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The BioPharmCatalyst has added Byrostatin to their watch list for upcoming results next week:
http://us13.campaign-archive1.com/?e=3da3a52f00&u=ce642b003b32103d28995373d&id=35829a11f3
burp, see post #3774 by cadfxguy.
Also Aegis, in both their report and their update note they say by end of April. What that tells me is that the company must have the data and are in the process of completing their own statistical review.
The Market Makers are absolutely aware that binary news is pending for NTRP and when they look at the Options market they see a bullish set-up.
IMO they are running the sell stops to accumulate inventory. They know, no matter what the Ph2b results, there is going to be a huge uptick in volume and they are going to be required to provide liquidity. Being short on inventory in a bull run can be very, very expensive for a MM.
"Not at all - allows for a 10-1 forward stock split that I hear is coming."
Well that is one way to deal with the ridiculously small float that this stock has. I'll take it!!
"The LT shareholers are lined up to sell on results" what proof do you have to back up that statement?
The private placement investors that I personally know have a very different game plan and it does not involve selling out of their investment if the Ph2b results upend the entire AD research field.
A new paradigm for AD treatment, one that works, is going to be worth significantly more than the initial run-up in stock price. It will take time for the true market valuation to be revealed, most likely by a Big Pharma partner or outright buyout.
Logically, it is obvious that Neurotrope sees raising funds at $20 bucks a share as a mistake. That is a yuge tell. It shows they expect to raise at a much higher valuation.
Think about it. Your run of the mill microcap scam company would already be in the market hawking shares and hiring some pump and dump PR company to beat the bushes for sucker investors before results are released not after.
That is just not the case.
Your logic is faulty. The part you are leaving out is that of the
150,000,000 shares authorized none have been sold or issued. It appears that NTRP will raise money after the Ph2b results are released not before.
If the Aegis report was a true pump job Neurotrope would already be in the market with an offering before results, that is just not the case.
The company has no debt, approximately $20 million in the bank, $50 plus million in outstanding warrants and options when exercised, and now, once results are out, the opportunity to raise additional funds at a much higher market cap. That will give them leverage when they negotiate with a Big Pharma suitor or they can pursue there own Ph3 and Ph2b open label follow-on studies .
Neurotrope has made all of the right moves.
Agreed runncoach, "If we are successful, we'll be the 2017 stock of the year and everyone will jump on the bandwagon. Big pharma will be all over us. That's how it works. They are in wait and see mode"
As I wrote last week concerning the Sachs Forum:
"The large and small players in the AD research field are vitally interested in their counterpart’s research and they all know NTRP is next in line for results. And they are all aware that if Dr. Alkon’s theories are validated and Byrostatin -1 shows efficacy the AD research field will undergo a massive shift in focus."
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=130504182
Link to Aegis Capital's update of their Neurotrope research report
NTRP: Inlicensing Activity Highlights Value of Alzheimer's Disease Therapies
http://www.investorvillage.com/smbd.asp?mb=19529&mn=183&pt=msg&mid=17076967
This article published in 2015 is a helpful summation of some of the science behind Neurotrope:
Risk Gene for Alzheimer's Disease May Aid Prevention
Researchers have identified the chain reaction that may lead to the disease.
A new study provides a clearer understanding of how the gene Apolipoprotein E4 (ApoE4) affects late, age-dependent Alzheimer's disease (AD). The findings may pave the way for better treatment and prevention, according to the researchers. The study was published in the Journal of Neuroscience, May 13, 2015.
THE VIEW FROM DUKE
SOPHIA WANG, MD, Staff Psychiatrist-Durham VA Medical Center; Asst. Professor of Psychiatry & Behavioral Sciences, Department of Psychiatry-Div. of Psychiatry/Geriatric Behavioral Health, Duke
Novel Treatments to Treat or Prevent AD are Much Needed
"Alzheimer's disease causes progressive, irreversible loss of memory, and affects more than 5 million Americans.
Novel treatments which can either treat or prevent Alzheimer's disease are much needed. Apolipoprotein E4 (ApoE4) is a well-established risk factor for late-onset Alzheimer's disease, but it is not well known how ApoE4 may increase the risk for Alzheimer's disease. Recent work now suggests that ApoE4 may increase the risk for Alzheimer's disease by indirectly lowering levels of brain-derived neurotrophic factor (BDNF). BDNF is important for building, repairing, and maintaining the connections between brain cells. The loss of BDNF is thought to be associated with the cognitive deficits seen in Alzheimer's disease. A new drug, bryostatin 1, may work by preventing ApoE4 from decreasing BDNF levels. Bryostatin is currently being tested in small-scale clinical trials to see whether it may benefit patients with Alzheimer's disease. If shown to be effective, bryostatin would be a novel class of drugs to treat this common, devastating disease."
ApoE4 is a major genetic risk factor for a majority of Alzheimer's patients. In fact, people with two copies of the ApoE4 gene are 10 times more likely to suffer from the disease. The link between ApoE4 and Alzheimer's is much like a domino effect: In a recent study, scientists found that the ApoE4 gene increases the activity of histone deacetylases (HDACs) in brain neurons. HDACs are enzymes that act like on/off buttons for genes. In response, this higher activity of HDACs reduces levels of DNA-programmed, brain-derived neurotrophic factor (BDNF).
Essential Synapses.
