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Jonathan Verenger
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Exciting Field In Cure For Parkinson's 3 comments
Dec 7, 2012 8:20 AM | about stocks: AMBS.OB, AMGN, BMY
I recently wrote an article covering some companies attempting tofind a cure for Parkinsons. As a follow up, I wanted to write about an exciting field of neutrophic factors that are being used in an attempt to treat Parkinsons.
Neutrophic factors are a family of proteins that are responsible for the growth and survival of developing neurons and the maintenance of mature neurons. Recent research has proven that neurotrophic factors promote the initial growth and development of neurons in the central nervous system and peripheral nervous system and that they are capable of restoring damaged neurons in test tubes and animal models. Neurotrophic factors are often released by the target tissue in order to guide the growth of developing axons. Currently, neurotrophic factors are being intensely studied for use in bioartificial nerve conduits because they are necessary in vivo for directing axon growth and regeneration. In studies, neurotrophic factors are normally used in conjunction with other techniques such as biological and physical cues created by the addition of cells and specific topographies.
In this article I'm going to cover 3 different neutrophic factors, glial cell-derived neurotrophic factor or GDNF, cerebral dopamine neurotrophic factor or CDNF, and mesencephalic astrocyte-derived neurotrophic factor or MANF as part of a two part series. Providing assistance in this article is Henri Huttunen, Ph.D., CSO and Partner from Hermo Pharma Oy Ltd., a privately owned, venture capital backed company based in Finland working on therapeutic approaches for currently untreatable medical needs, particularly Parkinson's disease. Hermo Pharma is a recent recipient of approximately $700,000 in grants from the Michael J. Fox Foundation.
It is important to start with GDNF since it was one of the first to be tested on humans via delivery directly to the brain. GDNF is a protein that, in humans, is encoded by the GDNF gene. GDNF is a small protein that potently promotes the survival of many types of neurons. GDNF showed promising results in two Parkinson's disease clinical trial and in a number of animal trials; however, a study came out later that reported the results as a placebo effect and as a result the clinical studies performed by Amgen (AMGN) and Medtronic (MDT)were halted. Additionally, a safe and easy method of delivery became a significant roadblock for GDNF. Work on perfecting the delivery of GDNF to the targeted is ongoing and it is still believed to have clinical importance for the treatment of ALS and more recent studies suggest it could be used in reducing drug and alcohol addiction.
Below is a Q&A I had with Henri. My comments and questions below are in bold for clarity:
Me: GDNF was at one point very promising yet clinical studies were halted after roughly $300 Million was spent on research. From what I can gather a big problem that GDNF ran into was the ways in which it was delivered. Are there alternative ways in which to deliver MANF/CDNF that would make it less risky for humans?
Henri: GDNF was one of the first biologicals to be tested in humans via intracerebral delivery. There are many simple technical reasons that contributed to the failure of GDNF, and as you correctly pointed out, many of these point to the delivery being critical for efficacy. In the past ten years, intracerebral delivery technology for protein drugs has developed quite a bit - of course many lessons were learned from the GDNF trials. Also, during this time deep-brain stimulator has become a widely accepted aid for PD patients. The surgical operation for implantation of DBS electrodes is highly similar to implantation of infusion catheters. So, in a way, we are now well-positioned to start testing the efficacy of therapeutic proteins - instead of developing delivery technologies. Prof. Steven Gill has recently initiated a new Phase 2 study with GDNF in Bristol, using improved delivery methods.
Me: Were the GDNF tests performed with a naturally occurring version (or variant) or with a modified or non-natural variant?
Henri: One important contributor of GDNF's failure in the clinic was likely its very limited distribution in the brain. Natural forms of GDNF and many other related proteins such as Neurturin (Ceregene) bind strongly to extracellular matrix proteoglycans which limit its distribution after infusion. There are some strategies in development to alter these sites in GDNF/Neurturin to improve their distribution in the brain. Very importantly, the natural forms of CDNF and MANF do not bind to these heparin-type proteoglycans and distribute much more widely than GDNF/Neurturin when injected into the brain.
Me: I am curious to know what ties you have with MANF. I see that you recently challenged patents held by another company called Amarantus BioScience (AMBS) which were held up in court. Does Hermo Pharma hold patents on this? Could you shed some light on this for me?
