While a chronic disorder like sleep apnea would be treated with CX1739 rather than CX717, the next step is to show that any Ampakine can affect sleep apnea, so they will begin with a pilot study using CX717. Cortex was talking about doing so during 1Q, and the point I made about a lack of placebo response, easy to measure apnea episodes, and each patient serving as their own control, is that they would probably know after 20 patients have spent two nights in a sleep lab whether CX717 affects the most common type of SA, obstructive SA, and/or the more likely-to-be impacted central/mixed type (figuring that out of 20 patients, 2 or 3 would be central/mixed).
Which means they'd know within a month, if they tap a couple of busy sleep labs (sleep apnea evals are routine, in contrast to RD assessment).
Why is this bigger? I've seen estimates of up to 20 million US sleep apnea patients in total. Even if only those with a central SA component were successfully treated, that's 3 million. And treatment would mean daily, ongoing medication administration.
I used to follow sleep apnea much more closely in the mid 90s, back when Provigil was in development, and that was one of the main goals, to treat the somnolence that results from sleep apnea. No drug therapy currently treats the SA itself, wearing a pressurized mask (CPAP) during sleep is the most effective, and hated, treatment.
Sleep apnea isn't just bigger than RD. Given the documented association with cardiovascular disease and even memory loss, this is one of the biggest untapped markets in all of medicine.If you doubt it, ask the Board's practicing neurologist, DavidAl.
My back of the envelope calculation for a drug that provides significant improvement in BOTH obstructive and central or mixed SA came out to $8 billion in the US. Annually. Just in the US.
I want to emphasize that the RD effects of CX717 are more predictive of effect in central/mixed SA. It is a different 'circuit' that controls the airway musculature critical in obstructive SA. But I went back through my cobwebbed neuroanatomy resources and found that the hypoglossal nerve begins in an area near, but not identical to, the Pre-Botzinger complex. Are there AMPA receptors there that will respond to CX717 by upping the stim of that musculature? And can it be done without impairing sleep itself? No one knows.
Those are the $8 billion questions yet to be answered. But answers in the affirmative would be....well they would change the valuation calculations considerably.
NeuroInvestment
