One Doctor's Hopeful Plan To Eradicate Alzheimer's
A new drug developed by Neurogeneticist Dr. Rudolph Tanzi could be part of a cure for Alzheimer's disease within the decade. Tanzi, who co-discovered all three early-onset familial Alzheimer’s genes, said he expects doctors to be managing Alzheimer’s
Perhaps frequent copiers of abstracts are not aware, but a scientist from whom they frequently borrow - Dr.Susan Lindquist of the Whitehead Institute - passed away prematurely last October 2016. Her death is indeed a loss for Science. However they should be reminded again that she was not and has never been a "Prana scientist"....a top-notch scientist, yes....and one whose work will be followed for the benefit of many.
IGXT (MC $46 M) NDA filing for MEGA thin-flim Cialis (better than Viagra) this month =10++ BAGGER Potential ! PLEASE read this guys and then join us to make big money .A LIFETIME OPPORTUNITY HERE GUYS !!!
2 US-NDA submission within 2 months ,lot of Cash and heavily underpriced at a valuation of just $46 million .1 Big drug partnered with Endo Pharma already under review by FDA market launch expected in 1H 2018 .Load up guys before she the MEGA news hit the wire and thank me later .GL
MarketCap $46 Million Cash ~$12 Million (including convertible debt) =cash untill 2021+ Price: 0.70
NDA submission for tadalafil (erectile dysfunction) thin-film version of Blockbuster drug Cialis in June or July NDA resubmission for Rizaport (migraine) in early Q3 Partnership for Tadalafil in 2H 2017
IntelGenx previously confirmed the bioequivalence of Tadalafil to Eli Lilly’s Cialis, which had sales of $1.5-billion in 2016 but faces generic competition in 2020. IntelGenx has an exclusive license for oral films from Lilly for its dosing patent, which would allow Tadalafil to enter the ED market in the U.S. free from patent litigation from Lilly. Dr. Matzen explains that Tadalafil, which offers a discrete dosing alternative, could enter the market in 2018, with up to three years of market exclusivity before Cialis is hit with generic competition.
Tadalafil is an erectile dysfunction (ED) treatment that boasts bioequivalence with Cialis, the current leading brand, and with a successful biostudy in-hand a 505(b)(2) NDA is set to be filed any day now, meaning that a full launch should be expected in mid-2018. Cialis is already winning-out over Viagra in terms of numbers of prescriptions, which is largely down to price and efficacy, but when Tadalafil comes to market with the same product in a more convenient and discreet delivery mechanism, IntelGenX should see a massive number of customers take-up its services.
IntelGenx has multi-faceted BD approach for its oral films
With a burgeoning pipeline of pharmaceutical oral films, IntelGenx’s (OTCQX:IGXT; TSXV:IGX) business development strategy is focused on partnering its product pipeline along with actively meeting with potential partners to explore manufacturing
Anyone else notice a pattern with regard to share price here? Down, up with no news, enticing the feeble-minded, then down again.
ACS Chem Neurosci. 2017 Jun 19. doi: 10.1021/acschemneuro.7b00187. [Epub ahead of print] Dihydropyrimidine-thiones and clioquinol synergize to target β-amyloid cellular pathologies through a metal-dependent mechanism. Tardiff DF, Brown LE, Yan X, Trilles R, Jui NT, Barrasa MI, Caldwell KA, Caldwell GA, Schaus SE, Lindquist S. Abstract The lack of therapies for neurodegenerative diseases arises from our incomplete understanding of their underlying cellular toxicities and the limited number of predictive model systems. It is critical that we develop approaches to identify novel targets and lead compounds. Here, a phenotypic screen of yeast proteinopathy models identified dihydropyrimidine-thiones (DHPM-thiones) that selectively rescued the toxicity caused by β-amyloid (Aβ), the peptide implicated in Alzheimer's disease. Rescue of Aβ toxicity by DHPM-thiones occurred through a metal-dependent mechanism of action. The bioactivity was distinct, however, from the 8-hydroxyquinoline clioquinol (CQ). These structurally dissimilar compounds strongly synergized at concentrations otherwise not competent to reduce toxicity. Co-treatment ameliorated Aβ toxicity by reducing Aβ levels and restoring functional vesicle trafficking. Notably, these low doses significantly reduced deleterious off-target effects caused by CQ on mitochondria at higher concentrations. Both single and combinatorial treatments also reduced death of neurons expressing Aβ in a nematode, indicating that DHPM-thiones target a conserved protective mechanism. Furthermore, this conserved activity suggests that expression of the Aβ peptide causes similar cellular pathologies from yeast to neurons. Our identification of a new cytoprotective scaffold that requires metal-binding underscores the critical role of metal phenomenology in mediating Aβ toxicity. Additionally, our findings demonstrate the valuable potential of synergistic compounds enhance on-target activities, while mitigating deleterious off-target effects. The identification and prosecution of synergistic compounds could prove useful for developing AD therapeutics where combination therapies may be required to antagonize diverse pathologies.
