EQUITY RESEARCH

INITIATION

Biotechnology Neurotrope, Inc. Buy

NTRP - NASDAQ May 16, 2018 Rebuilding Network Connections in Alzheimer's Disease -
Initiating Coverage with a Buy Rating, $16 PT
Closing Price 05/15/2018 $9.04
Rating: Buy Summary
12-Month Target Price: $16.00
52-Week Range: $3.40 - $9.94 • We are initiating coverage of Neurotrope BioScience with a Buy rating and
Market Cap (M): 71 $16 price target. Neurotrope’s bryostatin has a differentiated mechanism of
Shares O/S (M): 7.9 action that may induce synapse regeneration in Alzheimer’s Disease (AD), the
Float: 96.5% underlying cause of cognition impairment.
Avg. Daily Volume (000): 25
Debt (M): $0.0
• Phase 2 data (N=150) in patients with mod-sev AD demonstrated Severe
Impairment Battery (SIB) improvement, which continued to increase for
Dividend: $0.00 weeks after treatment ended, suggesting an impact on synapse regeneration/
Dividend Yield: 0.00% preservation.
Risk Profile: Speculative
Fiscal Year End: December • Confirmatory P2 is next, we see it as a “smart” move; Neurotrope, rather than
jumping right to a P3 study based on a small P2 study and subgroup analysis,
is stepping back and designing a second P2 study to validate dosing and to
Total Expenses ('000) zero in on the right patient population (initiate 2Q18, data mid-19).
2017A 2018E 2019E
1Q 3,090 2,013A 4,753 • Bryostatin is a platform drug with potential in several indications; stroke, TBI,
2Q 2,964 3,558 4,960 Fragile X, Niemann-Pick Type C and Rett Syndrome. P2 studies expected.
3Q 2,317 3,855 5,373
4Q 4,331 4,003 5,580 • Conclusion: By regenerating synapses and attacking AD at its core, we believe
FY 12,702 14,826 20,665 that bryostatin could emerge as a viable therapy in AD and potentially have
the clinical success that other approaches have not. In our view, positive P2
confirmatory data can position the company well for partnering opportunities
NTRP or to become an acquisition target for big pharma. Catalysts lay ahead; we see
Price (USD) Source: Factset Volume (MM)
11 0.35 upside at the current ~$70M valuation of the company.
10 0.3
9
Details
0.25
8 A Differentiated Approach to Alzheimer's Disease (AD): Bryostatin targets AD
0.2
7 by addressing the proximate cause of cognitive deficit, loss of synapses (only
6
0.15 direct link to AD and cognition, discovered 27 years ago, Abstract Link). It does so
0.1 by upregulating PKCε, which has demonstrated increased synaptogenesis in pre-
5
clinical models. Synapses are essentially the “wiring” of the brain, so it logically
4 0.05
follows that repairing this would help with a multitude of neurodegenerative diseases.
3 0 One of the key advantages to this approach is that it should produce a durable effect
Jul-17 Sep-17 Nov-17 Jan-18 Mar-18 May-18 as new synapses will not simply disappear after treatment stops. The majority of drug
Price Volume development in AD has focused on targeting Aβ and Tau. However, these attempts
have been largely unsuccessful. PKCε activation also upregulates enzymes which
degrade amyloid beta plaques and cleave the precursor proteins from which they
form but most importantly may regenerate synapses.
Phase 2 Study in Moderate – Severe AD: The P2 study (n=147) involved three
dosing cohorts, Placebo, 20 μg, and 40 μg. Patients who completed the trial taking
the 20 μg dose had an SIB improvement of 1.5 vs. a decline of 0.8 for placebo
(n=0.07), patients in the 40 μg cohort did not experience an improvement. The latter
is likely due to prior work demonstrating that higher levels of bryostatin induce PKCε
inhibition. The sub-group analysis of non-memantine patients at 15 weeks, showed
an increase in SIB of 6.36 over placebo (p<0.05) while no difference was observed
in the non-memantine patients. While it’s a small number of patients, the data are
suggestive of a signal from bryostatin. A second P2 study is planned for 2Q18, data
mid-19.
Caroline Palomeque Valuation: We model commercial launch of Bryostatin in the US in 2023 and the
(212) 895-3726 EU (with a partner and Neurotrope receiving royalties) in 2024. A risk adjustment of
cpalomeque@maximgrp.com 50% is factored in based on stage of development and trial risk. A 30% discount is
applied to the Free Cash Flow, Discounted EPS and Sum-of-the-Parts models which
Jason McCarthy, Ph.D. are equally weighted to derive a $16 price target.
(212) 895-3556
jmccarthy@maximgrp.com
SEE PAGES 16 - 17 FOR IMPORTANT DISCLOSURES AND DISCLAIMERS

