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NTRP - Neurotrope’s Approach to Treating Alzheimer’s Disease Through Its Product Bryostatin-1, an Activator of Protein Kinase C Epsilon (PKCe), Supported by Blanchette Rockefeller Neurosciences Institute (BRNI) Publication, Identifying PKCe as a Biomarker of Alzheimer’s
Neurotrope’s Collaborator BRNI, Publishes Article in the Journal of Alzheimer’s Disease describing correlation of PKCe levels and degree of disease


Plantation, FL – August 18, 2014 – Neurotrope, Inc. (OTCQB:NTRP)today announced that results from a new study, entitled, “PKCe Deficits in Alzheimer’s Disease Brains and Skin Fibroblasts,” published in the recent edition of the peer-reviewed Journal of Alzheimer’s Disease and co-authored by Tapan K. Khan, Ph.D.; Abhik Sen, Ph.D.; Jarin Hongpaisan, Ph.D.; Chol S. Lim, Ph.D.; Thomas J. Nelson, Ph.D., and; Dr. Daniel L. Alkon, each of the Blanchette Rockefeller Neurosciences Institute (BRNI), provide further indication of the role that protein kinase C epsilon (PKCe) may play in the potential treatment of Alzheimer’s disease (AD). Neurotrope is currently collaborating with BRNI on the development of its lead compound, bryostatin, a potent modulator of PKCe, for the treatment of patients with AD.

A major hurdle in the treatment of AD is that patients only show symptoms years after the disease has already taken hold. Most treatments have focused on stimulating the neurotransmitter activity of healthy neurons in the brain, or removing the beta-amyloid plaque or tau protein which builds up in the brain as a result of the disease. All drug development efforts to date that have targeted the removal of beta-amyloid or tau protein, have failed, and drugs approved for stimulating neurotransmitter activity have offered only short-lived, palliative results for patients. Further, these treatment strategies have had no effect on the progression of the disease and have yielded no improvement in patients’ memory or cognitive performance.

As reported in BRNI’s recently published study, in brain samples (consisting of autopsy-confirmed AD and age- and gender-matched control samples), blindly provided by the Harvard Brain Bank, the amount of PKCe was found to be significantly reduced in specific areas of the brain that are known to be targets in early AD. In these same brain areas, the study also showed that levels of A Beta oligomers (a toxic protein formed as a result of AD) are elevated when PKCe is reduced. Remarkably similar changes were consistently found in the skin cells of AD patients when compared to their age-matched controls and as compared to patients with non-AD dementias (skin samples for the study were obtained from the cell bank at the Coriell Institute for Medical Research). Additionally, low levels of PKCe in skin cells were strongly correlated with progression of the disease. The longer the patients had AD, the lower their levels of PKCe. Further, low levels of PKCe in the brain were significantly correlated with an accepted measure of disease severity, known as the Braak score.

Taken together, these findings indicate that the presence of low levels of PKCe support the enzyme’s potential value as an early therapeutic target in AD.


Dr. Alkon, Toyota Chair in Neurodegenerative Disease, Scientific Director and Professor, Blanchette Rockefeller Neurosciences Institute, and Chief Scientific Officer of Neurotrope, stated, “The results of this study are compelling and warrant continued research to fully explore the importance of PKCe in the identification and treatment of patients with AD. The data compiled from this study, and that related to Neurotrope’s lead compound, bryostatin -- which, in preclinical in vivo models has shown to play an important role in slowing or reversing AD and restoring cognition, memory and motor skills -- provides additional incentive to pursue what could lead to a major shift in the medical community’s approach to this debilitating and costly disease, which currently afflicts approximately 36 million people, worldwide.”