How refreshing. PRAN up 19 cents today and no-one bothers asking why. It's easily seen that volume remains lower than daily average and closing price has receded from the HOD. Doesn't take long for the opportunists to take a selling opportunity when it's there. No, no news today.
This is one possible way, may be others but this could be why eliminating iron could help mitochondria and slow down the degeneration of neurons (???).
Biometals. 2017 Jun 12. doi: 10.1007/s10534-017-0023-0. [Epub ahead of print] Iron-induced generation of mitochondrial ROS depends on AMPK activity.
Huang H1,2, Chen J1,2, Lu H1, Zhou M1,2, Chai Z1,2, Hu Y3,4. Author information
1 CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multidisciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. 2 University of Chinese Academy of Sciences, Beijing, 100049, China. 3 CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multidisciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. email@example.com. 4 University of Chinese Academy of Sciences, Beijing, 100049, China. firstname.lastname@example.org. Abstract
Deregulated iron homeostasis is generally believed to be implicated in neurodegenerative diseases, including Parkinson's disease. Nevertheless, it is not fully understood how iron overload can elicit neuronal cell damage. Here we examined mitochondrial reactive oxygen species (ROS) levels in human dopaminergic neuroblastoma SH-SY5Y cells upon iron exposure. A relatively high concentration of iron could significantly increase mitochondrial ROS levels in SH-SY5Y cells. Pharmacological activation of AMP-activated protein kinase (AMPK) almost completely inhibited the effect of iron on mitochondrial ROS. By contrast, AMPK inhibition aggravated the neurotoxicity of iron and enhanced the production of mitochondrial ROS. Collectively, these findings suggested that excess iron may be able to perturb mitochondrial function, and AMPK activity is important for the association of iron and mitochondria.
Prana Appoints David Stamler as Chief Medical Officer to Lead Clinical Development
MELBOURNE, AUSTRALIA. 5 June 2017: David Stamler, M.D., has joined Prana Biotechnology (ASX PBT, NASDAQ PRAN) as Chief Medical Officer and Senior Vice President, Clinical Development, based in San Francisco. Prior to joining Prana, Dr. Stamler worked for Teva Pharmaceuticals (NYSE TEVA), as part of Teva’s US$3.5 billion acquisition of Auspex Pharmaceuticals. Dr. Stamler led the development of a new drug for the treatment of Huntington’s disease, which was approved by the U.S. Food and Drug Administration (FDA) in April this year. This was the second neurological agent that Dr. Stamler has led through the approval process with the FDA. Dr. Stamler’s appointment follows a detailed review of the pharmaceutical assets and strategy at Prana over the last 6 months and marks a refocus on prioritising PBT434 for the treatment of parkinsonian movement disorders. PBT434 is a first-in-class therapy planned to enter Phase 1 clinical trials later this year. In parallel, the company is exploring new options for PBT2 and building its pipeline of drug candidates from Prana’s proprietary library for neurodegenerative diseases and other therapeutic fields that may potentially benefit from Prana’s compounds. Prana’s Executive Chairman and CEO, Geoffrey Kempler, noted: “Dr. Stamler is a seasoned and talented drug developer who brings more than 20 years of central nervous system (CNS) development experience and a deep understanding of the regulatory environment. We are very pleased that he has chosen to work with Prana and advance our portfolio of drugs for neurodegenerative diseases.” In commenting on his appointment, Dr. Stamler said: “There is a great need for new treatments for neurodegenerative diseases. Prana’s approach, along with their extensive chemical library and experience in translational research, make them ideally positioned to advance the field. Progressing PBT434 into the clinic will be very exciting, as it has demonstrated substantial functional improvements and impressive neuroprotective properties in numerous animal models. I am thrilled to be joining Prana to help bring new agents such as PBT434 to the clinic and, hopefully, to patients in need.” Dr. Stamler comes from Teva as VP, Clinical Development and Therapeutic Head, Movement Disorders where he was responsible for clinical-regulatory interactions leading to the approval of AUSTEDOTM (deutetrabenazine) for treatment of chorea associated with Huntington’s disease in 2017. Prior to Teva, Dr. Stamler was Chief Medical Officer at Auspex Pharmaceuticals, Inc. (which was acquired by Teva in 2015) and prior to this he served as Chief Medical Officer and Senior Vice President of Xenoport, Inc. where he led clinical development activities for their portfolio of CNS compounds.