Investment Risk:
Neurotrope’s products are not
approved and the company
currently does not generate
revenue.
Regulatory Risk:
Neurotrope’s products may
not be successful in clinical
trials and may not meet the
requirements for regulatory
approval(s).
Commercial Risk:
Neurotrope’s products are not
yet commercialized and
if/when they become
commercially available may
not achieve significant market
share.
Financial Risk: Neurotrope
is not profitable and may
need to raise additional
capital to fund operations.
Dilution Risk: Capital raises
to fund operations could
dilute investors.
Ownership:
Institutional: 16.4%
Insiders: 3.5%
Balance Sheet Summary:
Cash: $14.5M (1Q18A)
Debt: $0M (1Q18A)
Analysts Covering the
Stock (other than Maxim): 1
Maxim Group LLC
Neurotrope, Inc. (NTRP)
CORPORATE PROFILE
Neurotrope BioScience, Inc.
th
205 East 42nd Street, 17 Floor
New York, NY 10017
Company Background. Neurotrope BioScience, (NASDAQ:NTRP), formed in 2012, is at the forefront
of the biotech industry and is focused on developing new therapies with Bryostatin 1 for the treatment of
neurodegenerative diseases and developmental disorders. The company built a development pipeline
that includes various treatment approaches with Bryostatin 1 for serious and difficult-to-treat diseases
such as Alzheimer’s dementia and the Orphan diseases, Fragile X Syndrome (FXS) and Niemann-Pick
Type C (NPC).
Bryostatin was tested in a 148 moderate to severe Alzheimer's disease patient population across 26
sites in the U.S. First patients dosed January 2016 . Primary efficacy endpoint based on Severe
Impairment Battery Scale (SIB). Entry criteria was based on the MMSE score. Top line data was
released at Alzheimer's Association International Conference (AAIC) in July 2017. Please see the full
top line data set by reviewing our press release dated July 19, 2017. The company released additional
data on 01/07/18 at the Sachs Neuroscience Conference. These new findings on associative memory
mechanisms are guiding development of drug discovery with the potential to treat the loss of synapses
and to prevent neuronal death in neuro-degenerative disorders such as, Alzheimer's disease, stroke,
traumatic brain injury, fragile x, Neimann Pick type C, Rett Syndrome and attention-deficit disorders.
Senior Management:
Charles S Ryan, JD, PhD – Chief Executive Officer. Appointed CEO of Neurotrope BioScience in
February 2018, Dr. Ryan is an experienced executive with over 20 years of experience in drug
development. Prior to joining Neurotrope, he served as CEO of Orthobond, a private company focused
on creating proprietary surface modifications to enhance the function of medical devices or
pharmaceuticals. Prior still, Dr. Ryan was VP and General Counsel at Cold Spring Harbor Laboratory, a
preeminent non-profit institution focused in neuroscience, bioinformatics, cancer, genomics and plant
biology. From 2004 until the acquisition by Actavis plc in 2014, Dr. Ryan was SVP Chief Intellectual
Property Counsel for Forest Laboratories, a specialty pharmaceutical company in New York. At Forest
Laboratories, Dr. Ryan led hundreds of due diligence teams, managed all aspects of patent and
trademark litigations, developed cross-functional teams to establish a global strategy for hundreds of
products. Two of the company’s most significant drugs were Lexapro (for major depressive disorders)
and Namenda (for moderate to severe Alzheimer’s Disease). He began his career in biotechnology with
The Collaborative Group, Ltd., a bioscience company providing development, research and
manufacturing services to the pharmaceutical and skin care industries. Dr. Ryan earned his Ph.D. from
Stony Brook University, his J.D. from Western New England University, and his B.A. from The College
of Wooster.
Dr. Daniel Alkon. – President and Chief Scientific Officer. Dr. Alkon received his undergraduate
degree in chemistry in 1965 at the University of Pennsylvania. After earning his M.D. at Cornell
University and finishing an internship in medicine at the Mt Sinai Hospital in New York, he joined the
staff of the National Institutes of Health where during his 30 year career he became a medical Director
in the U.S. Public Health Service at the NINDS and Chief of the Laboratory of Adaptive Systems. In
1999, Dr. Alkon then became the founding Scientific Director of the Blanchette Rockefeller
Neurosciences Institute and occupied the Toyota Chair in Neuroscience at the Institute. In this position
he and his team conducted multidisciplinary research on the molecular and biophysical mechanisms of
memory and memory dysfunction in psychiatric and neurological disorders, particularly Alzheimer’s
disease. He was also a Professor at BRNI and a Professor of Neurology at West Virginia University until
September 2016. As an internationally recognized pioneer in research on brain-based neural networks
and the molecular basis of memory, he has authored hundreds of scientific articles as well as several
books including Memory Traces in the Brain by Cambridge University Press, and the popular book
Memory’s Voice by Harper Collins.
2
 Neurotrope, Inc. (NTRP)

