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I guess he saw the same Pattern I saw.. he had the AMBS Chart Deleted... sheesh..
thats funny... that AMBS Chart looks similar now to the pattern of last Aug/September... look what happened then.. thanks Chart Guy...
that AMBS chart means squat here
Really Means nada. ,no offense.
AMBS
GL2ALL
Lets not forget, that there is another possibility. Gerald is on record saying about data in regards to the Eye and "Ear". I don't have time now to look it up but its on the board here further back.
AMBS
GL2ALL
Nice find. That report had Lympro at Phase 2 And they described it as a neurotrophic factor companion diagnostic. ??????
Also many of those AD therapeutic candidates may be knocking at AMBS's door to buy lympro to screen clinical trial patients.
Seems as if Dr. Urano was looking for the Bio marker for DB and what he found was both the marker MANF and the possible therapeutic drug candidate in one.
AMBS.
Concurrently with this announcement, Amarantus announced that it has executed an Exclusive Option Agreement with the University of Massachusetts Medical School ("UMMS") to license intellectual property recently developed at UMMS to advance Amarantus' diabetes diagnostic development and commercialization program using Amarantus' lead protein MANF as a biomarker for beta cell stress.
"The commercial potential for MANF as a diagnostic test that could identify patients who would most greatly benefit from Oral-lyn represents a significant market opportunity," said Gerald Commissiong, Amarantus' co-founder and Chief Operating Officer. "Unlike therapeutics, diagnostics can be commercialized in a relatively short period of time. This collaboration significantly improves Amarantus' development pipeline, targeting a key medical need in a multi-billion dollar market with no commercial-stage competition."
"The joint efforts of many players, starting from the discovery of a new use of MANF at UMass Medical School for diabetes, and the synergies of two highly committed organizations, has allowed us to generate a unique opportunity to launch a commercial development program for MANF as a biomarker of cellular stress and stressed beta cells in diabetes," said Dr. Fumihiko Urano, associate professor at the University of Massachusetts Medical School, who identified MANF's role in this area.
http://markets.financialcontent.com/stocks/news/read/18673668/Generex_Biotechnology_and_Amarantus_BioSciences_Announce_Oral
"
This is an email reply from Gerald to me on that subject a while back. :
"While we canceled the deal with Generex, we maintain the option."
http://markets.financialcontent.com/stocks/news/read/18673668/Generex_Biotechnology_and_Amarantus_BioSciences_Announce_Oral
On Fri, Aug 30, 2013 at 6:07 PM, Gerald Commissiong <gerald@amarantus.com> wrote:
All will be revealed in time
Gerald E. Commissiong
President & CEO
"Be the change you wish to see in the world." Good quote at the bottom of Dr. Urano's signature. This is the difference from people who do and people who think it can't be done.
AMBS is lucky to have scientists like this gentleman who believe in the science and the potential for MANF.
Nice post
AMBS
Save your lectures and stay on AMBS topic.
Amarantus' LymPro May Be More Crucial For Alzheimer's Treatment Than We Think
In a very detailed and thorough article entitled "LymPro Looks Like The Real Deal - Amarantus Now A Buy" published on October 15, Seeking Alpha author Jason Napodano makes the case for Amarantus BioSciences (OTC:AMBS) based on the recent success of its Alzheimer's diagnostic platform, LymPro. LymPro is Amarantus' flagship Alzheimer's pipeline product, and is designed as a minimally invasive blood test that can detect the earliest stages of Alzheimer's disease [AD]. Readers should familiarize themselves with his piece in order to better understand what follows here.
In this article, I will summarize Napodano's points concerning the value, importance, and market need for LymPro, most of which I generally agree with. His target price for AMBS of $0.20 a share is based on Amarantus' current pipeline which includes LymPro among other assets. For his target price, I assume (though the author did not state this explicitly) a time horizon of 2H2014, given that Amarantus has no revenues and likely will not have any until LymPro's commercial launch at that time, assuming it clears CLIA approval. A share price of 4x the current one probably will not materialize until Amarantus can at minimum prove LymPro works and sells, which won't happen for at least another year.