"BDNF fosters the growth, maintenance, and repair of synapses—the process of how nerve cells signal to other cells," says lead researcher Daniel Alkon, MD, of the Blanchette Rockefeller Neurosciences Institute in Morgantown, W.Va. Synapses are essential for storing memories and processing thoughts and planning."The loss of synapses is the pathologic (disease-causing) change in Alzheimer's that most closely relates to its progressive cognitive deficits."
Previous autopsy studies have shown that many brains of Alzheimer's patients have deficits in BDNF, adds Dr. Alkon. "So we can now see a connection between ApoE4 and lower BDNF and an increased risk of Alzheimer's."
Shift in Treatment Focus.
Current drug therapy for Alzheimer's focuses on reducing the telltale physical signs of the disease—build-up of plaque on the brain caused by the clumping of proteins called beta amyloid, and twisted intracellular tau fibers in brain cells called "tangles." "Yet, so far these drug approaches have been singularly unsuccessful," says Dr. Alkon.
However, the new research could provide a major shift in how to approach treatment. "Synaptic loss can occur before the onset of beta amyloid plaques or tangles, so conventional anti-amyloid and anti-tau approaches are not targeting a critical pathway by which Alzheimer's disease may develop," says Dr. Alkon.
Using this new research as a guide, one way to tackle the disease may be with bryostatin drugs. Pre-clinical studies have found that bryostatins can prevent ApoE4 from hindering BDNF production, and thus stop the chain reaction that may lead to Alzheimer's. Clinical trials with Bryostatin are under way.
"This is a possible next step that could offer a different way to approach Alzheimer's disease treatment and even prevention, especially for people who may be at a higher risk," says Dr. Alkon.
In the microcosm of the AD research field Neurotrope’s results are next up:
While shareholders in NTRP are counting down the days until the Ph2b study results are released there is another group that is highly interested in the outcome.
Dr. Alkon gave the Keynote address at the Sachs Neuroscience and Biopartnering & Investment Forum (3-27-17) to some two hundred plus attendees, many of whom were representatives of the largest Pharmaceutical companies in the world. The CEOs of a number of NTRP competitors were also there to give their own company presentations. (see attendee list at bottom)
By design the Sachs Forum was set up to connect businesses involved in AD and Parkinson disease research with Big Pharmas that are looking at what is in the development pipeline for possible partnerships or buyouts.
Representative of many major Investment Funds were likewise prospecting for promising companies.
The large and small players in the AD research field are vitally interested in their counterpart’s research and they all know NTRP is next in line for results. And they are all aware that if Dr. Alkon’s theories are validated and Byrostatin -1 shows efficacy the AD research field will undergo a massive shift in focus.
The Sachs Forum format allowed company CEOs to meet one on one with Pharma and Investment Fund reps. Neurotrope had a number of such meetings with some of the largest Pharma companies in the world.
If the Ph2b results are what we are hoping for I expect that Neurotrope will be swiftly approached by Big Pharma companies who will immediately understand the market implications for Bryostatin.
Sachs Neuroscience Biopartnering & Investment Forum (3-27-17):
Confirmed Attending Companies Include:
A C Binder Corp.
AbbVie, Inc.
Abingworth LLP
Agent Capital, LLC
Alpha Bronze
Amorsa Therapeutics, Inc.
Angel Investor
APS International
Arbor Pharmaceuticals, Inc.
Arix Bioscience
ASDERA
Assembly Biosciences
Athyrium Capital Management
Avanir Pharmaceuticals
Avicenna Ventures
Axial Biotherapeutics
Bigger Capital Fund, LP
Bishop Capital Management
Boehringer Ingelheim Venture USA, Inc.
BrainStorm Cell Therapeutics, Inc.
Brendan E. Cryan & Co. LLC
Cambridge Cognition Ltd.
Cantabio Pharmaceuticals, Inc.
CastleRock Management
CBT Advisors
Cipla New Ventures
Clarus Ventures, LLC
Cognition Therapeutics, Inc.
Cortexyme
CureDuchenne Ventures
Dabar Investment Associates
Daiichi Sankyo, Inc.
Dawson James Securities, Inc.
Deca Ventures
Defined Health, a Cello Health business
Delwar Capital
Edison Investment Research
Eli Lilly and Co.
Embera NeuroTherapeutics, Inc.
Enso Ventures
Erydel
ESC Advisors
Exscientia Ltd.
F. Hoffmann La Roche Ltd.
First Republic Investment Management?
Flagship Ventures
Fountain Healthcare Partners
Fraser Finance
FreeMind Group
Goodwin Procter LLP
Hercules Technology Growth Capital, Inc.
Hereditary Neuropathy Foundation
ICR, Inc.
Johnson & Johnson
Katalyst Securities, LLC
KemPharm, Inc.
K-PAX Pharmaceuticals, Inc.
Landmark Family Office
Lauren Sciences LLC & Maya Sciences LLC
Lexington Capital Management
Little Gem Life Sciences
Lonza Walkersville, Inc.
Loop Capital Markets
Lysosomal Therapeutics, Inc.
M3 Biotechnology, Inc.
Mavericks Capital
MedPro Investors, LLC
Merck & Co., Inc.
Mergermarket
Mid Atlantic Bio Angels
Minoryx Therapeutics S.L.
Mizuho Bank
Momentum Biotech
MP Healthcare Venture Management, Inc.
NeuroRx, Inc.
NeuroTherapia, Inc.