INVESTMENT SUMMARY
Bull Case. Despite the high prevalence of Alzheimer’s Disease (AD), drug development has been largely unsuccessful to date for multiple
factors. Bryostatin’s unique MoA differentiates the drug versus other therapeutics in development by targeting/promoting the growth of synapses,
addressing the actual cause of cognitive deficit. Bryostatin has been tested in over 1500 patients as an anticancer drug and has a well-
established safety and tolerability profile, which partially “de-risks” the compound. In a P2 trial (N=150) in moderate to severe AD, Bryostatin
demonstrated improvements in Severe Impairment Battery (SIB) at 11 weeks of treatment which was maintained through 15 weeks. The results
were suggestive of a signal that synapses may be being regenerated and not just symptomatic relief. Neurotrope is moving Bryostatin into a
phase 2 confirmatory trial (vs moving directly to a P3 study) using the data from the previous trial to “fine tune” dosing and patient population (i.e.
memantine-free patients which experienced the most benefit in the prior trial). Data is expected in mid-2019. Bryostatin may expand into
additional indications including Fragile X and Neiman Pick Disease, as well as be partnered for non-AD indications. The AD market is >$5B and
made up of mostly palliative care and a few medications like memantine which only induce some symptomatic relief. Targeting the root of the
disease, loss of synapses, with Bryostatin could make it a blockbuster drug. Bulls recognize that AD drug development has struggled and there
is risk, though Byrostatin with a differentiated MOA (vs targeting tau, amyloid plaques etc) could potentially have success where others have
failed. Given the size of the market opportunity and the current market capitalization of $65M success is not yet factored in. Catalysts lay ahead
over the next 12-months as the AD trial gets underway and data emerges, as well as potential expansion to additional indications and
partnerships, pointing to upside.
Bear Case. Drug development across the spectrum of AD (mild to severe) remains difficult with multiple large phase 3 trials failing in recent
years, likely due (in part) to the complexity of the disease and heterogeneity of a large number of people the disease affects. Establishing
definitive proof of concept is difficult with small numbers of patients. The P2 study of Bryostatin in mod-sev AD, met statistical significance in an
FDA pre-specified, one-tailed t-test at p<0.01. This was, however, an exploratory trial that was not conducted to establish proof-of-concept
(POC). A post-hoc analysis was conducted in a subgroup of patients that were not receiving memantine and there appeared to be a more
pronounced benefit. In this analysis, a two-tailed t-test was highly significant with improvement delta of over 6 points. Still, the number of patients
was too small to represent POC. The company is going back to run another P2 study based on the prior study results which will take more time
and more capital to reach POC and attract a partner. AD, in the eyes of bears, is a big pharma game and may be outside the reach of a
microcap biotechnology company like Neurotrope and given the long list of drug failures in the space, bears expect bryostatin could follow a
similar path.
Our Take. Induce synapse regeneration and halt or reverse AD or other neurodegenerative diseases. This is the target of Bryostatin which
differentiates this drug in AD versus others that target tau and amyloid plaques or other areas. The bottom line in AD is that synapses are lost
which likely drives cognition and functional impairment. Bryostatin induces synapse regeneration by targeting the signaling molecule PKC3. In a
P2 study, patients experienced improvement in severe impairment battery (SIB) which continued to improve even after the drug was stopped.
The effect was more pronounced in patients not receiving memantine. Although a small number of patients, the data are suggestive of new
synapse preservation or regeneration which could potentially explain the continued improvement. In addition, Brystatin has a positive safety
profile, established over years or work in over 1,500 patients as an anti-cancer agent at the NIH. Good enough to go to P3? It could be but AD is
a complex disease where many other drugs have failed. Instead of racing to P3, Neurotrope is “smartly” in our view, taking a step back and
carefully designing a second confirmatory P2 study to further explore the results observed in the prior trial. Positive data in the next trial, which is
expected in mid-2019, would represent proof of concept and set the stage for phase 3 studies and potential partnering opportunities. In addition,
with a unique mechanism of action that may impact synapse regeneration, there are multiple other indications that Bryostatin could potentially
target and may also be attractive to a partner(s). The AD market opportunity is in the billions and with a $65M market capitalization for
Neurotrope today, success is not yet factored in. Why? AD has proven to be a very complex and difficult indication, many drugs have failed
which may cause investors to exercise caution. We believe that with a differentiated MOA, a strong safety profile and early signals of efficacy,
Bryostatin could potentially be successful in AD where others have failed. With data coming over the next 12 months, as well as potential
partnering opportunities we see upside at the current valuation of the company.