While target prices can never be exact, I do believe Napodano is generally correct in his assessment of a steep increase in AMBS shares come late 2014. What Napodano missed, however, is one critical point that could have a tremendous impact on the importance and value of LymPro and therefore on the valuation of Amarantus moving into the end of 2016, something that could significantly increase the target price for AMBS going into 2017. This same factor could also have a large impact on Eli Lilly (LLY) and BD Biosciences (BDX).
LymPro Recap
The difficulty in establishing a blood test for Alzheimer's has to do with the brain/blood barrier. Because of this nature-given shield, it is difficult to establish a diagnostic measure in the blood that is indicative of what is occurring in the brain. Amarantus has overcome this by stimulating peripheral blood lymphocytes (PBLs) with mitogenic stimulation that initiates the cell division cycle. (Mitosis = cell division, and mitogenic compounds cause cell division.) In healthy cells, a biomarker called CD69 increases in order to shut down what is interpreted as premature mitosis. In Alzheimer's patients however, CD69 is not increased and the PBLs enter the cell cycle inappropriately. This is not the case with other types of dementia, allowing AD to be specifically targeted by this diagnostic method.
A Phase 1 CLIA study of 88 patients showed a clinical sensitivity rate of 91% and a clinical specificity rate of 92%. The results were independent of the severity of the dementia caused by AD. A Phase II study partnering with BD Biosciences will be initiated in the next few months, and assuming success, the companies estimate commercial launch in the second half of 2014.
Napodano makes a valuation stab of $500M for LymPro based loosely on Eli Lilly's past acquisition of AD diagnostic Amyvid through its acquisition of Avid Radiopharmaceuticals for $300M upfront and $500M in backend consideration. Amyvid is a different Alzheimer's diagnostic that only works once a patient is already experiencing memory loss, making early detection unlikely.
The Dreary Alzheimer's Pipeline
The Alzheimer's clinical pipeline is especially dreary and has very few bright spots. Currently, there is no known cure for Alzheimer's, or even a treatment beyond minimal effectiveness in slowing symptoms. Alzheimer's is different from most other terminal illnesses because researchers not only do not fully understand the cause of it, but even the mechanism of its progression in the brain is very poorly comprehended. Researchers cannot even agree on what a treatment would theoretically have to do to cure AD.
To illustrate what I mean, take cancer. The cause of many types of cancer is poorly understood in terms of why some people become sick as opposed to others. However, in all cases of cancer, everyone agrees on what the disease is and on what has to be done theoretically to cure it. Namely, cancer cells keep dividing and growing, eventually crowding out healthy organs and killing the patient. The theoretical cure is to somehow get rid of the cancer cells without damaging the healthy ones. The only question is how, but everyone agrees on what has to be done and what to pursue.
Even poorly understood central nervous system diseases like Parkinson's and ALS, the causes of which are mostly unknown, are understood in terms of their mechanisms of action and what a theoretical cure would look like. In Parkinson's, dopamine-producing brain cells begin to die, so the theoretical answer is to regenerate them somehow. In ALS, motor neurons die, leading to the same theoretical answer as to a cure. Point being, even in poorly understood diseases of the central nervous system, researchers basically understand what needs to be done to cure them, but just don't know how yet.
Alzheimer's is different because researchers don't agree as to what to even target. For example, one prominent theory as to the mechanism of the progression of AD is amyloid plaque buildup in the brain, leading to the theory that clearing the plaque could lead to a cure, or at the very least a slowed rate of disease progression. Unfortunately, researchers have already succeeded years ago in engineering a protease that clears amyloid buildup in the brain (see here), but dementia persisted and disease progression was not even slowed, even in patients whose amyloid plaques were completely cleared. This could be because the brain damage, once the plaque builds up, is already done and irreversible, but nobody knows for sure.
It is because of this conceptual uncertainty as to what an AD cure would even consist of that a large percentage of AD clinical trials only focus on slowing symptoms and nothing more. Of the 20 industry sponsored phase III trials for AD currently open, 7 of them explicitly focus only on symptomatic expressions of the disease as primary and secondary endpoints rather than AD itself.