Neurotrope Bioscience, Inc.
New Enterprise Associates
New Frontier Capital, LP
New York Ventures
Nexeon Medsystems, Inc.
NI Research, Inc.
Noble Life Science Partners
NSIP LLC
Occidental Group
Oppenheimer & Co. Inc.
Origenis GmbH
Oryzon Genomics SA
P4G Capital
Park Avenue Capital?
Parkfield Fund LLC
Perseverance Capital
Pfizer, Inc.
Pharmasum Therapeutics AS
PJT Partners
Probiodrug AG
ProMIS™ Neurosciences, Inc.
ProPhase
Purdue Pharma L.P.
Quartet Medicine
Queen Mary University London
Raman Health Technologies, S.L.
Remiges Ventures
Sachs Associates Ltd.
SalubRx Therapeutics, Inc.
Sanofi
Shadow Lake Group, Inc.
Shaw Strategic Capital LLC
Stanphyl Capital
SternAegis Ventures
Sternberg Investments
Sunovion Pharmaceuticals, Inc.
SunRegen Healthcare AG
Syncrosome
Syzygy Therapeutics
T3D Therapeutics, Inc.
Tanaka Capital Management
The Alzheimer's Drug Discovery Foundation
The Astrologers Fund, Inc.
The Center for Performance Investing
The Michael J. Fox Foundation
TikoMed AB
TS Family Office
Union Square Advisors
vasopharm GmbH
Vector Resource Funds
Vista Point Capital
WallachBeth Capital
WBB Securities, LLC
Wells Fargo Advisors
WestPark Capital
Wotczak Group
YLM2012 Trust
Yorkville Advisors, LLC
Yumanity Therapeutics
YunTai Fund USA Office
http://www.sachsforum.com/2nbpi-attendees.html
Actually, for me, I am most encouraged by the pricing of the Option Grants. As you pointed out on the Investor Village board "I guess they truly will sink or swim with the shareholders based on results..."
To price the options at Market Value, after the stock price has tripled, would seem to indicate a solid vote of confidence by Management that the Ph2b study results are going to be positive with most if not all of the endpoints being met.
EP Vantage has over 3300 followers on Seeking Alpha:
EP Vantage is a forward-looking comment and analysis service tailored to the needs of pharma and finance professionals, focusing on the events that will define the future of companies, products and therapy areas. Written by experienced journalists, EP Vantage provides timely financial analysis of regulatory and patent decisions, marketing approvals, licensing deals, and M&A, giving fresh angles and insight to both current and future industry triggers. EP Vantage is powered by EvaluatePharma, the industry leader in consensus forecasts.
https://seekingalpha.com/author/ep-vantage/articles#regular_articles
SEEKING ALPHA:
Neurotrope Aims For Alzheimer's While Brigatinib Comes Late To The Alk Party
Apr. 14, 2017 1:44 PM ET| About: Neurotrope, Inc. (NTRP), TKPPY, Includes: BMY, RHHBY
EP Vantage
Newsletter provider, biotech, healthcare
EP Vantage
(3,321 followers)
Summary
Phase II data are expected this month from Neurotrope's Alzheimer's project Bryostatin-1.
The company will need to raise more cash in the not too distant future. As of March it had approximately $24.1m, sufficient to fund operations for the next 18 to 24 months.
Meanwhile, Takeda's Alk inhibitor brigatinib will go before US regulators by April 28 in second-line NSCLC.
Welcome to your weekly digest of approaching regulatory and clinical readouts. Phase II data are expected this month from Neurotrope's (NASDAQ:NTRP) Alzheimer's project Bryostatin-1, which aims to activate protein kinase-c, though the litany of failures targeting this tricky disease is hard to ignore.
Meanwhile, Takeda's (OTCQX:TKPPY) Alk inhibitor brigatinib will go before US regulators by April 28 in second-line NSCLC. This asset came through Takeda's acquisition of Ariad, and if approved it will be entering a crowded market: only this week Roche's (OTCQX:RHHBY) competing asset Alecensa proved itself in a first-line setting, reinforcing it as the one to beat.
PKC activation
Bryostatin-1's phase IIb study tests 20 or 40 micrograms administered intravenously over 45 minutes every other week after two initial loading doses in 148 patients with moderate to severe Alzheimer's, versus placebo.
Primary endpoints measure adverse events and change from baseline in the severe impairment battery, which assesses cognition, while secondary endpoints include activities of daily living, neuropsychiatric inventory and mini-mental state exam. Topline efficacy data are due this month.
Bryostatin-1 is a protein kinase-c-epsilon activator said to target multiple pathways, including activating synaptic growth factors and amyloid-beta degrading enzymes. A phase IIa study in nine patients with mild dementia showed good tolerability, and while there was no improvement in cognition Neurotrope said only a single dose was given and that previous animal studies showed improvement with multiple doses.
Three patients also have been treated in a compassionate-use program where the company has reported improvements in cognition and daily living, and even states the possibility of disease reversal, but obviously this will need to be proven in upcoming trials.
Neurotrope was formed in 2012 out of the Blanchette Rockefeller Institute. It was originally listed on the OTC bulletin board, but last month began trading on Nasdaq after a 1-for-32 stock consolidation, since which shares are up 161% and the market cap now sits at $137m.
The company will need to raise more cash in the not too distant future. As of March it had approximately $24.1m, sufficient to fund operations for the next 18 to 24 months. Funds will be used to complete a phase II study and start an open-label extension trial and a study in Fragile X syndrome.