Is It the last Rudy Tanzi's Twitter message about Prana? Just curious! He talks about his new Alzheimer's drug in clinical trials this year.
X axis : Stocks Price Correlation Coefficient Y axis : Quantity of stocks May-2016 1,000 Day Parameter 2,830 NASDAQ Stocks Price Analysis This stock mode of correlation coefficient is -0.1 In other words, the correlation coefficient of the other stoc
So is this progress while waiting for something (anything) to enter Clinical Trials?
ASX closed yesterday at $0.049 after trading the grand sum of $437 for the entire session.. That's some improvement over the several days of no trading during this year.
Prana as shown above is down to $2.11 now 1-1/2 hours after NASDAQ open with continued low volume. Any news?
Enjoy the Memorial Day week-end everyone. Take time to honor those who gave up all by their ultimate sacrifice. It puts to shame the jabbering self-serving idiocy seen everyday on some message boards.
Are there any activitites for this which has a potential for upside for pran in nasdaq
why such a low volume and such a big difference in bid and ask
I am not sure why some investors stick with Prana. Maybe they are afraid to admit defeat (it was not easy for me); maybe making a loss official is too painful. In any event, I believe that there are many stocks with more promise than Prana has and that are moving forward so that rewards may actually be realized in THIS lifetime. Prana has played it close to the vest for too long. It is not my way to be negative toward another's dream, but I do not see good faith here. My recommendation is that investors look to a company that is better managed, is more straightforward with, and fair to investors, and is progressing normally. There are many such opportunities in biotech and elsewhere.
I don't care how many degrees all of PRAN's associates have between them, or how many dozens of articles they've published over the past 20 years. As a publicly traded company, they are terrible. The stock is a loser.
Posts about PBT434 on The Science of Parkinson's disease
Posts about PBT434 written by Simon
For those interested, Prana have offices in the same street as The Florey Institute of Neuroscience and Mental Health. Prana co founder Colin Masters co heads the Neurodegeneration Division. heads the AIBL study,and several labs. Other labs whith ties to Prana are: Paul Adlard (Synaptic Neurobiology Laboratory) Kevin Barnham (Neurotherapeutics Laboratory) Ashley Bush (Oxidation Biology Laboratory)[co-founder] Robert Cherny (Prana Laboratory) David Finkelstein (Pre-clinical Parkinson's Disease Research Laboratory) Colin Masters (Neuropathology and Neurodegeneration Laboratory and The Australian Imaging Biomarker and Lifestyle Study) If you go to the Florey site you can see all of these labs are doing work for Prana. The Florey is probably the biggest neuro research institute in the southern hemisphere. When you add Rudy Tanzi at Harvard, the other Prana co-founder, Prana have access to an enormous amount of research. muscle for a company of it's size. [Rudolph Tanzi, PhD, is the vice chair of the Department of Neurology and Director of the Genetics and Aging Research Unit at Massachusetts General Hospital, and serves as the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School.]
To repeat my earlier themes: 1) Does anyone know how the employees of Prana (I think there are nine) spend their work days? 2) Has anyone noticed a pattern with regard to stock price related to inflated excitement, then selling after the sucker - er, I mean - investors have jumped on the bandwagon? Seems there are people who seek out a molecule that will help them tell an apparently compelling story, then exploit the heck out of it. Very profitable (albeit parasitic) careers have been made in this way.