Henri: Regarding the recent patent challenge, we strongly believe that the European Patent Office has made a significant mistake in granting the Amarantus's MANF patent a 90% sequence homology protection. The reason why we believe this is based on the following:
1.) Amarantus originally patented a non-natural form of the protein (probably a cloning artifact resulting in an amino acid change vs the naturally occurring form of MANF).
**My NOTE: Amarantus separately claims to have additional patents on the protein in SEC filings.
2.) A single amino acid change in a critical site in the MANF protein will entirely destroy its biological activity (several independent laboratories have confirmed this).
3) Their patent covers all sequences with 90% homology to MANF (182 amino acid protein --> variation in 18 amino acid residues allowed, 20 options for each position --> you do the math; the result is an astronomical number of variants!). According to the patent law this causes "an undue burden" to anyone who would like to test these variants for activity. This is the explanation why we have challenged the EPO granted patent on MANF for Amarantus.
Amarantus Therapeutics owns the MANF sequence patent. For clarity, human CDNF shares 59% amino acid identity with human MANF, so the MANF patents are by no means limiting CDNF development, or vice versa.
Me: Who owns the IP for CDNF?
Henri: Hermo Pharma owns all IP rights to CDNF. The composition of matter patent for CDNF has been granted in a large number of countries, including US and EPO region. In addition, we have filed a number of use patent applications for CDNF that are currently pending.
Me: Are there any large pharmaceutical companies involved in the research and testing of the novel family of neutrophic factors that MANF and CDNF are a part of?
Yes, there is interest in the big pharma. The field is burdened by the stigma caused by GDNF failures. Over the past 3-4 years, we have discussed with a large number of companies, small-mid-big pharma, and it has become very clear that if one of the small biotechs can provide proof of efficacy in human PD patients, this will bring the big players back in the game.
So what is the play?
At this time the only publicly traded company that is playing in this field is Amarantus (AMBS.OB). Amarantus owns sequence patents on MANF which were upheld in court after Hermo Pharma challenged them. As Henri mentioned, they challenged the patents because they believed that they covered too many possible variants of the protein and it therefore "causes "an undue burden" to anyone who would like to test these variants for activity". The only way I can interpret this is that anyone looking to test different variants of MANF will be forced to go through AMBS as it has patents "that cover all sequences with 90% homology to MANF".
After looking further at AMBS I came away with a list of some positives and negatives. Negatives always come first when assessing a micro-cap investment.
Negatives:
1.) Balance sheet is a risk, despite recent financing efforts. The company currently has roughly $600k in cash and a history of losses.
2.) There is still a stigma surrounding delivery methods of these neutrophic factors to the brain and other areas of the body; however, Henri seems to believe that there is already a good deal of progress on this front.
3.) Dilution risk - given that the company is very small and has had to issue shares in the past to raise capital, there is still further risk that they will need to raise capital via equity raises. Additional capital will need to be obtained through partnerships with larger pharma companies or through grants.
4.) The company is tiny, with only 3 full time employees and an outsourced clinical staff. While this is not uncommon (e.g., Hermo Pharma has 4 full time employees and an outsourced staff of around 20), it places additional emphasis on working with well seasoned advisors and directors that have had big pharma experience.
Positives:
1.) Probably the most important positive: Patent protection on MANF that was recently upheld in court.
2.) Almost equally as important, the company has a strong group of advisors with big pharma backgrounds and experience in bringing novel drug therapies to market. Below is a list of recently appointed advisor and what they had to say about the company's MANF program.
Dr. Joseph Rubinfeld, co-founder of Amgen, was recently appointed as an advisor to the company and had some very glowing things to say about MANF: "I believe in MANF," said Dr. Rubinfeld, "I have reviewed a great number of technologies in my 45 year career in the biopharmaceutical field, and I believe that MANF could be one of the biggest successes that I have ever seen. The fundamental scientific premise of reducing protein misfolding is basic, yet very profound. The data, while early, demonstrates very clearly at the cellular level and in animals that MANF reduces apoptosis, improves cellular function, and restores behavioural deficits in a number of disease models, including Parkinson's, Stroke, Myocardial Infarction and Traumatic Brain Injury. These are all indications with very large markets and clear unmet medical need. I believe that if we are able to further de-risk MANF with positive toxicology studies and early clinical data, the Company's new orphan drug strategy could get MANF to market rather expeditiously. MANF has the commercial potential to become a blockbuster drug."