Bryostatin is purified from Bugula neritina, a marine invertebrate first isolated in the 1960s. It was initially tested in oncology by the NCI, but proved ineffective. The private company Aphios also is investigating it pre-clinically in Alzheimer's with APH-0703 and its analogue APH-1104.
Numerous competitor failures have turned Alzheimer's into a development graveyard, but this has not stopped investment. Biogen (NASDAQ:BIIB) just paid $300m up front for Bristol-Myers Squibb's (NYSE:BMY) phase I anti-tau MAb BMS-986168, for instance.
Late runner
Takeda's brigatinib is filed for metastatic Alk-positive NSCLC patients resistant to or intolerant of Pfizer's Xalkori and has a PDUFA date set for April 28.
The market is getting increasingly crowded with the likes of Xalkori, Zykadia and Alecensa all competing for a small patient population - only 3-5% of NSCLC cases are Alk-driven. Roche reported topline data this week showing Alecensa beating Xalkori in the first-line setting, highlighting Alecensa's potential to become the best seller in this class.
Brigatinib was one of the main drivers of Takeda's move on Ariad, and it must show that it can compete with Alecensa to justify the $5.2bn price tag. Results from brigatinib's first-line trial Alta-1L are likely to emerge towards the end of 2018, while a study in Alecensa failures started last month (Therapy focus - Roche looks ready to rule another cancer niche, March 6, 2017).
Project
Trial ID
Details
Bryostatin-1
NCT02431468
Phase IIb, 148 patients with moderate to severe Alzheimer's
Bryostatin-1
NCT02221947
Phase IIa, 9 patients with mild Alzheimer's
Brigatinib
NCT02737501
Alta-1L, brigatinib versus Xalkori in first line use, primary completion April 2019
Brigatinib
NCT02706626
After treatment with 2nd generation Alk inhibitors, primary completion June 2018
Editor's Note: This article discusses one or more securities that do not trade on a major U.S. exchange. Please be aware of the risks associated with these stocks.
https://seekingalpha.com/article/4062492-neurotrope-aims-alzheimers-brigatinib-comes-late-alk-party?app=1&auth_param=l0ob:1cf22j9:64a92f1777b1d50aa73b856b96b7875a
Well, I don't know what happened to the scheduled interview on Varney and Co. with Dr. Alkon.
Looks like a story about retail stores closing was a bigger story.
I would tend to agree with you. Neurotrope, once they receive the results, will need time to review and complete their own statistical analysis. That process could take a couple of weeks. They could very well already have the data in hand.
Thanks Whatsupp, I corrected my message to Maple tree.
Varney & Co. is the morning program on Fox Business Channel here in the US. It is on 9:00am to noon EST.
Neurotrope BioScience CSO Dr. Daniel Alkon to be Interviewed Live Today on 'Varney & Co.' on Fox Business Read More...
NEW YORK, April 13, 2017 /PRNewswire/ -- Neurotrope, Inc. (OTCQB: NTRP), a clinical-stage biopharmaceutical company developing novel therapies for neurodegenerative diseases, including Alzheimer's disease, today announced that Dr. Daniel Alkon, Neurotrope's President and Chief Scientific Officer, will be interviewed live this morning by Stuart Varney on the Fox Business Network program, 'Varney & Co.'
Details of the broadcast are as follows:
Date: Thursday April 13th, 2017
Start Time: 11:45 am EDT
Network: Fox Business Network
Show: Varney & Co.
Host: Stuart Varney
Dr. Alkon will discuss the 'Neurotrope Difference.' Other companies targeting Alzheimer's and other neurodegenerative diseases target one mechanism of action. Neurotrope, through the upregulation of PKC epsilon, activates a multimodal mechanism of action targeting many pathways to stop the spread of toxic plaque and tau tangles while also regenerating synapses by activating Neurotrophic growth factors like BDNF, IGF-1, and NGF.
About Neurotrope
Neurotrope is at the forefront of developing a novel therapy to treat and potentially reverse moderate to severe Alzheimer's disease and other neurodegenerative diseases. The Company's world-class science is a paradigm shifting approach that treats some of the underlying causes of Alzheimer's disease.
The scientific basis of our treatment is activation of Protein Kinase C isozymes e and a by bryostatin, a natural product, which in mouse Alzheimer's disease models was demonstrated to result in repair of damaged synapses as well as synaptogenesis, the induction of new neuronal networks, reduction of toxic beta-amyloid generation, prevention of neuronal death, and enhancement of memory and learning, thus having the potential to improve cognition and behavior in Alzheimer's disease.
Neurotrope is conducting a Phase 2 trial of bryostatin in the treatment of moderate to severe Alzheimer's disease, as well as preclinical studies of bryostatin-1 as a treatment for Fragile X Syndrome, Niemann-Pick Type C disease and Rett Sydrome, three rare genetic diseases for which only symptomatic treatments are currently available. The FDA has granted Orphan Drug Designation to Neurotrope for bryostatin-1 as a treatment for Fragile X Syndrome. Bryostatin-1 has undergone testing in over 1,500 people establishing a large safety database.
Forward-Looking Statements
04/13/2017 | Press release | Distributed by Public on 04/12/2017 23:32
Neurotrope BioScience CSO Dr. Daniel Alkon to be Interviewed Live Today on 'Varney & Co.' on Fox Business Read More...
