bristol myers squibb is only aiming to get it on formularies as adjunct therapy, at least for the foreseeable future. that's also what EMERGENT-3 was designed to support; it doesn't have use of other antipsychotics in its exclusion criteria. in fact, they exclude patients with early psychosis or treatment resistance. (it would probably be unethical to jump straight into using an investigational drug as monotherapy for such a serious disease even within a clinical trial, anyway, especially considering potential diminished capacity to consent)
it would be incredibly interesting and great if muscarinic antagonism is an entirely different treatment modality than D2 antagonism, but it's possible that karXT's mechanism of action is actually rooted in downstream dopaminergic changes that are impacted by changes in acetylcholine. we have yet to see if karXT has noninferiority as monotherapy, but we also don't know whether or not it exacerbates the metabolic side effects of dopaminergic antipsychotics when used as adjunct therapy.
i think the most interesting outcome would be discovering that not all schizos are the same type of schizo, with some responding better to cobenfy because they have a muscarinic etiology. i've thought a lot about this due to the existence of anticholinergic psychosis... how different does that feel from psychosis induced by stimulant use or use of antiparkinsonian drugs? this is why i'd like to try datura some day, for science...
![heh :heh: :heh:](/forum/data/assets/smilies/01cf23a43158bded0a7de04385a84f.png)