Finances. Neurotrope BioScience, Inc. ended 1Q18 with $14.5M in cash and operating expenses of just over $2M. The company has cash
runway into 2019 and through the confirmatory phase 2 trial of Bryostatin in Alzheimer’s Disease. The announcement of partnership(s) could
bring upfront payments that may extend the runway further. As a microcap biotechnology company we expect that Neurotrope will likely need to
raise capital multiple times to fund ongoing and planned clinical programs and we factor in potential future dilution into our model.

Maxim Group LLC 3

 Neurotrope, Inc. (NTRP)

Exhibit 1. Upcoming Catalysts for Neurotrope

Product Geography Indication Event Timeline Impact

Bryostatin US Alzheimer's Disease Initiate P2 Confirmatory Trial 2Q18 +
Bryostatin US Fragile X Syndrome Initiate clinical development, P2 study 3Q18 ++
Byrologs US Multiple Announce Partnership(s) to Advance Pipeline Products 2018-2019 +
Bryostatin US Alzheimer's Disease Complete enrollment of the P2 study 1H19 +
Bryostatin US Alzheimer's Disease Topline data from P2 study mid-19 ++
Bryostatin US Fragile X Syndrome Report P2 data 2H19 ++
Bryostatin US Alzheimer's Disease Initiate P3 pivotal studies 2020 ++
Stock Si gni fi ca nce Sca l e: + of modera te i mporta nce; ++ hi gher l evel ; +++ very i mporta nt
Source: Compa ny reports a nd Ma xi m Foreca s ts

Exhibit 2. Neurotrope Bioscience Pipeline

Product Indication Development Pre-IND Phase I Phase II Phase III Marketed

Bryostatin - 1 Alzheimer's Disease
Bryostatin - 1 Fragile X Syndrome
Bryostatin - 1 Neimann Pick Type C
Byrologs Pipeline
Source: Company Reports and Maxim