Neurotrope BioScience CSO Dr. Daniel Alkon to be Interviewed Live Today on 'Varney & Co.' on Fox Business
NEW YORK, April 13, 2017 /PRNewswire/ -- Neurotrope, Inc. (OTCQB: NTRP), a clinical-stage biopharmaceutical company developing novel therapies for neurodegenerative diseases, including Alzheimer's disease, today announced that Dr. Daniel Alkon, Neurotrope's President and Chief Scientific Officer, will be interviewed live this morning by Stuart Varney on the Fox Business Network program, 'Varney & Co.'
Details of the broadcast are as follows:
Date: Thursday April 13th, 2017
Start Time: 11:45 am EDT
Network: Fox Business Network
Show: Varney & Co.
Host: Stuart Varney
Dr. Alkon will discuss the 'Neurotrope Difference.' Other companies targeting Alzheimer's and other neurodegenerative diseases target one mechanism of action. Neurotrope, through the upregulation of PKC epsilon, activates a multimodal mechanism of action targeting many pathways to stop the spread of toxic plaque and tau tangles while also regenerating synapses by activating Neurotrophic growth factors like BDNF, IGF-1, and NGF.
About Neurotrope
Neurotrope is at the forefront of developing a novel therapy to treat and potentially reverse moderate to severe Alzheimer's disease and other neurodegenerative diseases. The Company's world-class science is a paradigm shifting approach that treats some of the underlying causes of Alzheimer's disease.
The scientific basis of our treatment is activation of Protein Kinase C isozymes e and a by bryostatin, a natural product, which in mouse Alzheimer's disease models was demonstrated to result in repair of damaged synapses as well as synaptogenesis, the induction of new neuronal networks, reduction of toxic beta-amyloid generation, prevention of neuronal death, and enhancement of memory and learning, thus having the potential to improve cognition and behavior in Alzheimer's disease.
Neurotrope is conducting a Phase 2 trial of bryostatin in the treatment of moderate to severe Alzheimer's disease, as well as preclinical studies of bryostatin-1 as a treatment for Fragile X Syndrome, Niemann-Pick Type C disease and Rett Sydrome, three rare genetic diseases for which only symptomatic treatments are currently available. The FDA has granted Orphan Drug Designation to Neurotrope for bryostatin-1 as a treatment for Fragile X Syndrome. Bryostatin-1 has undergone testing in over 1,500 people establishing a large safety database.
Forward-Looking Statements
http://www.publicnow.com/view/403DBEE0317C8A6A44C937CD70ED7778DC286160?2017-04-13-07:01:05+01:00-xxx8310
Here is a link to a PDF of the entire article:
http://www.jbc.org/content/early/2016/06/21/jbc.M116.730440.full.pdf?with-ds=yes
Neurotrope's (NTRP) stock structure is set-up for huge move if results of Ph2b AD study are positive.
Maybe seven to seven and half million shares outstanding. A float of probably two and a half to 3 million (miniscule!). And NO OPTIONS which means you have to have extremely deep pockets to dare to go short. After hours positive news and the stock could open up fifty bucks or more.
Neurotrope:
AEGIS Capital: Buy Rating of $31 share
NTRP: Has Neurotrope Pulled An Alzheimer's Sword From The Stone?
Summary We are initiating coverage of Neurotrope with a Buy rating and a price target of $31 per share. The company is developing Bryostatin-1 as a stimulator of PKCε, an early regulator of brain cell growth and repair. A Phase IIb trial has completed enrollment in Alzheimer’s disease, with data expected in late April 2017.
Bryotstatin-1 stimulates PKCε, a protein involved in the formation of new memories. Data shows that it acts as an early "regulatory control" that stimulate synaptic growth and other neuronal pathways involved in the brain. We believe its mechanism of action can affect several important pathologies of the disease.
Phase IIb Trial Results Expected In Late April to May The primary endpoint in trial is the change in Severe Impairment Battery (SIB), a clinical tool evaluating several cognitive functions. Safety and efficacy are also endpoints. Each of the secondary endpoints evaluates specific effects of Bryostatin-1.
Bryostatin Clinical Trials Have Both High Risk and High Reward The only treatments for Alzheimer’s disease (AD) are drugs that lessen symptoms with little to no effect on disease progression. The mechanism of disease is unclear and subject to widely varied opinions in the medical community. Dozens of clinical trials in AD have failed, making it a high risk indication for development. If the Bryostatin-1 Phase IIb trial is successful, it could be the first disease-modifying therapy that prevents AD progression and restores lost memory. If the Phase IIb trial is partially successful (meets some but not all of its endpoints) we believe it could still have therapeutic value in AD and other neurological diseases where cognitive function or development is affected.
Valuation We expect NTRP to be driven by the results of its Phase IIb clinical trial, currently scheduled to be reported in late April 2017. Marketed drugs that provide a modest reduction in symptoms have had annual sales in the $2 billion to $5 billion ranges. Products for AD intended only to slow the progression of disease or reduce symptoms have achieved market valuations in the $1 billion range after positive Phase II data, which we believe reflects the high unmet need and sales potential for effective AD drugs. Neurotrope's market valuation is currently about $145 million, which we believe discounts the current uncertainties and high risk before the data announcement.