Taken together, this is what makes the AD clinical pipeline so dreary. But one of these trials does provide a ray of hope for treating the disease itself, the results of which could have serious implications for the valuation and importance of LymPro, and in consequence the valuations of Amarantus, Eli Lilly, and BD Biosciences. What follows is the critical point I believe Napodano overlooked.
The Missing Piece
In his piece, Napodano correctly writes:
We point investors to the high profile failures of Pfizer / J&J's bapineuzumab in 2012 or Eli Lilly's solanezumab in 2012 or semagacestat in 2010. Elan's failures with bapineuzumab have been well chronicled following the phase II data in 2008. However, Pfizer and new partner, J&J, pushed forward in phase III, thinking they had identified a sub-group of patients without a gene called ApoE4 though post hoc data mining. Some 4,100 patients, 4 years and $500 million later, the phase III trial still failed. Despite not learning much from their failure with semagacestat in 2010, Eli Lilly's solanezumab failed a phase III study in Alzheimer's disease in 2012.
Solanezumab is a monoclonal antibody designed to clear amyloid plaques in the brain, as mentioned before, and successfully does so, but does not cure or significantly slow AD. Despite these failures however, evidence suggests that cognitive decline was slowed somewhat in these trials. Now Eli Lilly is at it again with a solanezumab Phase III trial, but with a very interesting twist: a different type of Alzheimer's patients. Namely, patients that have no disease symptoms at all, but have tested positive for a dominant genetic mutation that is known to cause early onset Alzheimer's. This mutation is called Autosomal Dominant Alzheimer's. It is extremely rare, but provides the only opportunity to test amyloid-clearing treatment in completely asymptomatic patients that will, with a high degree of certainty, develop Alzheimer's in the future.
It is this trial, with results due in December 2016, that could have enormous implications for AD in general and Amarantus' LymPro in particular. While Napodano's analysis is by-and-large accurate for what it is considering, the results of Eli Lilly's trial on Autosomal Dominant Alzheimer's patients could fundamentally change the whole scenario.
How exactly? If, for example, a significant portion of these asymptomatic patients were to show delayed onset of their Alzheimer's, or perhaps even its prevention due to clearing amyloid plaque before buildup even begins and brain damage ensues, it would mean by implication that the earliest detection of Alzheimer's possible in spontaneous cases would be absolutely critical to delaying or perhaps even preventing the disease. As of now, LymPro is the best candidate for the earliest possible presymptomatic Alzheimer's detection.
Assuming Lympro's Phase II success, which would clear the way for CLIA approval and commercialization in 2H2014, investors will have to wait until the completion of Eli Lilly's solanezumab Phase III trial on Autosomal Dominant Alzheimer's patients in December 2016 to see if these asymptomatic patients respond to it, as signified by delay in the disease. If they do, LymPro could prove to be a lot more crucial to the Alzheimer's world than we all thought.
http://seekingalpha.com/article/1773372-amarantus-lympro-may-be-more-crucial-for-alzheimers-treatment-than-we-think
and yet it is on plan to be commercialized in 2014 with a peak Market Potential of OVER 500 Million Dollars..
you left out the part of Companion Diagnostics... very important part to help find a cure
luckily we have Doctors and Scientists with positive attitudes working to find cures.. unlike --- well you know
Gl2U...
what some people don't realize is that the job of a good CEO is to have the right people in the right places at the right time..
DR. ADAM SIMON & DR. COLIN BIER
Dr. Bier will be working closely with Dr. Adam Simon, current member of the Company's Corporate Advisory Board, to finalize and implement the Company's commercialization strategy for LymPro to both maximize potential revenue and position LymPro as a potential companion diagnostic for therapeutic
http://www.amarantus.com/about-us/board-of-advisors
DR. David A. Lowe, PhD
will be overseeing the translational development of MANF through first-in-man clinical studies, as well as advising on the development of the LymPro Test® blood diagnostic for Alzheimer's disease, PhenoGuard Protein Discovery Engine and potential additions to the Amarantus portfolio.
http://ir.stockpr.com/amarantus/company-news/detail/964/amarantus-appoints-david-a-lowe-phd-to-board-of-directors
well done Gerald. nice choices to run these Divisions..
all in your opinion, which i think is worth Zero here on AMBS. thats my opinion.