Dr. Robert Zimmerman from Bayer (BAYZF): "I have been involved with Amarantus formally and informally for the past three years supporting the founders as they work tirelessly to advance MANF to a stage where it has real commercial potential," said Robert J. Zimmerman, SD. "While that effort has been centered on Parkinson's disease, I believe additional opportunities exist to diversify this therapeutic candidate. Ischemia/reperfusion, cardiovascular disease, stroke, traumatic brain injury, diabetes and potentially other disease conditions appear to be impacted by MANF based upon preclinical studies and the literature."
Clinton O. Allen from Bristol Myers Squibb (BMY): "I am very excited to join Amarantus at this critical time in its growth cycle," said Clinton O. Allen, newly appointed advisor to Amarantus. "The team at Amarantus has been working tremendously hard over the last few years to bring the MANF Program closer to actualizing its true potential. Now that the Company is looking at various partnering and funding opportunities to drive shareholder value, it is an opportune time to join the team in order meticulously evaluate proposals and make recommendations for future growth."
3.) The company has received two separate grants from the Michael J. Fox Foundation in 2010 and 2011 as well as a grant from the Center of Excellence in Apoptosis Research.
If AMBS is able to continue showing positive results in toxicology studies and preclinical data it is possible that larger pharmaceutical companies will seek a partnership with them. Having patent protection will certainly help them in negotiations and having a recent patent challenge upheld in courts could prove to be quite positive for them.
RISKS:
As always, micro caps are subject to significant risks and uncertainties. The micro cap field is littered with a lot of pump and dump companies and traders looking for short term moves. Volatity in this space is very high. Please do your own due diligence.
Disclosure: I am long AMBS.OB.
Additional disclosure: After doing a good deal of research on this field I am long AMBS. Please understand the risks of micro cap companies. They are highly volatile and subject to significant risks.
Themes: Biopharmaceutical, Pharmaceutical Stocks: AMBS.OB, AMGN, BMY
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Coolbluelake Comments (331)
Jonathan, your research on Parkinson's must have taken you a great deal of time and effort to accumulate. Outstanding work. Thank you. Gregg
8 Dec 2012, 12:46 PM Reply ! Report Abuse Like 0
olsen46 Comments (2)
Might interest the author to know a large segment of the population who suffer from Parkinson's Disease feel the Amgen Trials with GDNF were pulled purely for financial reasons; seems the delivery system was too costly. A book chronicling the trials was written by investigative reporter, Nick Nelson, titled "Monkeys In The Middle: How One DrugCompany Kept A Parkinson's Breakthrough Out Of Reach". And Big Pharma is reluctant to embark upon further trials with neurotropic factors needing intraputamenal infusion because "The field is burdened by the stigma caused by GDNF failures." What failures exactly, other than the one involving making egregious amounts of money?
14 Dec 2012, 02:25 AM Reply ! Report Abuse Like 0
olsen46 Comments (2)
Might interest the author to know that a large segment of the population with Parkinson's disease feel the Amgen trials with GDNF were pulled purely for financial reasons; the delivery system was too costly. A book chronicling the trials was written by an investigative reporter, Nick Nelson, titled "Monkeys in the Middle: How One Drug Company Kept a Parkinsons Disease Breakthrough Out of Reach".And Big Pharma is reluctant to continue trials with neurotropic factors needing intraputamenal infusions because "The field is burdened by the stigma caused by GDNF failures". What failures exactly? Other than the one associated with money?