To value NTRP, we began by estimated earnings for the first year of profitability. We assume first revenues in 2020, and base our estimates on a cost of $1,500 per month. We use a probability adjustment of 75% of revenues to allow for the high risk of failure in clinical trials for Alzheimer’s disease. We further discount FY2021 EPS of $5.96 by 30% per year, with a multiple of 15X for a price target of $31 per share.
Alternatively, we considered the valuations for comparable companies in clinical development for Alzheimer’s disease. Based on expected sales of drugs that are intended to slow the decline in cognitive function or reduce symptoms, we believe our estimates for Bryostatin-1 are conservative. Our price target correlates with a market capitalization of about $330 million compared with about $145 million today. See Risk Factors and Valuation Methodology on page 17.
Please click here for full report: https://aegis.bluematrix.com/sellside/EmailDocViewer?encrypt=fe256461-2876-435f-afb5-e92484e957c0&mime=pdf&co=aegis&id=eden.rahim@NextEdgeCapital.com&source=mail
150,000,000 authorized but none sold or issued. It appears that NTRP will raise money after the Ph2b results are released not before.
5 things to know in Texas energy this week
Apr 10, 2017, 8:33am CDT
• Plano, Texas-based Torchlight Energy Resources Inc. (NASDAQ: TRCH) is drilling a third test well in the Orogrande Basin, in Texas near the New Mexico border. It reached an agreement for development over the next 10 years last week with University Land, an endowment that manages mineral interests in West Texas. “It’s going to become the major asset of the company,” Torchlight CEO and Founder John Brda said on a conference call. “What you’re looking at is the potential for a billion-barrel field.”
http://www.bizjournals.com/houston/news/2017/04/10/5-things-to-know-in-texas-energy-this-week.html
Aols is mentioned in this Bloomberg article today:
https://www.bloomberg.com/news/articles/2017-04-11/the-u-s-needs-a-new-nerve-gas-antidote
Maple tree, this study (which I posted earlier) along with the Aphios data confirm the role of PKC epsilon in AD progression:
Independent Confirmation of Dr. Alkon's research
The scholarly article below was referenced twice by Dr. Alkon in recent presentations at both the Oppenheimer and Sachs Forums. I believe for Dr. Alkon this study independently confirms an element of his theoretical framework for the role of PKC epsilon in modulating Alzheimer’s disease. The study addresses one aspect of the multi-modal effect of treatment with Byrostatin. The reduction of amyloid plaque pathology.
Briefly, the study took mice that genetically express AD at an early stage in their life cycle. Then this mouse model was further genetically manipulated with a gene to produce higher than normal levels of PKC epsilon (the brain agent that Byrostatin stimulates to treat AD). The premise was, will higher levels of PKC epsilon prevent AD symptoms in animals that always develop the disease. This study showed that these double transgenic mice had lower amyloid plaque deposits and Alzheimer’s disease expression confirming an important theoretical aspect of Dr. Alkons work.
PKCe increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice
Choi et. al.
March 31, 2006
Abstract
Deposition of plaques containing amyloid ß (Aß) peptides is a neuropathological hallmark of Alzheimer's disease (AD). Here we demonstrate that neuronal overexpression of the e isozyme of PKC decreases Aß levels, plaque burden, and plaque-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-mutant forms of the human amyloid precursor protein (APP). Compared with APP singly transgenic mice, APP/PKCe doubly transgenic mice had decreased Aß levels but showed no evidence for altered cleavage of APP. Instead, PKCe overexpression selectively increased the activity of endothelin-converting enzyme, which degrades Aß. The activities of other Aß-degrading enzymes, insulin degrading enzyme and neprilysin, were unchanged. These results indicate that increased neuronal PKCe activity can promote Aß clearance and reduce AD neuropathology through increased endothelin-converting enzyme activity. http://www.pnas.org/content/103/21/8215.full
The other things I am loving is the stock structure. Maybe seven to seven and half million shares outstanding. A float of probably two and a half to 3 million (miniscule!). And NO OPTIONS which means you have to have extremely deep pockets to dare to go short. After hours positive news and the stock could open up fifty bucks or more. Longs will rejoice and shorts will drop dead.
I have not examined Aphios' patent(s) for an analog compound of Byrostatin (it is not for Bryostatin-1).
My point was, in my post on Seeking Alpha (dkitt), that Aphios is still years behind NTRP in the regulatory process of getting a FDA approved drug to market and as Whatsupp just explained "in a recent talk by Dr Alkon, he said that NTRP patent covers any PK epsilon enhancing drug. I.e. Any company that sells such a drug has to go through them."
There are interesting comments at the end of the Dendrite Research
article concerning independent research by Aphios that show confirmation of Dr. Alkon's AD theories:
Neurotrope BioScience: Upcoming Alzheimer's Trial Results May Propel Share Price
https://seekingalpha.com/pro/checkout/4046795?notice=pro
The Streets Real Money column just put out this article. TRCH is the third one discussed:
3 Independent Energy Stocks That Are Ready to Rock
3. Torchlight Energy (TRCH) (+23.7% ytd). Unlike EPM and GST, TRCH shares have performed very well thus far in 2017. This is a transformational year for Torchlight, as the company looks to drill the first well on its Hazel project in the Midland Basin by mid-year.
At present, Torchlight has virtually no current productive assets -- "PDP" in oil industry parlance -- and proving up Hazel is key to solidifying TRCH's operating future. Management has been looking to raise capital to fund drilling and for other corporate needs, and I believe the capital markets will support such a transaction.