Paul Freiman and Charles S. Ramat, Neurotrope’s Co-Chairmen and Co-Chief Executive Officers, noted, “We believe that our Company’s focus on modulating the levels of PKCe, instead of on the removal of beta-amyloid and tau protein, represents a novel, promising model for tackling what has been a highly frustrating and disappointing approach to treating this patient population. While still early stage, bryostatin has shown the potential to restore synaptic structures and functions damaged by AD, and as such, holds the promise of becoming a new, first-in-class treatment which may provide significant improvement in quality of life. The results of BRNI’s most recent study, as published in the Journal of Alzheimer’s Disease, lend additional credibility to our development of bryostatin which just recently entered a Phase 2a study.” As previously announced, management expects to report a top-line analysis of the Phase 2a study by the end of the first quarter of 2015.


Messrs. Freiman and Ramat went on to say, “The potential for bryostatin goes beyond just the treatment of patients with AD. Due to the compound’s ability to activate PKCe and to therefore stimulate the formation of new synaptic connections, the drug may have applicability to other neurodegenerative brain diseases, including patients suffering from traumatic brain injuries, stroke or mental retardation.”

About The Blanchette Rockefeller Neurosciences Institute
Located in Morgantown, WV, BRNI, at West Virginia University, is a unique, independent, non-profit institute dedicated to the study of memory and finding solutions to memory disorders. BRNI was founded in 1999 in memory of Blanchette Ferry Hooker Rockefeller, an Alzheimer's patient and mother of U. S. Senator John D. Rockefeller IV. BRNI is operated in alliance with West Virginia University as well as in collaboration with other academic institutions.

About Bryostatin
Bryostatin is a natural product produced by a marine invertebrate organism called Bugula neritina and is isolated from organic matter harvested from the ocean. Several variations of this complex product have been achieved in recent years in various academic chemistry laboratories, including bryostatin derivatives being developed through an exclusive license with Stanford University and the existing license agreement with BRNI. These approaches may represent alternative sources of drug supply.

About Neurotrope
Neurotrope was formed in October 2012 principally to license, develop and commercialize various novel therapeutic and diagnostic technologies from BRNI. Neurotrope’s pipeline, under its license from BRNI, includes the drug candidate, bryostatin, for the treatment of Alzheimer’s disease; a minimally invasive, diagnostic biomarker analysis system which would assess the presence of Alzheimer’s in patients. A Phase 2a study with bryostatin in the treatment of Alzheimer’s disease is currently underway. In addition, Neurotrope has a world-wide, exclusive license agreement with the Icahn School of Medicine at Mount Sinai to utilize its proprietary information and data package for the use of Bryostatin-1 in the treatment of Niemann-Pick Type C Disease, a rare disease, mostly of children who are afflicted with Alzheimer- like symptoms. Also, as part of its license from BRNI, the Company, under its BRNI license, the rights to pursue treatments for a number of orphan diseases, including Fragile X Syndrome. The Company’s preclinical and clinical efforts are focused on the development of conventional small molecules that are extraordinarily potent in the activation of the enzyme PKCe, which has been shown to play a central role in the regrowth or repair of nervous tissues, cells or cell products.

Please visit www.neurotropebioscience.com for further information.

http://www.neurotropebioscience.com/Welcome_to_Neurotrope_BioScience/Press_Treating.html

>Bryostatin was originally created as an anti-cancer chemotherapy. When BRNI scientists extensively tested PKC activators against Alzheimer’s disease models, they discovered the drug’s hidden potential to stop Alzheimer’s disease. Over the past six years, the drug has shown remarkable possibilities. In preclinical testing, BRNI scientists experimented with Bryostatin on three species of Alzheimer’s disease transgenic mice, each species based on different human Alzheimer’s disease genes. The test results revealed that Bryostatin, and a related class of drugs discovered at BRNI, can reduce the toxic Alzheimer’s disease protein A Beta and the deposits of A Beta called amyloid plaques, restore lost synapses, and protect against the loss of memory functions. In related preclinical testing, Bryostatin has been shown to enhance and restore memory by rewiring connections in the brain previously destroyed by stroke, head trauma, or aging itself.<

http://www.brni.org/scientific_research/clinical_trials.aspx