In2it, It's a long story, but here's a synopsis from the 10-K (see below). The artifact absolutely wrecked Cortex, and it's been a fight for survival ever since. Pre-artifact, they had very strong pharma partnering interest in CX-717/ADHD (perhaps up to $30 mil in upfronts), but it all fell apart when the artifact surfaced. Cortex spent a long time trying to show that the cellular tissue changes were an artifact of the fixative process, but the FDA wouldn't allow the compound to go into an ADHD Phase 2b (longer term dosing). Cortex then went after the respiratory areas (RD and then SA), but severe financial issues have dogged the company ever since -
>>> Regulatory Issues with CX717
In late March 2006 the Neurology Division of the FDA notified us that it was placing CX717 on clinical hold due to concerns related to some preclinical animal toxicology data. After submitting a response to the Agency in September 2006, the clinical hold was lifted in October 2006, but the FDA limited the approved dosage levels of the compound. Those dosing limitations impacted our plans to conduct further clinical testing of CX717. We submitted additional data to the Neurology Division in April 2007 that demonstrated that the animal toxicity issues were postmortem, fixative-induced effects. In July 2007, the Neurology Division removed the dosing restrictions, and allowed us to resume our clinical trial with CX717 in Alzheimer’s disease at all dose levels requested prior to the hold being placed on the compound.
In September 2007 we submitted a Notice of Claimed Investigational Exemption for a New Drug (an “IND”) to the Division of Psychiatry Products of the FDA to allow us to proceed with longer term human clinical studies of CX717 for ADHD. In October 2007, the Division rejected our IND application. At this time, we do not anticipate submitting further data to the Agency for CX717 as a treatment for ADHD, but we continue to advance additional preclinical AMPAKINE compounds such as CX1739 that may be a potential therapy for the indication.
The data developed during the additional toxicology studies conducted during 2006 and 2007 clearly demonstrated that the postmortem toxicology artifacts seen with CX717 did not occur with short dosing periods, but were found only after chronic dosing at very high dose levels in animals. We believe that by developing an acute use for CX717 we can mitigate any perceived risks associated with chronic doses of the compound. The risk/benefit ratio for the treatment of patients with life-threatening disorders, such as respiratory depression, is significantly different than that for the treatment of ADHD.
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