I got an email reply from Larry Glass last week which I thought was very interesting and exciting.
After a few days I thought that perhaps I should post it on Hotcopper. I asked him if that was ok and he had no objection. He stated that there is nothing that hasn’t been previously disclosed either in published papers or presentations.
So below it is in full and unedited. Just to let you know that he first responds to a question I have about the animal testing (was it tested on monkeys, basically). He then goes on to state why they are optimistic about nnz2256.
Remember that nnz2256 is derived from something that already works in humans.
His reply really shows why this is worth being a long term hold and not a quick trade. This stock really should be worth in the 12c to 21c range now imho, as Bell Potter has stated.
ok, here is his reply:
.............
Hi Paul,
No, NNZ-2566 was not tested in non-human primates. To my knowledge, there are no laboratories in North America, Europe or Australasia that conduct TBI studies in monkeys; the animal ethics committees won’t approve such studies, particularly if they involve recovery (reawakening). Even pig, cat and dog studies that include recovery following experimental TBI can be hard to get approved. Our focus on preclinical studies all along has been to look for three things: evidence of functional recovery, evidence of relevant physiological and molecular effects and a reasonable therapeutic time window. Basically, we weren’t especially impressed with the short term studies that use infarct size as the primary outcome measure and administer the test compound before or immediately after the injury is induced. Many of the preclinical efficacy studies on NNZ-2566 have been published (let me know if you have trouble finding them). I don’t want to get overly technical here but it’s hard to explain without getting into the science at least a little. Summarizing why we’re optimistic:
In virtually every model in which NNZ-2566 has been tested (stroke, hypoxia-ischemia, penetrating head injury, closed head injury), we have employed functional outcomes such as neurologic function (e.g., foot faults on a balance beam) and cognitive function (e.g., memory tested in a Morris water maze) and have evaluated the effect as long as one month following injury. Across all the models and all the studies, outcomes have improved.
The mechanisms by which NNZ-2566 exerts a neuroprotective effect (primarily inhibition of neuroinflammatory cytokines as well as inhibition of microglial activation and apoptotic gene expression) are directly relevant to the complex pathophysiologic processes (often referred to as a cascade) that occur following brain injury in people (as they are in other mammalian species). Most of the drugs that have been tried in TBI were specifically targeted at a particular event (e.g., free radical release, NMDA antagonism, etc.) whereas NNZ-2566 has multiple effects at different stages of the cascade, including both early and late stage processes. The effects on secondary physiologic events such as seizures (and we’ve seen the effects on both convulsive and non-convulsive seizures in various models) bolster our belief that the effects observed at the molecular level will be manifested in relevant secondary effects and clinical benefits.
Depending on the model and the severity of the experimental injury, the therapeutic time window has been up to 5 hours following injury. The therapeutic time window in rats most likely translates into a longer window in humans. The pathogenic process in humans appears to develop over many hours which is why we’re dosing for 72 hours.
All that said, do we know that NNZ-2566 is going to work? Obviously not. Clinical trial design is a big part of showing that a drug works (or doesn’t). We’ve relied on scientific advisors to help us design the current trial who are among the world’s leading experts not just in TBI therapy but in clinical trial design per se. We also believe that the trial is large enough and has a sufficiently wide range of functional and physiologic endpoints to be definitive. That’s a big part of the advantage of having the funding from the US Army available.
Let me know if you have any further questions or comments. (For clarity, there’s nothing in my response that hasn’t been previously disclosed either in published papers or presentations.)
Best,
Larry
Larry Glass
CEO
Neuren Pharmaceuticals
3 Bethesda Metro Center, Suite 700
Bethesda, MD 20814
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