Ann: Webcast Today - New Data from bioMUSE Natural History Study, page-40

ATH434 is an iron chelator with moderate binding affinity. Therefore chance for the study to meet the primary endpoint of removing brain iron seemed significant, IMHO.

There is however , as per my knowledge, lack of any data from preclinical models related to ATH434's potential to reduce brain volume loss. So making this a new primary endpoint it a big guess for me and IMHO a risk, though I hope to be wrong. I can't wait to hear our the yhesterday's webcast.

Let me quote chatgpt4 as well:

Considering the mechanism of action of ATH434, which targets iron dysregulation and the aggregation of alpha-synuclein, there is a plausible basis to suggest that ATH434 could potentially influence factors contributing to brain volume loss in MSA patients. By aiming to reduce pathological iron accumulation and inhibit alpha-synuclein aggregation, ATH434 might mitigate some of the neurodegenerative processes that lead to neuronal death and, subsequently, brain atrophy.However, whether ATH434 can directly decrease brain volume loss in MSA patients, including those at advanced stages, would require specific evidence from clinical trials measuring changes in brain volume through imaging techniques like MRI. Such trials would need to demonstrate that the drug can significantly impact the underlying neurodegeneration associated with MSA to convincingly argue that it can reduce the rate of brain volume loss. Until such data are available, the potential of ATH434 to decrease brain volume loss remains a hypothesis grounded in its expected impact on the disease's pathology.