These results strongly suggest that we revisit previous drug targets such as ?-secretase and BACE, as small compounds modulating these activities might be, in the long run, the only cheap and feasible prevention for AD. The alternative might be to reconsider active immunization. A big kudo to Lars Lannfelt, the inventor of this antibody - - Bart De Strooper UK Dementia Research Institute@UCL and VIB@KuLeuven As someone who studies disease mechanisms, I’m not sure this study informs questions of AD etiology. To my mind this study, along with other amyloid antibody trials, is better positioned to inform the question of how toxic Aß is in people’s brains. One would think if this approach was to have a transformative effect, the answer would be very toxic, if no effect then not toxic, and if a small effect then a little toxic. Data from Clarity would seem to argue Aß is more on the minor than major end of the toxicity spectrum. - - Russell Swerdlow University of Kansas Third, some clarity (pun intended) on why this particular antibody seemed to be a bit more effective and a bit safer than Aduhelm and other previous anti-Aß antibodies is important. Is the intent-to-treat population or the dosing regimen different enough to explain the apparent success? Or are the antibodies different enough both in terms of effector function, aggregate binding profile and avidity, to explain the difference, especially with respect to side effects? I know lecanemab is advertised as targeting toxic oligomers better, but I remain agnostic about that claim as the underlying reason for its apparent efficacy. - - Todd E. Golde Goizueta Institute @ Emory Brain Health