GL2U
not at all, they publish the positive data when they have it. these are ongoing studies and grants awarded to independent researchers. just be glad it involves AMBS's lead targeted Therapeutic in someway.
I do not have an Issue with the CEO as some do here.. BH beat me to it..
If Gerald was doing such a bad job he would not be able to attract the Immense talent onto the BOD & BOA.. all of which have publicized their happiness in being associated with AMBS.
GL2ALL
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE - MANF
Project Funding Information for 2013:
Total Funding: $304,756
2013 Award Notice Date: 13-SEP-2013
http://projectreporter.nih.gov/project_info_details.cfm?aid=8452819&icde=18489718
2013 Award Notice Date: 8-JUN-2013
Total Funding: $344,920
http://projectreporter.nih.gov/project_info_details.cfm?aid=8488313&icde=18489803
DESCRIPTION (provided by applicant): Synopsis: Our long-term objective is to determine the roles of ER stress in the heart. Using a genomics approach we identified a group of genes induced by the ATF6 branch of the ER stress response (ERSR) that encode proteins predicted to have para/autocrine effects on the heart. These proteins, which we call ER stress-inducible cardiomyokines (ERS-CMKs), are unique, since they are synthesized in, and secreted from the heart during stresses, e.g. ischemia, that impair synthesis and release of most other proteins. The focus of this proposal is the ERS-CMK, mesencephalic astrocyte-derived neurotrophic factor (MANF), which is novel since it functions intra- and extracellularly to affect cardioprotection. In this proposal cardiomyokines (CMKs) are defined as proteins secreted by the heart that may exert para/autocrine effects, in part, by direct binding to heart cells, as well as binding to resident and, perhaps non-cardiac-derived stem cells to affect their function. Most CMKs are synthesized and folded in the rough ER, routed to the Golgi, then to secretory vesicles before secretion. In the absence of ER stress, conditions are optimal for expression, folding and, thus, secretion of functional CMKs. However, some stresses impair protein folding in the ER, activating ER stress, which decreases CMK transcription, translation, folding and secretion, thus leading to a loss of CMK function. ER stress leads to activation of ATF6, a nodal sensor of ER stress that increases transcription of many known ERSR genes that encode ER-targeted proteins that directly augment ER-protein folding. We showed that the ATF6 branch of the ERSR, which is activated during ischemia, protects the heart from damage during ischemia and reperfusion, ex vivo and in vivo. Microarray analyses of mouse hearts revealed numerous ATF6-inducible genes that encode proteins predicted to be ER-targeted and secreted (ERS-CMKs). One ERS-CMK, MANF, is unusual, since it is either retained or secreted, depending on the stress. Overexpression of MANF, or addition of recombinant MANF (rMANF) to culture medium, protected cardiomyocytes, while MANF knock-down increased simulated I & I/R-mediated cell death. Hypothesis: The specific hypothesis addressed in this proposal is that ischemia, which is known to activate ER stress, induces the ERS-CMK, MANF, in an ATF6-dependent manner, and acts intra- and extracellularly to protect the heart from ischemic damage. The Specific Aims that address this hypothesis are to: 1. examine expression of MANF in the ischemic mouse heart subjected to ATF6 gain- and loss-of-function, 2. determine the effects MANF gain- and loss-of-function in the ischemic heart, in vivo, and 3. dissect the functions of intra- and extracellular MANF, delineate the structural features of MANF required for its activities, and identify signaling mechanisms responsible for MANF function in cardiomyocytes.
