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We waited a long time for a real gene therapy, though we were promised it would be easy. So now we are feeling optimistic about the other recalcitrant biomedical challenges. What about a first-in-class drug for schizophrenia? Where are we with that?

Well, in the same old place it turns out. Although excellent data had accumulated on inhibition of certain voltage-gated sodium channels, namely the Nav 1.3, 1.7 and 1.8 types, in a variety of neuropsychiatric phenotypes, the pharmaceutical champion of this approach, Newron Corp., was hit with FDA concerns over central nervous system (CNS) effects of their lead inhibitor, evenamide.

Now the FDA expressing a “concern” is like the Fed Chairman dropping a hint: It's a nuclear bomb. Companies have pre-meetings and pre-pre-meetings with the FDA just to discuss WHETHER they will submit something, much less how or what is contained in their submission. It's like seeking permission to marry into a highly traditional family: You gotta bring gifts for everyone and the uncle has to introduce you to the family friend who introduces you to the gardner who introduces you to Dad. Lots of protocol. And even then, Dad has to REALLY like what he sees. Well, Dad didn’t like what Newron showed him, so it's go to jail, do not pass GO, pay to get out.

Now, nobody’s talking about what exactly these CNS effects were. But we at GeneCentrix would have a few questions up front. For example, what other drug targets (off-targets) might evenamide have affinity for? And are any of these expressed in the CNS? For that matter, are Nav 1.3, 1.7 and 1.8 expressed in the CNS? And where exactly? if a Nav targeted by evenamide is expressed in the visual cortex and the CNS effect was visual, ummm . . . wouldn’t we want to know that? Did the company do this analysis? Probably not. Why? Because there are no good tools for doing it. Well, there is one . . .


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