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I rarely ever short BUT this is too perfect lol got a BIG short position at $40.35 i'm not covering till this shit is dead. Im sorry my bull brothers this is just too perfect. :(
SLIPPING FAST....$37'S SOON
aGREED,,,, when up too much too fast= http://www.finviz.com/quote.ashx?t=PRTA
How many chances do you want to buy in bro?? $39...$40...
Are you stopping by jimmybobs Option Millionaires board? Folks doing well with many trades.
Thanks just getting into options so I'm pretty excited only my second trade..
Institutions quietly loading all day!
Uh oh do I see $44?
My money says $50 coming...
Haha in right here. Bought in the $37's last night and at $40.00 this morning. My chips on the table......
44.30 > Looking solid!
SO QUIET NOW....WHAT HAPPENED GUYS???? $35 SOON
Witnesseth
More institutions may be loading here on today's news.
Holding a few shares long term!
May be a keeper! Phase II & phase III results could possibly be explosive as well.
Prothena up big premarket on PRX002 trial results in PD
32 MINUTES AGO PRTA
Prothena (NASDAQ:PRTA) is up 46% premarket on light volume in response to its announcement after the close yesterday of positive results in Phase 1 trial evaluating its product candidate, PRX002, for the treatment of Parkinson's disease. After one dose, levels of a key protein, alpha-synuclein, dropped up to 96%.
Previously: Phase 1 study shows safety of Prothena Parkinson's disease drug candidate plus significant reduction in key PD-related protein (March 19)
Uh oh $44. DMC making bank from $37...
This equity will easily go to $400.+ like BIIB is doing. Yes $400.+
Were sitting on 27M float.
Swiss drug giant Roche ( OTCPK: RHHBY ) was up .09 in AH. Wonder why Roche shares were little changed.
Parkinson's disease is a degenerative disorder of the central nervous system that affects one in 100 people over age 60, and after Alzheimer's disease is the second most common neurodegenerative disorder. There are an estimated seven to ten million patients living with Parkinson's disease worldwide. Current treatments for Parkinson's disease are only effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists. As the disease progresses and dopaminergic neurons continue to be lost, these drugs eventually become less effective at treating the symptoms. In contrast, PRX002 targets disease-causing alpha-synuclein, and may slow or reduce the neurodegeneration associated with aberrant forms of alpha-synuclein.
LOL....Appreciate the PROFESSIONAL DD!
THIS POS WILL NEVER SEE $50
Yeah AH $37.28 but wondering if I should flip here or hold and see if $50 hits Tomm.
Highest PT is $53. Barring an offering, which I don't doubt at all, maybe this could hit that mark tomorrow...
Anyone playing this??
Prothena Reports Robust Reduction of Free Serum Alpha-Synuclein of up to 96% After Single Dose of PRX002, a Novel Protein Imm...
Source: GlobeNewswire
All Doses of PRX002 Found to be Safe and Well Tolerated, Meeting Primary Objective of Phase 1 Single Ascending Dose Study
Results of Study Demonstrate Rapid and Dose-Dependent Reduction of Free Serum Alpha-Synuclein, Potential Disease-Causing Protein in Parkinson's Disease
DUBLIN, Ireland, March 19, 2015 (GLOBE NEWSWIRE) -- Prothena Corporation plc (Nasdaq:PRTA), a late-stage clinical biotechnology company focused on the discovery, development and commercialization of novel protein immunotherapy programs, today announced positive results from a Phase 1 single ascending dose study of PRX002, a monoclonal antibody for the potential treatment of Parkinson's disease and other related synucleinopathies. PRX002 is the focus of a worldwide collaboration between Prothena and Roche.
PRX002 was safe and well-tolerated, meeting the primary objective of the study. Further, results from this study showed that administration of PRX002 leads to mean reduction of free serum alpha-synuclein levels of up to 96%. These overall results were highly statistically significant (p<0.00001). Reduction of free serum alpha-synuclein, a protein potentially involved in the onset and progression of Parkinson's disease and the target of PRX002, was shown to be robust, rapid and dose-dependent after just a single dose.