Alzheimer's Disease
Alzheimer’s Disease (AD) is a chronic neurodegenerative brain disease which starts slowly and progresses causing short term memory loss,
problems with language, disorientation, mood swings, loss of motivation and behavioral issues. At the later stages of the disease, bodily
1
functions are lost which ultimately leads to death. AD is responsible for 60-70% of dementia cases and the estimated prevalence of the disease
2
ranges from 11.4M to 59.4M worldwide. The disease can be categorized into four stages based on the degree of cognitive impairment. Pre-
dementia, also known as mild cognitive impairment (MCI) is often considered a prodromal stage of AD and is often mistaken for normal signs of
3
aging. Study results estimate that people with MCI progress to AD at a rate of 10-15% per year. Early AD is when definitive symptoms begin to
show and a diagnosis can be made. This stage is characterized by losses in short term memory and decreased language fluency. These
changes may only be noticed by close friends and family. The person is usually able to complete most tasks independently and communicate
basic ideas, but may need assistance with more cognitively demanding activities. As the patient progresses into moderate AD, the symptoms
become more evident. Long-term memories start to become affected and the person may not recognize family members, speech becomes
noticeably impaired due to inability to recall vocabulary. At this point in the disease confusion with daily tasks inhibits independence and full-time
care is often required. During advanced AD, the patient is completely dependent on the caregiver and verbal language ability is reduced to
phrases or even single words. Ultimately the patient will no longer be able to perform the simplest tasks and will be bedridden. The process of
progression from early AD to death is approximately 8 to 10 years on average.
Physiopathology. The dominant hypothesis for the cause of Alzheimer’s Disease, the amyloid cascade hypothesis, has to do with the build-up
of beta-amyloid plaque and neurofibrillary tangles. Beta-amyloid (Aβ) plaques are clumps of insoluble peptides which build up in the brains of
Alzheimer's patients. Beta-amyloid is produced by the abnormal cleavage of a neuronal membrane protein, amyloid precursor protein (APP).
APP is normally cleaved by α-secretase and γ-secretase, which releases soluble fragments that can be disassembled and repurposed. In
Alzheimer's patients, the APP is cleaved by β-secretase and γ-secretase which released the beta-amyloid protein. Beta-amyloid self assembles
into insoluble fibers which clump together to form beta amyloid plaques that interfere with neuronal function. One of the consequences of these
plaques is the release of inflammatory cytokines due to microglial activation. This creates neuroinflammation which enhances beta-amyloid
4
deposition, creating a vicious cycle. Neurofibrillary tangles occur when the tau proteins, which stabilize microtubules in the neuron, are
deformed and separate from the microtubule, causing it to fall apart. Microtubules give neurons their structure and facilitate molecular transport.
When they disassemble, neural connections separate and eventually cause neurons to die.

1
Burns, A., and S. Iliffe. “Alzheimer's Disease.” BMJ, vol. 338, no. 1, 5 Feb. 2009.
2
Brookmeyer, Ron, et al. “Forecasting the Global Burden of Alzheimer’s Disease.” Alzheimer's & Dementia, vol. 3, no. 3, 2007, pp. 186–191.
3
Grundman, Michael. “Mild Cognitive Impairment Can Be Distinguished From Alzheimer Disease and Normal Aging for Clinical Trials.” Archives of Neurology, vol. 61, no. 1, Jan.
2004, p. 59
4
Cai, Zhiyou, et al. “Microglia, Neuroinflammation, and Beta-Amyloid Protein in Alzheimer's Disease.” International Journal of Neuroscience, vol. 124, no. 5, Dec. 2013, pp. 307–
321.

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Synaptic Loss. Synapses act as the wiring for the brain, allowing electrical and chemical signals to pass between neurons. As synapses
activate, the connection between the two neurons strengthens, resulting in the formation of memory through a process known as long term
5 6
potentiation. One of the common characteristics across all memory disorders is the loss of synaptic function. In AD, synaptic loss is the only
pathological finding that correlates with the degree of cognitive deficit; Amyloid plaques and neurofibrillary tangles are only weakly correlated.
Current research suggests that Aβ is involved in synaptic loss and has been shown to reduce PKC (Protein Kinase C) isomers, which are known
7
to protect against synaptic loss. This downregulation could be could be linked to Aβ induced synaptic loss. The majority of drug development is
focused on eliminating Amyloid and Tau but none have been effective in halting the progression of the disease leading some to believe that it is
8
an incomplete picture, especially considering that cognitive deficits and synaptic loss can be present in the absence of amyloid plaques.
The Current Standard of Care for AD offers small symptomatic relief and is palliative in nature. It consists of medication, psychosocial
intervention, and caregiving. Five medications are currently available for Alzheimer's which fall into two categories: acetylcholinesterase
inhibitors and NMDA receptor antagonists. Acetylcholinesterase inhibitors include tacrine, rivastigmine, galantamine and donepezil which reduce
the rate at which acetylcholine is broken down. This combats the decrease in acetylcholine caused by the death of cholinergic neurons. There is
some evidence of efficacy in mild to moderate AD but there has not been any significant evidence to show delay of onset of AD in patients with
9
MCI. NMDA receptor antagonists, such as memantine, work by blocking NMDA receptors and inhibiting their overstimulation by glutamate. This
prevents excessive amounts of glutamate from causing cell death. There has been a small benefit observed using memantine in patients with
10
Alzheimer's.
The Market for Alzheimer's Disease was worth $4.9B in 2013, for symptomatic relief of AD, of which 57% was spent on MCI, 10% was spent
on mild AD, 23% on moderate AD and 10% on severe AD. For a disease-modifying drug, the market size could increase 10x. The
pharmaceutical market for AD is dominated by 4 drugs, Namenda (Memantine), Aricept (Donepezil), and Exelon (Rivastigmine) and Memary
11
which is a memantine drug in Japan. Together these drugs represent 80% of sales for AD. This market is expected to grow due to an aging
population and life expectancy improvements. Since the solutions on the market do not adequately treat the disease, drug companies are
pursuing a number of therapeutic targets. These include nicotinic receptors, 5HT receptors, neurogenesis, neuroinflammation, the amyloid
cascade, tau & GSK-3, PDE inhibition, HDAC & sirtuin, and mitochondria. With limited clinical success in the space, Neurotrope is exploring a
novel mechanism for addressing AD, PKCε activation.
Exhibit 3. Neurons in a Healthy Brain versus Neurons in an Alzheimer's Brain. Two types of lesions are found in the brains of individuals
with Alzheimer's. The first is amyloid plaques which are groups of molecules which clump together and build up in the brain. The other type is
neurofibrillary tangles, which consist of abnormal tau proteins. When the abnormal tau proteins detach from the microtubules, the neuron begins
to degenerate and can no longer communicate with other neurons.