That's the short-term story, but the longer-term cachet -- or Big Gold, if you will -- in the TRCH story is its Orogrande play in Hudspeth County near El Paso, TX. While Orogrande is not currently producing, the two development wells TRCH has drilled there have yielded a wealth of information. In my conversation with TRCH CEO John Brda, he noted that the initial data have done nothing but reinforce his bullishness on the Orogrande, and he singled out the extreme porosity of the rock there as an especially positive characteristic.
So, TRCH has the long-term upside, GST has the near-term catalyst in its upcoming shareholder vote and EPM has the stability of its dividend and debt-free balance sheet. It's a great time to be initiating positions in the smaller E&Ps, and I believe each of the three mentioned stocks will outperform the markets for the balance of 2017.
http://realmoney.thestreet.com/articles/04/07/2017/3-independent-energy-stocks-are-ready-rock
In the most recent 10K NTRP states that it has relinquished its rights to the AD diagnostic test in order to focus on treatment of AD and other neurodegenerative diseases. I assume those rights were returned to CRE (Cognitive Research Enterprise the successor organization of BRNI:
Discontinued Research
We had planned to develop two other lines of research related to learning and memory disorders: (i) drug prototypes that activate or inhibit the enzyme carbonic anhydrase to modulate the attention status of animals, which may have had applications for attention deficit disorder and post-traumatic stress disorder, and (ii) generalizing the application of a blood-brain-barrier delivery system to a variety of drugs through a contract research service to be offered to other pharmaceutical companies seeking to improve the penetration of their drug prototypes into the brain.
We have decided, however, to focus our efforts on neurodegenerative diseases, which are the most advanced programs in our portfolio, and therefore will not be pursuing either the drug candidate for activating carbonic anhydrase or the blood-brain-barrier delivery system.
We also relinquished rights to the AD diagnostic system under the terms of the February 2015 SOW (see below).
page 14
https://www.sec.gov/Archives/edgar/data/1513856/000114420417014012/v461285_10k.htm
I would suggest you call the company and speak to Noreeen.
I don't know why they have not put out a press release yet.
The Nigerian inspection team has already made their trip to the Dominican Republic. The next step, as I understand it, is for NAFDAQ to approve their report.
Wildginger, wow, this quote from that 2011 article brings us to were we are now...a few weeks away from Neurotrope's Ph2b trial results
"Researchers led by Daniel Alkon, scientific director and professor at Blanchette Rockefeller Neurosciences Institute at West Virginia University, were trying to work out how memories are stored on the molecular level when they discovered that PKC plays a critical role in the process. “It’s a very powerful regulator of molecular switches that send signals, especially at the most important junctions in the brain called synaptic junctions—the connections in the brain between neurons,” he says. “We discovered when we form memories we actually induce the formation of new synapses, and that’s regulated by protein kinase C and a whole host of other molecular players in the orchestra that protein kinase C regulates.”
With this understanding, Alkon’s team wondered whether PKC might be relevant to the memory loss associated with Alzheimer’s disease. “It turns out that the central molecular pathways of the pathophysiology of Alzheimer’s disease all involve protein kinase C,” Alkon explains. This led Alkon to several compounds that activate PKC, of which bryostatin 1 was the most potent.
“We found that PKC activators are remarkably effective in animal models of Alzheimer’s disease in addressing virtually all of the aspects of Alzheimer’s disease,” Alkon says.
These compounds “enhance memory. They correct memory deficits. They restore lost synapses and prevent the loss of synapses. They prevent the death of neurons. They prevent the amyloid plaques. And they prevent the neurofibrillary tangles. All of those are hallmarks of Alzheimer’s disease,” Alkon continues. “There’s no one therapy except activators of protein kinase C that does that.” These findings, he argues, suggest a new way of looking at Alzheimer’s disease.
Animal tests with bryostatin 1 have also shown that it restores memory after strokes and traumatic brain injuries. “Essentially what it’s doing is building new connections in the brain and preventing the death of neurons,” Alkon says. “It also has the potential of enhancing memory in normal patients or aging patients or depressed patients. We believe that there is a tremendous potential here.”
Alkon recently received approval to begin a Phase II clinical trial using bryostatin 1 to treat Alzheimer’s. He wants to partner with a private-sector company before moving forward, however."
WSJ article (anyone with a WSJ subscription who can provide excerpts):
The FDA Can Declare War on Alzheimer’s
Flexible standards for drug approval would help patients.
https://www.wsj.com/articles/the-fda-can-declare-war-on-alzheimers-1491347437
mcbio, regarding Neurotrope's (NTRP) upcoming release of Ph2b AD study results in 147 moderate to severe Alzheimer’s patients due by the end of this month you ask: "Is there any strong independent data to suggest activating protein kinase C epsilon would work in AD?"
This study provides some context using NTRP's lead drug
Byrostatin -1 to restore synaptic loss, the underlying cause of AD according to Neurotrope:
Bryostatin-1 Restores Blood Brain Barrier Integrity following Blast-Induced Traumatic Brain Injury
"Bryostatin-1 has been successfully used in numerous animal models of neural injury including TBI, ischemic stroke, auditory neurodegeneration, and Alzheimer’s disease and is currently under investigation in clinical trials...For example, bryostatin-1 protects against loss of pre-synaptic synaptophysin and loss of post-synaptic spinophylin following TBI in mice... Likewise, bryostatin-1 decreased apoptosis and prevented deficits in synaptogenesis in a global model of cerebral ischemia..."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5000781/
Also, the scholarly article below was referenced twice by Dr. Alkon, the lead researcher and CSO of NTRP in recent presentations at both the Oppenheimer and Sachs Forums. I believe for Dr. Alkon this study independently confirms an element of his theoretical framework for the role of PKC epsilon in modulating Alzheimer’s disease. This study addresses one aspect of the multi-modal effect of treatment with Byrostatin. The reduction of amyloid plaque pathology.