Abstract Text:
Proteins secreted by the heart are called cardiokines. After secretion, cardiokines, such as cytokines, growth promoters and stem cell homing factors affect ischemic damage, as well as stem cell survival and engraftment. But ischemia impairs protein folding and secretion, and negatively impacts stem cell-mediated regeneration. However, we discovered a secretion process that resists this inhibition, enabling the release of certain beneficial cardiokines, just when they are needed the most. The objectives of this study are to examine the functions of, and molecular mechanisms governing this secretion process in cardiac myocytes, in vitro and in vivo, and in cardiac stem cells. We discovered this process while studying the beneficial cardiokine, mesencephalic astrocyte-derived neurotrophic factor (MANF), which resides in the endoplasmic/sarcomplasmic reticulum (ER/SR). Our hypothesis is that 1) GRP78 regulates the secretion of beneficial ER stress cardiokines from cardiac myocytes and cardiac progenitor cells by mediating the conditional retention of proteins in the ER/SR, and 2) CPCs are specially configured with a novel cytosolic form of GRP78 that enhances survival, as well as cardiokine secretion during ER stress.We will address this hypothesis by using MANF as a model cardiokine, GRP78 gain- and loss-of-function, cultured cells and mouse hearts, /\AV9-mediated in vivo gene transfer, and zero-distance live cell cross linking in the following specific aims: 1- to determine the mechanism by which GRP78 regulates cardiokine secretion from cardiac myocytes, 2- to assess GRP78-regulated cardiokine secretion in the heart, in vivo, and determine the effects of disrupting this secretion on ischemic damage and regeneration, and 3- to examine the effects of GRP78 in the ER, as well as a novel, cytosolic form of GRP78 on cardiokine secretion, responses to ER stress and survival of cardiac stem cells. The results of these studies will facilitate the design of therapeutic strategies aimed at enhancing the secretion of beneficial cardiokines that minimize damage and maximize regeneration.
http://projectreporter.nih.gov/project_info_description.cfm?aid=8452819&icde=18489718
http://projectreporter.nih.gov/project_info_description.cfm?aid=8488313&icde=18489803&ddparam=&ddvalue=&ddsub=&cr=2&csb=default&cs=ASC
AMBS - MANF
Next catalyst for Lympro = Phase 2 commencement
A Phase II study partnering with BD Biosciences will be initiated in the next few months, and assuming success, the companies estimate commercial launch in the second half of 2014.
Next catalyst for Lympro is not until LATE 2014
It is estimated that the market opportunity for Retinitis Pigmentosa exceeds $10B annually
http://globenewswire.com/news-release/2013/08/12/566161/10044574/en/Amarantus-Announces-Positive-Orphan-Data-for-MANF-in-Retinitis-Pigmentosa.html
LymPro Looks Like The Real Deal - Amarantus Now A Buy by Jason Napodano.
Quote:Becton, Dickinson & Co is an expert in flow cytometry. In fact, BD Biosciences may be the best in the world in this area. That's why Amarantus engaging with BD for LymPro sample analysis and analytical performance was so important. Amarantus now has one of the world's bests in flow cytometry looking at the issues that causes unacceptably high intra-sample variability during Provista's Phase II study. The news today (LINK) from Amarantus announcing that BD has validated the previous findings from the Phase I study and established Analytical Performance (reliability and reproducibility) of the test is an enormous leap forward.
In the simplest analogy, LymPro is a highly specific and sensitive smoke detector, and where there is smoke, there is usually a fire. And given the size of this market, LymPro has $500 million potential with CLIA approval. Data from this Phase II CLIA study noted above is expected around the middle of 2014. This data will include analytical performance characteristics and reproducibility of the assay. Assuming positive data, we believe Amarantus could be in position to file for CLIA clearance and hear back by the end of 2014.
Journal of Molecular Neuroscience 2013-11-01 MANF ( AMBS )
Mesencephalic astrocyte-derived neurotrophic factor inhibits oxygen-glucose deprivation-induced cell damage and inflammation by suppressing endoplasmic reticulum stress in rat primary astrocytes.