Mesencephalic astrocyte-derived neurotrophic factor
MANF, ARP, mesencephalic astrocyte-derived neurotrophic factor, ARMET
The protein encoded by this gene is localized in the endoplasmic reticulum (ER) and golgi, and is also secreted. Reducing expression of this gene increases susceptibility to ER stress-induced death and promotes cell proliferation. The protein was initially thought to be longer at the N-terminus and to contain an arginine-rich region but transcribed evidence indicates a smaller open reading frame that does not encode the arginine tract. The presence of polymorphisms in the arginine-rich region, including a specific mutation that changes the previously numbered codon 50 from ATG to AGG, have been reported in a variety of solid tumors; however, these polymorphisms were later shown to exist in normal tissues and are thus not tumor-related. [provided by RefSeq, Jun 2010] (from NCBI)
Sponsored links
Antibodies onlineMANF (Human)
AbD serotecMANF
Papers on MANF
Qualitative and quantitative evaluation of derivatization reagents for different types of protein-bound carbonyl groups.
New
Hoffmann et al., Leipzig, Germany. In Analyst, 07 Oct 2013
Among the many reported reagents, 2,4-dinitrophenylhydrazine (DNPH), biotin hydrazide (BHZ) and O-(biotinylcarbazoylmethyl) hydroxylamine (ARP) are the most frequently used.
Transcriptional regulation of mouse mesencephalic astrocyte-derived neurotrophic factor in Neuro2a cells.
New
Kiuchi et al., Gifu, Japan. In Cell Mol Biol Lett, 30 Sep 2013
Mesencephalic astrocyte-derived neurotrophic factor (MANF) is a novel type of trophic factor.
Armet/Manf and Creld2 are components of a specialised ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.
New
Briggs et al., Manchester, United Kingdom. In Hum Mol Genet, 15 Sep 2013
Intracellular retention of mutant matrilin-3 causes ER stress and induces an unfolded protein response (UPR) including the upregulation of two genes recently implicated in ER stress: Armet and Creld2.
Roles of Pro-angiogenic and Anti-angiogenic Factors as well as Matrix Metalloproteinases in Healing of NSAID-Induced Small Intestinal Ulcers in Rats.
New
Takeuchi et al., Kyoto, Japan. In Life Sci, 27 Aug 2013
The healing of these ulcers was significantly delayed by the repeated administration of MMP inhibitors such as ARP-101 and SB-3CT.
Advanced Reduction Processes: A New Class of Treatment Processes.
New
Abdel-Wahab et al., College Station, United States. In Environ Eng Sci, May 2013
These experiments identified the combination of sulfite activated by ultraviolet light produced by a low-pressure mercury vapor lamp (UV-L) as an effective ARP.
ARP2/3 localization in Arabidopsis leaf pavement cells: a diversity of intracellular pools and cytoskeletal interactions.
New
Szymanski et al., West Lafayette, United States. In Front Plant Sci, Dec 2012
Actin filaments do not form spontaneously; instead filament nucleators, such as the evolutionarily conserved actin-related protein (ARP) 2/3 complex, can efficiently generate new actin filament networks when in a fully activated state.
Functions for the cardiomyokine, MANF, in cardioprotection, hypertrophy and heart failure.
Review
Glembotski, San Diego, United States. In J Mol Cell Cardiol, 2011
The subject of this review is the cardiomyokine, mesencephalic astrocyte-derived neurotrophic factor (MANF).
Altered expression of Armet and Mrlp51 in the oocyte, preimplantation embryo, and brain of mice following oocyte in vitro maturation but postnatal brain development and cognitive function are normal.
GeneRIF
Jin et al., Hangzhou, China. In Reproduction, 2011
The change in Armet expression lasted while the change of Mrpl51 disappeared after birth.
Coup d'Etat: an orphan takes control.
Review
Impact
Tsai et al., United States. In Endocr Rev, 2011
Cloning of their cDNAs demonstrated the existence of two distinct but related genes: COUP-TFI (EAR-3, NR2F1) and COUP-TFII (ARP-1, NR2F2).
Mesencephalic astrocyte-derived neurotrophic factor (MANF) has a unique mechanism to rescue apoptotic neurons.
GeneRIF
Permi et al., Helsinki, Finland. In J Biol Chem, 2011
MANF and C-MANF protect neurons intracellularly as efficiently as Ku70.
Widespread cortical expression of MANF by AAV serotype 7: localization and protection against ischemic brain injury.