"There is genetic and pathological evidence that supports a causal role of alpha-synuclein in Parkinson's disease," said Todd Sherer, PhD, CEO of the Michael J. Fox Foundation for Parkinson's Research. "We applaud Prothena and Roche for their pioneering work in developing a potentially disease-modifying therapy for this progressive neurodegenerative disease that affects millions worldwide."
The Phase 1 double-blind, placebo-controlled, single ascending dose study enrolled 40 healthy volunteers. All volunteers enrolled were randomized 3:1 into five escalating dose cohorts (0.3 mg/kg, 1 mg/kg, 3 mg/kg, 10 mg/kg or 30 mg/kg) to receive either PRX002 or placebo. No hypersensitivity reactions or drug-related serious adverse events were reported. PRX002 demonstrated favorable pharmacokinetic properties, supporting the current dosing frequency in the on-going Phase 1 multiple ascending dose study in patients with Parkinson's disease. There were no treatment emergent adverse events (TEAEs) in greater than 10% of subjects. The only TEAEs in greater than 5% of subjects were vessel puncture site pain, headache and viral infection. All PRX002-related adverse events were mild and no dose limiting toxicities were observed.
"We are extremely pleased with the results of the Phase 1 single ascending dose study as the mean reduction of free serum alpha-synuclein of up to 96% demonstrates the pharmacodynamic effects of PRX002," commented Gene Kinney, PhD, Chief Scientific Officer and Head of Research and Development at Prothena. "Importantly and for the first time in humans, we demonstrated that this robust, rapid and dose-dependent reduction of free serum alpha-synuclein was safe and well-tolerated. Thus, this approach may translate into a clinically meaningful delay or reversal of disease progression in patients with Parkinson's disease. We look forward to building upon these data with results from the on-going, multiple ascending dose study in patients with Parkinson's disease expected in the first half of 2016, where we will also be measuring levels of PRX002 in the cerebrospinal fluid and assessing additional biochemical, imaging and clinical biomarker endpoints. Separately, we are excited to co-host a symposium with Roche on March 21 at the 12th International Conference on Alzheimer's and Parkinson's Diseases and Related Neurological Disorders (AD/PD(TM) 2015) to continue to raise awareness of the role of alpha-synuclein as a target for Parkinson's disease."
Prothena Shares to Be Added to Russell Global Index
DUBLIN, Ireland, June 17, 2013 (GLOBE NEWSWIRE) -- Prothena Corporation plc (Nasdaq:PRTA), a clinical stage biotechnology company focused on the discovery and development of novel antibodies for the potential treatment of a broad range of diseases, announced that the trading of its ordinary shares will be included in the Russell Global Index when Russell Investments reconstitutes its comprehensive set of U.S. and global equity indexes on June 28, 2013, according to a preliminary list of additions posted June 14, 2013 on www.russell.com/indexes.
Membership in the Russell Global Index, which remains in place for one year, means automatic inclusion in the appropriate large-cap, small-cap, all-cap indexes as well as the applicable style, sector and country indexes. Russell determines membership for its equity indexes primarily by objective, market-capitalization rankings and style attributes.
"We are very pleased to join the Russell Global Index" said Dale Schenk, PhD, President and Chief Executive Officer of Prothena. "It is well established that investors rely on the Russell Indexes for true market representation and we expect our inclusion to have many benefits, including increased liquidity and broader exposure to institutional investors."
Russell indexes are widely used by investment managers and institutional investors for index funds and as benchmarks for both passive and active investment strategies. According to Russell, approximately $4.1 trillion in assets currently are benchmarked to Russell indexes.