Source: McGill University12

5
Lynch, M. A. (January 1, 2004). "Long-Term Potentiation and Memory". Physiological Reviews. 84 (1): 87–136.
6
Sun, Miao-Kun, et al. “Towards Universal Therapeutics for Memory Disorders.” Trends in Pharmacological Sciences, vol. 36, no. 6, 2015, pp. 384–394.
7
Hongpaisan, J., et al. “PKC ε Activation Prevents Synaptic Loss, Aβ Elevation, and Cognitive Deficits in Alzheimer's Disease Transgenic Mice.” Journal of Neuroscience, vol. 31,
no. 2, 2011, pp. 630–643., doi:10.1523/jneurosci.5209-10.2011.
8
Ghezzi, L. et al. (2013) Disease-modifying drugs in Alzheimer’s disease. Drug Des. Dev. Ther. 7, 1471–1479
9
Raschetti, Roberto, et al. “Cholinesterase Inhibitors in Mild Cognitive Impairment: A Systematic Review of Randomised Trials.” PLoS Medicine, vol. 4, no. 11, 2007.
10
Mcshane, Rupert, et al. “Memantine for Dementia.” Cochrane Database of Systematic Reviews, 19 Apr. 2006.
11
“Global Alzheimer's Disease Drugs Market 2017-2021 .” Business Wire, 4 July 2017, www.businesswire.com/news/home/20170704005296/en/Global-Alzheimers-Disease-
Drugs-Market-2017-2021--.
12
“Amyloid Plaques and Neurofibrillary Tangles.” THE BRAIN FROM TOP TO BOTTOM, McGill Univeristy, thebrain.mcgill.ca/flash/d/d_08/d_08_cl/d_08_cl_alz/d_08_cl_alz.html.

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Exhibit 4. Synaptic Loss Precedes Amyloid Formation and Neuronal Loss. While the prevailing dogma in AD research is centered around
the buildup of neurofibrillary tangles and amyloid plaques, the loss of synapses can often occur before the presence of amyloid plaques or later
in the disease in the absence of amyloid plaques, leading some to suggest that new targets for medication should be explored.

Source: Neurotrope BioScience Corporate Presentation

Bryostatin is a natural product isolated from an invertebrate marine organism called Bugula Neritina. The compound was originally explored for
potential anticancer applications due to immunomodulatory activities including induction of cytokine release and expansion of tumor-specific
lymphocyte populations through its activation of PKCs. After more than 60 phase 1 and 2 clinical trials, the effect produced by Bryostatin was not
13
clinically meaningful enough to warrant progression to phase 3. While the compound may not be effective as a cancer treatment, it was found
to be a potent activator of PKCε which may be an effective mechanism for treating AD through restoration of synaptic function in damaged
neurons. In vitro and in vivo animal models have demonstrated a partial restoration of synaptic function after PKCε activation. Neurotrope has
begun a clinical program in AD to test the effectiveness of Bryostatin in humans. With over 60 previous trials in cancer, the drug already has a
strong safety and tolerability profile.