GeneRIF
Harvey et al., Baltimore, United States. In Exp Neurol, 2010
Pretreatment with adeno-associated-virus vector containing human MANF reduces the volume of cerebral infarction and facilitates behavioral recovery in experimental stroke rats.
Solution structure and dynamics of mouse ARMET.
GeneRIF
Nagata et al., Kyoto, Japan. In Febs Lett, 2010
the solution structure of ARMET
Novel CDNF/MANF family of neurotrophic factors.
Review
Saarma et al., Helsinki, Finland. In Dev Neurobiol, 2010
In this review, we discuss novel evolutionary conserved family of NTFs consisting of two members in the vertebrates, cerebral dopamine neurotrophic factor (CDNF) and mesencephalic astrocyte-derived neurotrophic factor (MANF).
Induction profile of MANF/ARMET by cerebral ischemia and its implication for neuron protection.
GeneRIF
Shen et al., Hefei, China. In J Cereb Blood Flow Metab, 2010
These results suggest that cerebral ischemia-induced ARMET expression may be protective to the neurons
A KNOX family TALE.
Review
Tsiantis et al., Oxford, United Kingdom. In Curr Opin Plant Biol, 2009
Recent evidence for direct KNOX regulation by myb-related ARP proteins and epigenetic silencing by polycomb repressive complexes have also shed light on the mechanisms defining KNOX gene expression.
Characterization of two classes of small molecule inhibitors of Arp2/3 complex.
Impact
Pollard et al., New Haven, United States. In Nature, 2009
Polymerization of actin filaments directed by the actin-related protein (Arp)2/3 complex supports many types of cellular movements.
Delta traffic takes a sh-Arp turn.
Impact
Schejter, In Nat Cell Biol, 2009
In the Notch pathway, the transmembrane ligand Delta is internalized and then re-established on the surface of signal-sending cells to allow the productive binding and activation of the Notch receptor on neighbouring cells.
The rate of N-WASP exchange limits the extent of ARP2/3-complex-dependent actin-based motility.
Impact
Way et al., London, United Kingdom. In Nature, 2009
Taking advantage of this, we have analysed the dynamics of neuronal Wiskott-Aldrich syndrome protein (N-WASP), WASP-interacting protein (WIP), GRB2 and NCK, which are required to stimulate actin-related protein (ARP)2/3-complex-dependent actin-based motility of vaccinia virus, using fluorescence recovery after photobleaching.
Chapter 5. Nuclear actin-related proteins in epigenetic control.
Review
Roy et al., Athens, United States. In Int Rev Cell Mol Biol, 2008
A theme emerging from plants and animals is that in addition to their role in controlling the general compaction of DNA and gene silencing, isoforms of nuclear ARP-containing chromatin complexes have evolved to exert dynamic epigenetic control over gene expression and different phases of multicellular development.
Tropomyosin-based regulation of the actin cytoskeleton in time and space.
Review
Impact
Hardeman et al., Westmead, Australia. In Physiol Rev, 2008
The functional specificity of tropomyosins is related to the collaborative interactions of the isoforms with different actin binding proteins such as cofilin, gelsolin, Arp 2/3, myosin, caldesmon, and tropomodulin.
ContactTerms Of UseImprint & Disclaimer©2002-2012 Transinsight GmbH
MANF Trophic factor as a potential Novel Therapeutic agent for TYPE1 Diabetes
Diabetes Grants Of 2013
Timo Ylikomi from Tampere received the Diabetes Research Foundations large grant
The foundations large grant, 100 000 Euros in total for two years, was awarded to M.D. Timo Ylikomi from the University of Tampere. Ylikomi's research group has developed a fat cell model, through which insulin resistance may be studied. In total the Foundation awarded 400 000 Euros to 20 researchers.
This year the Diabetes Research Foundation received 80 grant applications of which 55 were centered on type 2 diabetes research, 21 on type 1 diabetes research and 14 on gestational diabetes research. Six applications were focused on other types of diabetes. One application may focus on several types of diabetes.
Almost a third of the applications were sent by researchers working at the University of Helsinki. Researchers from the Kuopio unit of the University of Eastern Finland were the second largest group of applicants.
Since its establishment in 1976 the Foundation has awarded over five million Euros in grant funds. People part of the Foundations administration are not eligible to receive its grants.