The Russell Global Index, which Russell estimates captures approximately 98% of investable securities globally, is reconstituted annually and all sub-indexes are recalibrated to accurately measure current market realities for each market segment. These investment tools originated from Russell's multi-manager investment business in the early 1980s when the company saw the need for a more objective, market-driven set of benchmarks in order to evaluate outside investment managers.
Russell launched the Russell Global Index in 2007, leveraging the popular methodology from its U.S. indexes. The broad-market Russell 3000® Index serves as the U.S. component to the Russell Global Index.
Total returns data for the Russell Global Index and other Russell Indexes is available at http://www.russell.com/indexes/data/Global_Equity/Russell_Global_returns.asp.
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These same scientists also pioneered significant scientific discoveries with cell adhesion molecules, leading to the discovery and development of Tysabri® (natalizumab), which is now approved for use in relapsing forms of multiple sclerosis and sold by Biogen Idec.
Athena was acquired by Elan Corporation in 1996, and its discovery and development activities were incorporated into Elan Pharmaceuticals at that time. In December 2012, Elan completed the successful demerger of its discovery and early development efforts resulting in Prothena, which is an independent publicly traded company with a strong pipeline of discovery programs, early stage clinical assets and preeminent scientists.
Instead of focusing on a specific therapeutic indication or platform technology, Prothena focuses on what we are best at – elucidating the contribution of protein misfolding and cell trafficking dysfunction to disease states and developing therapeutic approaches that interact in novel ways with proteins. Today, we are building a broad pipeline of compounds that could deliver the next generation of breakthrough therapies by drawing from our vast knowledge of in these areas of biology.
Amyloidosis is a term used for a variety of conditions that result when a normally soluble protein misfolds and accumulates, which can become toxic to organ tissue. Amyloidoses can affect any organ in the body, including the brain and peripheral organs. For example, the misfolding and aggregation of the amyloid beta (Aβ) peptide leads to a build-up of amyloid protein in the brain, which most scientists believe is the primary cause of Alzheimer’s disease. The scientific discoveries the team has made in Alzheimer’s disease led to the discovery of potential methods for intervening in the amyloidosis that occurs in other parts of the body. Amyloidogenic proteins including amyloid light chain (AL), amyloid A (AA) and transthyretin (TTR) are believed to cause toxicity in peripheral organs under pathological conditions. Collectively, the peripheral diseases caused by these proteins are known as systemic amyloidoses.
Our goal is to develop new product candidates that target these misfolded proteins, and our lead candidate, NEO001, has begun Phase 1 clinical testing in AL amyloidosis patients.
Synucleins are a family of proteins, of which there are three known members: α-synuclein, β-synuclein, and ?-synuclein. The α- and β-synuclein proteins are found primarily in brain tissue. The ?-synuclein protein is found primarily in the peripheral nervous system and retina, as well as several tumor types. While the role synuclein proteins play in normal cellular functioning has not been fully determined, there are data to suggest that synucleins assist with the stability of cellular membranes and/or their turnover.
Mutations and changes in the levels of α-synuclein have been associated with multiple neurodegenerative illnesses, including Parkinson’s disease. This protein is also a prominent component of Lewy bodies and Lewy neurites (abnormal protein clusters on the inside of neurons). Lewy bodies and Lewy neurites are pathological hallmarks of several neurological disorders collectively known as synucleinopathies. Synucleinopathies include Parkinson’s disease; dementia with Lewy bodies; multiple system atrophy; and certain other neurological disorders. In synucleinopathies, the α-synuclein protein is believed to misfold and aggregate to form the protein structures that are thought to contribute to the pathology of the disease.
Current treatment options for Parkinson’s disease and other synucleinopathies focus on providing symptomatic benefit; our goal is to slow the progression of disease. To achieve this, we have developed monoclonal antibodies intended to slow or reduce the neurodegeneration associated with α-synuclein misfolding and/or its transmission. The lead candidate in this portfolio, PRX002, is expected to begin Phase 1 testing in 2014.
