The easy answer would be to cite Provigil, extensively used in sleep apnea, but it's not really the answer, since Provigil doesn't actually affect the sleep apnea itself at all--it just deals with the resultant symptom of sleepiness.
So the correct answer is theoretical and not yet established: if there is a difference between lower dose required to activate the pre-Botzinger complex, and that which causes increased alertness and decreased sleep, that would be the 'sweet spot' for intervention. That sweet spot may not exist, which means sleep apnea might not be viable, or it might be much more difficult to access (i.e. could there be an Ampakine tailored to the receptors in the pre-Botzinger complex, but which would not have activity elsewhere? I doubt anyone yet knows the answer to that question).
So I am not building sleep apnea into my projections, and a partnership deal would probably include it as: 'If CX**** receives FDA approval for sleep apnea, another milestone payment of $XX million will be paid.'
NeuroInvestment