Grant For MANF
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.
Review Article
Functions for the cardiomyokine, MANF, in cardioprotection, hypertrophy and
heart failure
Christopher C. Glembotski
?
The SDSU Heart Institute and the Department of Biology, San Diego State University, San Diego, CA 92182, USA
abstract
article info
Article history:
Received 5 August 2010
Received in revised form 1 October 2010
Accepted 4 October 2010
Available online 21 October 2010
Keywords:
Cardiomyokine
MANF
ER stress
Cardioprotection
Hypertrophy
We define cardiomyokines as heart-derived secreted proteins that affect cardiovascular function viaautocrine, paracrine and/or endocrine mechanisms. The subject of this review is the cardiomyokine,mesencephalic astrocyte-derived neurotrophic factor (MANF). The expression of MANF is increased in the
ischemic heart, in part, through activation of ER stress, a condition that drastically impairs the expression and
secretion of most cardiomyokines. This novel function of MANF suggests that it may have important roles in
the ER stressed, ischemic heart. Consistent with this are recent
findings showing that MANF protects against
ischemic damage, and that it is anti-hypertrophic. Accordingly, in light of its function as a potentially secreted
cardiomyokine, MANF has translational potential as a novel therapy for ischemic heart disease.
Thank You Bioman. I really appreciate it
Thank You!
I just have a basic experience in options.
Bioman,
Option stategy seems to be practical. Would you just use call options or other bullish option strategis? What time frame options do you reco. One year options sound good, though they may be pricey.
Do these call options have the same upside as stocks? I believe they should be better because of the leveraging.
Do You use options in IRA accounts or regular a/cs.
Lot of questions here.
Thanks for your time
GLTA
Thank You!
GLTA
Bioman,
I am considering taking a position here. I want to know what the fully diluted share count when all the warrants A and B are excercized from the recent financing.
Thank You
Other Preclinical Programs TNGN is working with:
Tengion Neo-GI Augment™
Based on Tengion's understanding of hollow organ regeneration and clinical advances with the Neo-Urinary Conduit™, as well as principles demonstrated with its Neo-Bladder Augment™ product, Tengion is seeking to partner a preclinical stage asset for gastrointestinal regeneration. Tengion continues to advance this technology through the patent process and seeks scientific community input for these product candidates through scientific publications and presentations.
Tengion is advancing the Neo-GI Augment technology with the goal of using a patient's own cells to build gastrointestinal solutions for patients who have a need for esophageal or intestinal tissue.
Now think about all the patients that has GERD: GERD leading to Barretts esophagus and Esophageal cancer.
Can TNGN help patients grow GI/esophageal tissues with their own cells: I bet they CAN with their platform.
What other programs TNGN is working on?
Tengion Neo-Vessel Replacement™
Based on the principles demonstrated with its Neo-Bladder Augment™, Tengion is also seeking to partner its Neo-Vessel Replacement™ technology. Tengion has published several scientific papers outlining its progress with Neo-Vessel Replacement™ product candidates and continues to advance this technology through the patent process.
Tengion's Neo-Vessel Replacement is being advanced with the goal of using a patient's own cells to build blood vessels for patients that need vascular access for dialysis and for patients who are receiving peripheral bypass surgery or coronary artery bypass surgery.
Am I reading these right?
GI tissues for GERD!!!! HUGE potential!!!
Esophageal/ intestinal tissue for Cancer patients.
Buliding blood vessels for patients receiving peripheral bypass surgery or Coronary artery bypass surgery!!!!
What else Celegene knows that I have no clue about.
WOW!!! WOW!!!! Wow!!!
GLTA
Thank You Seel!
From the website:
Neo-Urinary Conduit: already in phase 1, seven patients completed. 3 more to go. They opened further sites at Sloan kettering, Baylor and University of Michigan. Now the active clinical test centers is 5.
What are findings? well, From website again:
Tengion has gained insights from the seven patients implanted to date including affirmation that the surgical procedure for a NUC implantation does activate urinary tissue regeneration in patients with bladder cancer, and a better understanding of the initial post-operative care required to maintain the patency and durability of the regenerated urinary tissue. Information already gained from this trial is being analyzed and will further support ongoing plans for a potential Phase 2/3 clinical trial.