Our scientists have maintained an interest in the biology of T-cell migration. In other words, determining how T-cells leave the circulatory system by attaching and migrating across blood vessel walls. We have made several fundamental scientific contributions that further our understanding of cell adhesion molecules and their role in allowing particularly pathogenic cells and proteins to transfer out of the circulatory system and into tissue sites where they initiate the damage associated with a variety of autoimmune diseases. These initial discoveries led to the development of Tysabri® (natalizumab), a highly effective drug that prevents inflammatory cells from entering the brain during periods of multiple sclerosis relapse, which is marketed by Biogen Idec.
There is a significant amount of literature suggesting Th17 cells are the primary cause of a variety of inflammatory diseases. Since Th17 cells represent a relatively small proportion of the overall T-cell population, we have focused on targeting these cells specifically in order to leave the majority of immune function intact.
Our approach is designed to prevent Th17 cells from leaving the blood vessels and infiltrating the tissue by blocking the interaction of a key cell adhesion protein, explicitly expressed on the surface of Th17 cells, with its binding partner on the blood vessel. As such, our approach differs with some other approaches that have focused directly on targeting individual cytokines released by Th17 cells, particularly IL-17. The same cell adhesion molecule is called the melanoma cell adhesion molecule (MCAM). MCAM appears to be critical for Th17 migration and has been reported to be upregulated on a variety of metastatic tumor cells that may utilize a similar molecular approach to spread to new tissue sites. We believe there is enormous potential in conducting discovery and development work in Th17-mediated inflammatory diseases and cancer. We are testing a portfolio of monoclonal antibodies that we have developed to selectively block MCAM-mediated cell adhesion. We have selected a lead candidate for clinical development and anticipate initiating Phase 1 clinical testing in 2015.
Our Discovery team continues to deliver new approaches to Prothena’s pipeline in a number of therapeutic areas as we progress our lead programs clinically. We are confident the important discoveries made to date and continued future innovation will ensure a profound impact on human health for decades to come.
Prothena’s research and development pipeline includes three lead therapeutic antibody programs that we are advancing aggressively: NEOD001 for the treatment of AL and AA Amyloidosis; PRX002 for the treatment of Parkinson’s disease; and PRX003 for the potential treatment of inflammatory disease and metastatic cancers. NEOD001 is in Phase 1 development, and in both 2014 and 2015, we anticipate moving one or more of our other product candidates into the clinic.
Prothena’s pipeline includes several discovery-stage programs studying antibodies that may offer potential treatments for Alzheimer’s disease and Type 2 Diabetes. The Company continues to generate additional novel antibodies against other targets involved in protein misfolding and cell adhesion.
Prothena employs three distinct strategies to ensure we are allocating our resources towards the appropriate antibody and target disease, potentially increasing the likelihood each compound will complete Phase 3 development successfully. We leverage our insight into the pathology of diseases involving protein misfolding and cell adhesion to employ biomarker endpoints in order to detect signals of clinical efficacy early in the clinical development process. We collaborate with scientists who are recognized as experts in our disease areas of interest to test and characterize our potential therapeutic antibody candidates. We seek feedback and guidance on our programs from leading clinical experts. We believe these strategies give us the opportunity to make the most educated decisions about our compounds throughout the development process.
Dr. Dale Schenk, Chief Executive Officer of Prothena, was most recently Chief Scientific Officer and Executive Vice President at Elan Pharmaceuticals where he provided the leadership and scientific direction for Elan’s research and development programs. Prior to joining Elan, Dr. Schenk was a founding scientist of Athena Neurosciences, which was acquired by Elan Pharmaceuticals. Dr. Schenk has pioneered the immunotherapeutic approach for the treatment of amyloidosis, as exemplified for Alzheimer’s disease. Dr. Schenk’s work in this area, as well as in early detection, testing and other pathways to the disease, has led to the most advanced potential treatment approaches for Alzheimer’s disease. Dr. Schenk earned his BA and PhD in Pharmacology and Physiology from the University of California, San Diego.