Briefly, the study took mice that genetically express AD at an early stage in their life cycle. Then this mouse model was further genetically manipulated with a gene to produce higher than normal levels of PKC epsilon (the brain agent that Byrostatin stimulates to treat AD). The premise was, will higher levels of PKC epsilon prevent AD symptoms in animals that always develop the disease.
This study showed that these double transgenic mice had lower amyloid plaque deposits and Alzheimer’s disease expression confirming an important theoretical aspect of Dr. Alkons work.
PKCe increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice
Choi et. al.
March 31, 2006
Abstract
Deposition of plaques containing amyloid ß (Aß) peptides is a neuropathological hallmark of Alzheimer's disease (AD). Here we demonstrate that neuronal overexpression of the e isozyme of PKC decreases Aß levels, plaque burden, and plaque-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-mutant forms of the human amyloid precursor protein (APP). Compared with APP singly transgenic mice, APP/PKCe doubly transgenic mice had decreased Aß levels but showed no evidence for altered cleavage of APP. Instead, PKCe overexpression selectively increased the activity of endothelin-converting enzyme, which degrades Aß. The activities of other Aß-degrading enzymes, insulin degrading enzyme and neprilysin, were unchanged. These results indicate that increased neuronal PKCe activity can promote Aß clearance and reduce AD neuropathology through increased endothelin-converting enzyme activity. http://www.pnas.org/content/103/21/8215.full
resident1, fair enough and I should have explained that the study addresses one aspect of the multi-modal effect of treatment with Byrostatin. The reduction of amyloid plaque pathology.
Perhaps the article referenced below that was posted by runncoach on the Investor Village board is more to your point:
Bryostatin-1 Restores Blood Brain Barrier Integrity following Blast-Induced Traumatic Brain Injury
"Bryostatin-1 has been successfully used in numerous animal models of neural injury including TBI, ischemic stroke, auditory neurodegeneration, and Alzheimer’s disease and is currently under investigation in clinical trials...For example, bryostatin-1 protects against loss of pre-synaptic synaptophysin and loss of post-synaptic spinophylin following TBI in mice... Likewise, bryostatin-1 decreased apoptosis and prevented deficits in synaptogenesis in a global model of cerebral ischemia..."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5000781/
The scholarly article below was referenced twice by Dr. Alkon in recent presentations at both the Oppenheimer and Sachs Forums. I believe for Dr. Alkon this study in particular may be the best independent confirmation of his own research and independently confirms a key element of his theoretical framework for the role of PKC epsilon in modulating Alzheimer’s disease.
Briefly, the study took mice that genetically express AD at an early stage in their life cycle. Then this mouse model was further genetically manipulated with a gene to produce higher than normal levels of PKC epsilon (the brain agent that Byrostatin stimulates to treat AD). The premise was, will higher levels of PKC epsilon prevent AD symptoms in animals that always develop the disease. This study showed that these double transgenic mice had lower amyloid plaque deposits and Alzheimer’s disease expression confirming an important theoretical aspect of Dr. Alkons work.
PKCe increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice
Choi et. al.
March 31, 2006
Abstract
Deposition of plaques containing amyloid ß (Aß) peptides is a neuropathological hallmark of Alzheimer's disease (AD). Here we demonstrate that neuronal overexpression of the e isozyme of PKC decreases Aß levels, plaque burden, and plaque-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-mutant forms of the human amyloid precursor protein (APP). Compared with APP singly transgenic mice, APP/PKCe doubly transgenic mice had decreased Aß levels but showed no evidence for altered cleavage of APP. Instead, PKCe overexpression selectively increased the activity of endothelin-converting enzyme, which degrades Aß. The activities of other Aß-degrading enzymes, insulin degrading enzyme and neprilysin, were unchanged. These results indicate that increased neuronal PKCe activity can promote Aß clearance and reduce AD neuropathology through increased endothelin-converting enzyme activity. http://www.pnas.org/content/103/21/8215.full
Neurotrope Nears Breakthrough In New Alzheimer's Treatment
Apr. 3, 2017 4:46 PM ET
About: Neurotrope, Inc. (NTRP)
by: Sharon di Stefano
Sharon di Stefano
Biotech, healthcare, small-cap, special situations
(1,144 followers)
Summary
An extraordinary way to treat Alzheimer’s reaches Phase II.
Top line data expected in April 2017 in placebo controlled study of bryostatin-1 in 148 moderate to severe Alzheimer's patients.
Healing underlying causes versus symptoms can transform Alzheimer’s medicine.
Lead drug bryostatin, from a natural source, can be synthesized for manufacturing efficiency.
Common risks are translation of early results to larger trials, and competition.
Full article:
https://seekingalpha.com/article/4059932-neurotrope-nears-breakthrough-new-alzheimers-treatment?auth_param=v6t5:1ce5bcr ;
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