Neo-Kidney Augment Program Update
In April 2013, Tengion announced the acceptance of the Company's Clinical Trial Application (CTA) filed with the Medical Products Agency in Sweden to initiate a Phase 1 clinical trial to evaluate the safety and delivery of its second clinical program, the Neo-Kidney Augment, in patients with Chronic Kidney Disease (CKD). The Neo-Kidney Augment is being developed with the goal of using a patient's own kidney cells to augment or replace renal function for patients with CKD who are rapidly progressing toward end stage renal disease (ESRD), and is intended to prevent or delay the need for dialysis or kidney transplant by catalyzing the regeneration of functional kidney tissue in patients with ESRD.
The Phase 1 clinical trial in Sweden will involve delivery of an active regenerative dose of Neo-Kidney Augment in patients with CKD. Tengion plans to enroll up to five patients in 2013 and will follow each patient for up to two years. Additionally, the Company plans to submit an Investigative New Drug filing for the Neo-Kidney Augment to the U.S. Food and Drug Administration during the second quarter of 2013, paving the way to initiate the U.S. Phase 1 trial in the fourth quarter of 2013 and provide initial human proof-of-concept data in 2014.
This will be HUGE!!!!!!!!!!!!
Please check your PM that I sent recently from he other site.
GLTA
Is this a quiet period for this stock? When can we expect some PR?
Thanks
GLTA
Thank You. What got my attention was Natty's article on SA. He is very detailed and does excellent research to find unidentified Gems.
Getting in 50% below what the institutions paid on an average sounds great!
GLTA
Sorry for the confusion. Not trying to "sell". I was just asking the input from a fellow poster "seel".
Could you please point me some key posts are posters to look at for my DD.
TIA
GLTA
Yes Indeed! Its reassuring to read posts from Knowledgeable people.
Thank You!
Can you check out my post on the other IHUB board today. I am not a premium member, so I couldn't PM.
GLTA
Trying to DD on this stock. I came across the article from SA
http://seekingalpha.com/article/1544122-institutions-increase-ownership-in-venaxis
What do you think SEEL?
Thanks
GLTA
Thank You Seel:
Here are a few posts from YMB from aj, who's been in the stock since IPO and adding every month:
ajabraham2002 • Jul 25, 2013 7:58 PM
If You Really Thought the Market Cap. Was 1-3 Million...
you really shouldn't be making unequivocal predictions about the share price. The warrants have always been a huge part of the equation. The article that came out two days ago argued that this is a value trap b/c Yahoo! finance shows a market cap of less than 5 million. Give me a break. People who buy on that basis are the most marginal shareholders imaginable. I have gone to a shareholder meeting. I have seen the urinary conduit up close, in a sealed container. I have spoken to the CFO in person. This is a legitimate company run by smart people trying to develop technology invented by brilliant, world-class medical doctors and scientists. You buy this company if you believe in the regenerative potential of autologous stem cells and if you believe that Dr. Atala, with his decades-long head start, is the scientist most likely to deliver first and deliver best on that potential.
ajabraham2002 • Jul 2, 2013 1:01 PM
I think a lot of small shareholders bought at the IPO and have since been busted out of this name, big time. The vast majority of the company is owned by Celgene and a few other private equity and venture capital firms in the form of convertible debt and warrants that appear the value the company at b/w .69 and .75 per share, currently. The warrants that were issued during the previous round of financing expire in early 2014. I'm not sure about the duration of the ones issued during the current round. With Celgene, a 50 billion dollar market cap biotech, backing Tengion now wholeheartedly, I think the future is bright. They have the right of first refusal on all three pipeline products-- the neo-urinary conduit, neo-kidney augment and an esophageal product which is currently in the pre-clinical phase. The neo-kidney product, which should receive approval for human testing by the end of this year, is the first potential, blockbuster product as the dialysis/kidney market is roughly 4 billion per year. If Tengion could receive just a fraction of that, it could potentially be an enormous catalyst. The neo-urinary conduit should complete phase I by the end of this year, and all indications are that it will be deemed a safe substitute for the current method. I believe eventually regenerative medicine will revolutionize medical care, and Tengion is CLEARLY at the forefront of the industry. Yesterday's news is probably the most significant news to ever come out pertaining to this company, and the price action confirms it. On a technical basis, resistance in the .69-.75 range should be fairly intense, but when it is broken, I think this stock could really take off. Lastly, as I stated, I believe the board is empty b/c so many small shareholders have been eliminated during the swoon from $50 to .30. Those who are left are partnered with some of very knowledgeable and deep-pocketed investors. These are all just my opinions, though, and not professional advice
GLTA
I agree that TNGN is further in the research compared to ONVO. The research been going on for more than 3 decades, and I beleive the time is NOW, because the fear of bancruptsy is removed with Celgene's backing. Kidney market is $23 billion a year HUGE!!!.