Dr. Gene Kinney, Head of Research and Development, was most recently Senior Vice President, Pharmacological Sciences at Elan Pharmaceuticals and head of Nonclinical Research at Janssen Alzheimer Immunotherapy R&D. Prior to joining Elan, Dr. Kinney was Senior Director, Head of Central Pharmacology and acting lead for Bioanalytics & Pathology at the Merck Research Laboratories. During his tenure at Merck, Dr. Kinney contributed to the strategic direction and oversight of drug discovery activities and led a number of nonclinical discovery and clinical development programs targeted for the treatment of neurodegenerative diseases (e.g., Alzheimer’s and Parkinson’s diseases) and psychiatric conditions (e.g., schizophrenia and depression). Dr. Kinney also has held positions at Bristol-Myers Squibb and was an Assistant Professor at the Emory University School of Medicine, Department of Psychiatry and Behavioral Sciences. Dr. Kinney earned his BA from Bloomsburg University and his MA and PhD from Florida Atlantic University.
Dr. Nickerson, Head of Corporate and Business Development of Prothena, was most recently Vice President and Head of Business Development at Elan Pharmaceuticals. During her tenure at Elan, Dr. Nickerson was responsible for opportunity evaluation, diligence, negotiations and contracting for Elan external opportunities. Dr. Nickerson established a broad network of collaborations for Elan with academic investigators, not-for-profit disease-focused foundations and industry collaborators. She has led efforts to build Elan’s pipeline of products for neurodegenerative disease, including license of ELND005, which currently is in Phase 2 clinical trials for bipolar disorder and agitation and aggression in Alzheimer’s disease. She was instrumental in establishing Neotope Biosciences and served as Head of Business Operations for Neotope from 2010 until 2012. Dr. Nickerson previously was a Senior Scientist at Celera Genomics (Axys Pharmaceuticals) from 2000 to 2002 where she led preclinical programs developing novel therapeutics for oncology. Dr. Nickerson earned her BSc and PhD in Experimental Medicine from McGill University and her MBA from the University of California, Berkeley Haas School of Business.
Mr. Nguyen, Chief Financial Officer, has 15 years of finance experience in the healthcare, banking and private equity industries. Prior to joining Prothena, he held management positions at Somaxon Pharmaceuticals, Inc., including Senior Vice President, Vice President, Chief Financial Officer, and Investor Relations, until its sale in 2013. Previously, Mr. Nguyen was Vice President, Chief Financial Officer and Investor Relations at Metabasis Therapeutics, Inc., until its sale in 2010. Before entering the biotech industry, Mr. Nguyen was a vice president in the Healthcare Investment Banking group at Citi Global Markets, Inc., and served in healthcare investment banking at Lehman Brothers, Inc. Mr. Nguyen has a BA from Claremont McKenna College and an MBA from UCLA Anderson School of Management.
Dr. Koller, Chief Medical Officer, is a board-certified neurologist with more than 20 years of experience in the life sciences industry, developing small molecules and biologic therapeutics for a diverse array of indications. Prior to joining Prothena, Dr. Koller served as Chief Medical Officer at Sonexa Therapeutics. Previously, Dr. Koller held clinical development roles and leadership positions at several life sciences companies, including Athena Neurosciences, Elan Pharmaceuticals, Syntex Pharmaceuticals and Wyeth Pharmaceuticals. Dr. Koller has extensive expertise in clinical trial design, having been involved in the clinical development of numerous INDs and NDAs targeting a broad array of indications, including Alzheimer's disease, multiple sclerosis, cervical dystonia, pain, epilepsy, migraine, stroke, anxiety, and depression. Dr. Koller has a BA from Franklin and Marshall College, an MPH with an emphasis in epidemiology from the University of Texas at Houston and his MD from the University of Maryland, Baltimore. Dr. Koller completed fellowship training in neuromuscular diseases at the University of Southern California.
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