Neurotrope, Inc. announced dosing of the first patient in its ongoing, long-term Phase 2 study of Bryostatin-1 for the treatment of Alzheimer's disease ("AD"). The study will be conducted in collaboration with the National Institutes of Health ("NIH") under a $2.7 million grant to Neurotrope. The new Phase 2 clinical study, which is expected to enroll approximately 100 patients, will evaluate Bryostatin-1 in the absence of Namenda® (memantine) for a six-month period, which will include two 11-week dosing cycles.  The study will focus on AD patients with pre-specified moderately severe (Moderate Stratum; MMSE-2 baseline score 14-10) and moderate (MMSE-2 baseline score 18–15) disease, including a patient population that demonstrated the most evidence of benefit in a prior study, and will focus on assessing sustained cognitive benefit as measured by the Severe Impairment Battery ("SIB") score, a widely accepted measure of cognitive function in advanced dementia patients.   Analysis of the data will be conducted in consultation with Dr. Richard Thompson, Senior Scientist from the Bloomberg School of Public Health at Johns Hopkins University.  This Phase 2 study is supported by Phase 2 clinical data from a completed pilot trial (NTRP101-202) which evaluated Bryostatin-1 in the absence of Namenda® in a short-term, 11-week treatment protocol.  In this prior study, Bryostatin-1 (20 mcg) was well tolerated and showed early signals of cognitive benefit, including improvement of 5.0 points in SIB score compared to baseline in the Moderate Stratum cohort in the non-Namenda® group.  This SIB score improvement was sustained throughout the treatment period and persisted for four weeks following completion of treatment.  A second pilot trial (NTRP101-203) using the same treatment protocol (Bryostatin-1 in the absence of Namenda® for 11 weeks) showed a similar SIB improvement compared to baseline for the Moderate Stratum cohort.We believe that the Neurotrope therapeutic strategy is a first-in-class for the potential regeneration of synapses lost in neurodegenerative diseases such as AD, Multiple Sclerosis and Fragile X mental retardation.  The signals of cognitive benefit observed during their Bryostatin-1 pilot trials were sustained over several weeks and, thus, may indicate the generation of new synapses in pre-clinical models caused by the activation of the PKC epsilon – BDNF (brain derived nerve factor) pathways by bryostatin and related compounds in the Neurotrope platform.