Agreed. As you have said your preferred strategy would be pursuing a phase II proof of concept in tbi, could you give a simplified explanation of how you see the Moa/drug working in tbi as opposed to iih.
do you think it is as simple as
patient has excess CSF, therefore this drug will reduce it
Or do you think the outcome could differ due to maybe the way the CSF is produced, more rapid in tbi etc
open ended question to anyone who has info
ta
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