Any thoughts on Bryostatin and PKC down regulation? That could be a factor holding the stock down.
How long and often was the CU patients treated with Bryostatin?

Excerpt from Benzinga article in February:

Neurotrope holds around 70 patents on its bryostatin and even more importantly, the rights to use PKC epsilon for treatment of AD. Alkon put it this way, "Suppose somebody else, let's say Lilly, came up with a new PKC epsilon activator, and let's say that it had good efficacy. The drug they came up with would be theirs, but to use it to treat Alzheimer's they'd have to work with us." And of the prospect of teaming up with pharma partners? "We'd be happy to work with them."

I hope that's true.

Maple Tree, that new bryolog by Aphios doesn't make you a little uncomfortable?
I know of Dr. Alkon's statement that Ntrp has the rights to all AD treatments using PKC activation, but I think the company needs to clarify this issue more. I don't think BP will partner if there are patent concerns.

I believe it was two weeks ago at the Sachs presentation Dr. Alkon said they will release the ph2a results in about two weeks. That would be about now. Any thoughts on possible results data that could move the s/p up or down?

"If NTRP works and proves it in a couple of weeks, the retail investments will not be meaningful."

Can you explain that part? Thanks.

Couldn't the company sell some shares out of the shelf into the market before release without announcing it? I would not fault them if they did. Just a little insurance.

Penny Double, I noticed that you haven't said anything about the science.
How will anything you're talking about affect the trial results, and if positive the soaring of the stock price that will ensue?

Runncoach are you sure that is the patent you wanted to post?

Also, patents are difficult to interpret if you're not use to reading them.

So what is Aphios angle? They do have a patent to use Bryostatin for neurologic disorders.

I've been trying to understand this patent issue. Here's an exert from a recent Benzinga article.

Neurotrope holds around 70 patents on its bryostatin and even more importantly, the rights to use PKC epsilon for treatment of AD. Alkon put it this way, "Suppose somebody else, let's say Lilly, came up with a new PKC epsilon activator, and let's say that it had good efficacy. The drug they came up with would be theirs, but to use it to treat Alzheimer's they'd have to work with us." And of the prospect of teaming up with pharma partners? "We'd be happy to work with them."

What do you think of Aphios' bryostatin patents?

Ok, I'm lazy. But does anyone have good links to Bryostatin's cancer trials? I want to review what doses were used, the frequency of dosing, and length of the trials.

runncoach, your post-
"I haven't studied AVXL's MOA to any extent which is why I don't post about them or on that board, but based on the statement you posted on that PR, it does lend to comparisons I suppose. Bryostatin is multi modal, neuroprotective, blocks some genetic issues that factor into many Alz cases and that's besides regenerating and regrowing synapses. If any of that is a component of their new drug then that would be further confirmation of our MOA IMO. Of course we are years further down the road on this MOA than anyone else from what I've seen. If AVXL holders are now excited by synaptogenesis then that's pretty ironic"

I was thinking the same thing. And I hope Avxl success.

Someone more computer savvy than I should supply some links to Dr. Alkon's presentations to the new article out.

You do know that Ntrp's trial is also going after moderate AD. They are not on their death bed. Wonder what was it the FDA saw to allow a shorter trial?

I was thinking would it be considered insider-trading for a company to buy or sell on unblinded non-public data.

Can the company sell shares after the data has been unblinded and before the results are made public?

I'll repeat, there is no "theory" in Ntrp's approach, and the animal testing has been checked off. Now it all boils down to can Bryostatin regenerate synaptic networks in humans. We will see soon.

If the trial produces very good results, say a reversal of the disease, where would you say the SP would end that day.

Kld2, the company will raise some of the money before data release but not nearly all. It would be irresponsible not to because there are no guarantees. But if you have confidence in you DD then don't let it scare you, relax.

"The approved drugs keep patients above baseline for <6 mos typically and then nosedive. Donepezil can be of benefit out to a year, best case."

Did any of these "nosediving" drugs for which you speak rebuild synaptic networks? Ok then.

Just read most of the Reddit posts. I laughed so hard I was crying.

Here's one post:

"True that. I work for a big name biotech with an amyloid plaque removal therapy in phase 3. That shit is gonna fail and I'm gonna get laid off"

By you including beta amyloid in the runnings, tells me why you don't see that PKC is clearly the winner here.

I would think the shorters were Adam's gang not the warrant holders, judging by the coordination with his article.

Any opinions on the shorts that drove the price down? Are they still short or did they recover without pushing the price back up?

The fact that Ntrp's approach to Alz is the only approach ever to not be a theory, puts us ahead of all past and present trials. If the synaptic networks can regenerate it will improve cognition.

"Chances are slim the results will be unambiguously positive. I hope they are but this is very, very, very ,........ far from likely."

This trial isn't targeting mild Alz or MCI. The results will not be ambiguous, it will be definite, with no doubt, one way or another. I say it will be greatly positive.

Can I get a "Small If" here? Now, if the failed trials were an assorted types of different approaches then I would agree with a "Big If". But that was not the case.

What makes getting decent results a " Big If"?

What was the question asked by the lady second to the last question? I could not hear her, apparently Dr. Alkon couldn't neither, he didn't give an answer.

Dr. Alkon stated that there was a measurable increase in PKCe (targeted engagement) after one dose in the Ph2a trial.Those measurements are retrievable and verifiable. Nothing was really expected by most people after one dose of Bryostatin. No reason to make up verifiable statistics that could ruin his long earned good reputation.

What red flag do you think it could possibly be other than maybe not supporting cognitive effect after one dose?

With all due respect Frontiers, I understand tapering down expectations, but I hope that you are wrong.
If Bryostatin's efficacy comes in at the low end of "at lease as well as memantine", we are in big trouble. This is an IV drug. And if Bryostatin's results places it in the "will eventually find a place in AZD treatment" category, we are in big trouble. You say "will eventually find a place in AZD treatment" as if there is a lot of other options to squeeze in between.

Anything pertinent to us.

With the amyloid theory the question was rather the buildup of plaque lead to cognitive deficiencies. In NTRP's approach is there anyone questioning rather synaptic loss leads to cognitive deficiencies? There's a difference here.

"With all due respect how do you think the amyloid theory believers would answer these questions before their P2 results were known?"

Are you referring to the first one or two failed trials, or the next dozen that followed them over the cliff? There is a difference. I can understand why long ago people thought the world was flat, but when evidence shows other wise you must change. There is a proven tight correlation between cognitive deficiencies in AD and synapses loss, and a very loose correlation between cognitive deficiencies and amyloid buildup. You can't compare a flat world with a round world.

What was the approach of PRANA?

Here's the reason I give this trial an 80% chance of having a positive result. The way I see it is you have 2 questions to ask yourself. How much do you believe in the approach and how much do you believe in the drug.

1. Do you believe that if the brain can regenerate synaptic networks, it would help AD patients?

2. Do you believe that Bryostatin can regenerate synaptic networks in humans as it did in mice?

I say yes to both.

The believers in the amyloid theory only got one of the two questions right. Some of their drugs got # 2 right, the drugs reduced the plaque, but they got #1 wrong, the theory was incorrect.

But still, what percent of the failed trials had virtually the same theory? Now, I would think that most people would say that IF the drug can regenerate synaptic nerves the chance of positive results would be very high. Do you think?

I don't think NTRP's approach is grasping in the dark. I think it has an 80% chance of success. Imo