Hua Zhao, Yi Liu, Lei Cheng, Ben Liu, Wen Zhang, Ying-Jun Guo, Lin Nie
PMID 23760988
Abstract
Astrocyte inflammation plays important roles both in physiological and pathological processes in the central nervous system (CNS). Ischemic injury in the CNS causes damage to astrocytes and the release of proinflammatory cytokines, such as tumor necrosis factor-a, interleukin-1ß, and interleukin-6. This current study investigates whether mesencephalic astrocyte-derived neurotrophic factor (MANF) inhibits oxygen-glucose deprivation (OGD)-induced cell damage and inflammatory cytokine secretion by suppressing endoplasmic reticulum stress in rat primary astrocytes. We found that MANF alleviated OGD-induced astrocyte damage and rescued the cell viability, and the upregulation of GRP78 (endoplasmic reticulum (ER) stress marker) and NF-?B p65 (one of the central mediators of proinflammatory pathways) induced by OGD were significantly reduced by preincubation of MANF. In addition, the increases of secretion and mRNA expression levels of the proinflammatory cytokines IL-1ß, IL-6, and TNF-a in astrocytes induced by OGD were significantly suppressed by MANF. These findings demonstrate that MANF shows the potential to alleviate cell damage and inflammation in rat primary astrocytes by suppressing ER stress, indicating that MANF plays an important role in astrocyte inflammation and functioning and may suggest a promising strategy for neuroprotection in the CNS.
http://www.sigmaaldrich.com/catalog/papers/23760988
Now please tell me these last 2 posters do not deserve to be on ignore? whoever on the AMBS board became less intelligent if they read those last posts.
Wow. Unreal.
ok i will take your advice and Add & hold til then
thats not too soon,. you need to buy a calendar
Soon huh....
Soon bankrupt
"The Company expects to be in a position to submit the necessary data package to CLIA to support the intended use statement "aid in the diagnosis of Alzheimer's disease," and commercial launch of LymPro in the second half of 2014 as a Laboratory-Developed Test (LDT) through CLIA."
Revenue stream is on plan,,, CLIA clearance = Revenue
We see a three-pronged approach to generate revenues with LymPro. The first would be to gain approval under the CLIA clearance, which would allow clinical diagnostic labs to utilize LymPro to aid in the diagnosis of Alzheimer's disease as an adjunct diagnostic either in a research or private payor situation. Ultimately, the company's goal is to obtain approval under the FDA's de-novo pre-market notification 510(k) or Premarket Approval (PMA) process. This type of clearance would facilitate LymPro being used as a companion diagnostic product in combination with one or more therapeutic agents.
Under this secondary scenario, uptake is facilitated through greater coverage with Medicare or private institutions and by treating physicians writing prescriptions for the companion therapeutic. We could see utility with LymPro in the diagnosis of patients that fit the subset of the Alzheimer's disease population companies like Pfizer and J&J are going after with bapineuzumab or Eli Lilly with solanezumab. Other companies like Merck, Lundbeck, and Roche are also testing new Alzheimer's therapeutic agents that might show improved outcome if companioned with a diagnostic such as LymPro. The Holy Grail for these companies is to identify a patient population that responds to their drug, i.e. mild Alzheimer's disease with moderate beta-amyloid or tau tangles, and couple the therapeutic approach to a diagnostic kit proven to identify this population. Instead, most continue to gamble big dollars on studies boomed to fail. Under this scenario, we see the peak revenue potential for LymPro in the $250+ million range.
The final market strategy for LymPro would be to achieve market penetration as a stand-alone diagnostic for early-detection or in "high risk" patients. This would essentially be taking the CLIA clearance and expanding to full FDA approval for commercial sales, with uptake facilitated by (yet to be generated) clinical data and full insurance reimbursement with CMS. With 98% sensitivity and 96% specificity as demonstrated in the previous clinical studies, LymPro has $500+ million potential in our opinion.
http://seekingalpha.com/article/1347691-amarantus-lympro-could-be-a-game-changer-for-alzheimers-diagnosis
Look at this statement:
"Sell if you can, because this is going down very hard."
You could have just posted this, instead of fabricating the rest of your spiel and would have reached more people to attempt to obtain you new entry price.
Why else would you want (need) AMBS to go down?
PS. AMBS's partner will take LymPro to market. Amarantus only has to prove it works. They are on that path and $400,000 is the tab for the next validation step. Give or take. Read that statement in the Companies filings.
Step up your efforts , u will need to.