There was a mention that The Popular Sci. article has a 8 page article on this technology and ONVO mentioned 16 times. If investors starting looking for opportunities for bargain basement price of under a buck, more exposure to TNGN. Just matter of time, this will be real BIG.
GLTA
Amazing opportunity TNGN. If they grab 1% of the 28 billion market of just one product Neo-kidney, their price would be atleast 10x of the current price. This is like buying ONVO for under a buck.
JMO and GLTA
Thank You very much Seel. I respect your opinion a lot. I follow You here and and other sites like SA. You are correct, the Neo Kidney augment is HUGE $27 Billion. The CEO is very experienced and hopefully minimize the dilution from warrants by buying back like Onvo did before uplisting. While the technologies of TNGN and ONVO appear different on the surface, I believe they are complimentary. While doing my DD, I noticed that while ONVO is years away from printing fully functional organs, TNGN can deliver native-like kidney and bladder tissues right now.
Regenerative medicine is no longer a futuristic Sci-fi idea, but is very relevant right now. The applications and potential are humungous, mind boggling and beyond comprehension. I am long ONVO, NVIV and TNGN. I hold ONVO and NVIV from $4. I've been looking for opportunities in BioPrinting, did reading on Dr Attala's work, but wasn't aware that he was the brains behind TNGN until Ron mentioned it a few posts ago. Then the light bulb went off. Yours and Ron's Comments were very helpful, I took a full position at $1.07. Kind of disheartening to see SP was down sharply, but I am in here for the long Term.
Thank You very much for all Your DD and sharing with the rest of us.
GLTA
I took a big position recently in TNGN. The article from SA writes about TNGN as a value trap. Should I be worried. What do you think?
Thanks
GLTA
Thank You Chauncy. I appreciate it. I started a small position last week. Will load up this week
GLTA
Genstock
I am a newbie and I am trying to do my DD. How can you justify the lofty valuations like $20 pps for Henc, When they only get 28% of the revenues. I am just wondering. You compare to BEXP which rose from <1 to 38 pps. Could you please help me understand? I read all your posts and also Chaunceys. Thank You very much for your your analysis.
GLTA
Nice Article this morning on SA. CTIX mentioned.
http://seekingalpha.com/article/1557622-3-disruptive-biotech-companies-moving-on-to-higher-exchanges?source=yahoo
GLTA
JB
Would ctix benefit from the bio printed human tissues from organovo(onvo) to
expedite the clinical trials and toxicity studies.
Thanks
Pi
A question for the experts:
Can our company CTIX use the bioprinted human tissue produced by Organovo (ONVO) to expedite the human trials?
TIA
Pharminvestor
Thank You TP and Bio for the welcome. The more I read about the company, and possibilities here, the more ming boggling it gets. I know I am in good company, good managements and awesome group here. GLTA
Hello Karin,
I am a newbie. Just started following the company after reading your posts here and at SA. There are so many knowledgeable people here like Yourself, Progressive, Wildnano, Bigjeff to name a few. I really like the risk/reward ratio here and took a full position with 24k shares at av pps 1.67. I am very excited to be here and look forward for great gains in the years ahead.
I have a question for you: I am looking at ASCO poster, the slide about "Expression level of p21 is a biomarker for Kevetrin". I tried to zoom so I can see, but couldn't do it. Is this info. from the Ph1 trial or from the preclinical models.
TIA
Pharminvestor