We are proud to be the first group to unite the different stakeholders in the concussion debate and believe the United Nations will set the stage for this truly global discussion."
http://ir.stockpr.com/amarantus/company-news/detail/974
A global health issue... there are not many venues better than this to hold this event.
nice connections used by Jack Brewer
http://jackbrewer.net/read_news.php?id=13
this AMBS promo seems to be by a third party not directly controlled by AMBS.... and the others listed where not compensated... just picking the stock to look good when it goes up..
http://stockpromoters.com/View-Stock-Promotions-By-Symbol.aspx?symbol=ambs&ctl00%24ContentPlaceHolderyy%24Footer1%24Image2.x=0&ctl00%24ContentPlaceHolderyy%24Footer1%24Image2.y=0
Also that other site p&d. Com is full of incorrect info .. especially the part where they swear they do not short sell stocks they publish...
Cool. I picked the right answer.
ONO Pharma who is conducting research with AMBS's MANF on Diabetes and Neuro-Degenerative Diseases is also tied to Novartis on an AD drug
ONO & NOVARTIS working on AD Drug --
In December 2005, Ono signed an agreement with Novartis Pharma AG on the co-development and commercialization in Japan of ONO-2540/ENA713D for the treatment of Alzheimer's disease. It was launched in July 2011 by Ono as "Rivastach® Patch" and by Novartis Pharma KK as "Exelon® Patch". The drug is the first transdermal patch developed using rivastigmine (oral drug), which is currently in use in over 70 countries outside Japan for the treatment of Alzheimer's disease. The drug is expected to reduce the burden on caregivers in dosing control.
http://www.ono.co.jp/eng/alliances/license/novartis.html
MANF DB Grants
Saarma, Mart, professor, the University of Helsinki, 25 000 Euros
MANF trophic factor as a potential novel therapeutic agent for type1 diabetes
Identifying the mechanisms that lead to the death of insulin producing beta cells may help to find new prevention methods of type 1 diabetes. MANF (Mesencephalic astrocyte-derived neurotrophic factor) protects and restores nervous cells with a dopamine neurotransmitter in the animal model of Parkinson’s disease. In order to study the biological role of MANF, the research group has developed a knockout mouse model (MANF KO). Surprisingly, the MANF KO mouse developed severe diabetes soon after its birth, as a result of advancing beta cell mass reduction.
This research venture studies molecular-level mechanisms where MANF regulates beta cell survival and dissemination in the islet cells of normal knockout mice. In addition to this, the research group aims to develop a transgenic mouse model that can be used when studying whether or not excessive manifestation of MANF can prevent the development of diabetes in mice.
http://www.diabetestutkimus.fi/en/grants/recipients/year_2013
6 quarters. Were not in the if response. Lets be clear. Stop twisting. Lol. I had to say that.
GL2all
@JNapodano: @68Tele_ @spence18 6 quarters. If they call the warrants, more like 12-15 quarters. Burn very dependent on R&D though for MANF.
You didn't like his answer to your question. ?
@68Tele_: @JNapodano @spence18 At $500k/month and no JVs or grants, when do they run out of cash?
I clearly understood his opinion.. you did not because you are disputing his Opinion!!!
The asset is moving to phase 2... the market potential is X the valuation he gave is his opinion and happens to be supported by analysts you yourself just posted.. valuation is based on sales, market potential involves sales projections..
Therefore, the entire Amarantus Diagnostic division is worth an estimated $50 million today.
Amarantus' LymPro May Be More Crucial For Alzheimer's Treatment Than We Think
for what I believe
even better, the more who want it the higher the price for MANF
not accurate, AMBS did change corporate structure and created Amarantus DX for possible spin off of their diagnostic assets and decided not to do it at the moment, but they still can.. and Gerald is on record talking about how valuations of their Diagnostic assets can made based off of multiples of sales. which keeping to plan (which they have) should commence in the 2nd half of 2014
Unsupportable by any publicly disclosed information from AMBS, by any AMBS Diagnostcs analyses/valuations done and published so far and of course by recent trading volume and direction.
Novartis - AMBS's MANF white paper was written by a Swiss Neuro firm for a reason
NeuroAssets
MANF white paper.
Prepared by
David A. Lowe PhD & Roman Urfer PhD
NeuroAssets Sàrl, Vevey, Switzerland
www.neuroassets.com
both of whom have heavy connections to Novartis