PKCε Activation Leads to Synaptogenesis. Synaptic loss is among the only pathological finding in the brains of AD patients which are
correlated with the degree of dementia in vivo. Staining results that examine the level of synaptic markers show a significant reduction in AD
14
patients’ brains. The more widely accepted markers, Aβ and Neurofibrillary tangles, are only weakly correlated to dementia. Protein Kinase C
enzymes (PKCs) are a family of protein kinase enzymes which have demonstrated the ability to promote synaptic growth in normal brains and
15
prevent synaptic loss in pathological brains, in particular PKCε. Upon activation, PKCε migrates to the cell membrane where it activates
signaling enzymes which lead to increased DNA transcription, synaptic maturation, increase in growth factors (nerve growth factor and brain-
derived neurotrophic factor [such as BDNF, NGF]), apoptosis inhibition and reduction of Aβ and phosphorylated Tau. These events have a
number of secondary effects in the neuron such as an increase in the number of pre-synaptic vesicles and an increase in the number of
mushroom spines associated with individual synaptic buttons. The end result is that neurons are able to form more synapses which assist in
learning and memory and have demonstrated a regenerative effect in pre-clinical models of AD. PKCε activation represents a new therapeutic
target which has the potential to expand treatment beyond simply lowering the presence of Aβ and tangles, to restoring synaptic networks lost
during neurodegeneration and preventing further loss.

PKCs Also Reduce Amyloid Beta. While Bryostatin acts primarily via increased synaptogenesis, PKC activation also leads to reduction in
amyloid beta. PKCε activates three enzymes involved in Aβ, two of which degrade the beta oligomers and one which prevents plaque formation.
The activation of endothelin converting enzyme and neprilysin leads to amyloid beta degradation, and the induction of alpha-secretase cleaves
amyloid precursor protein through phosphorylation of the Erk enzyme. This effect was confirmed in preclinical models predisposed to amyloid
deposit formation, whereby PKCε activation interrupted the amyloid formation.

Preclinical Models. Bryostatin was tested in Tg2576 AD transgenic mouse strains. In the pathogenic mice, researchers found that Bryostatin
restored normal or supranormal levels of PKC α and ε, while simultaneously reducing the level of Aβ. The researchers also noted that Bryostatin
prevented or even reversed hippocampal synaptic loss and memory impairment at 5 months postpartum. The researchers also tested Bryostatin

13
Trindade-Silva, AE; Lim-Fong, GE; Sharp, KH; Haygood, MG (December 2010). "Bryostatins: biological context and biotechnological prospects". Current Opinion in
Biotechnology. 21 (6): 834–42.
14
Hongpaisan, J., et al. “PKC ε Activation Prevents Synaptic Loss, Aβ Elevation, and Cognitive Deficits in Alzheimer's Disease Transgenic Mice.” Journal of Neuroscience, vol. 31,
no. 2, 2011, pp. 630–643.
15
Ibid.

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in the much more rapidly progressing 5XFAD strains and found that it similarly prevented cognitive deficits. The results suggest that PKC
16
activation plays an important role in preventing and even reversing the effects of AD.

Phase 2 Data. The P2 study of Bryostatin (n=147) enrolled patients with late stage AD to examine the safety and preliminary efficacy of
Bryostatin. The primary endpoint was reduction in the Severe Impairment Battery (SIB), which is a measure of severity of dementia, after twelve
weeks of treatment. The study involved 3 dosing cohorts (Placebo, 20μg, and 40μg) and data was further divided into the modified intent to treat
(mITT) population (n=135), which included all patients who received the study drug and had completed at least one efficacy/safety assessment,
and the completer population (n=113), which included patients who completed the 13-week protocol and cognitive assessments. For the 20μg
dose, patients in the completer population experienced a mean SIB increase of 1.5 vs a decrease of -1.1 in the placebo group (p<0.07) while the
mITT population experienced an increase of 1.2 vs -0.8 for placebo (p<0.134). No effect was observed in patients taking the 40μg dose, this was
17
not surprising as Bryostatin was originally investigated for PKC downregulation, which is expressed at higher doses. The results did not meet
the standard criteria for statistical significance and thus the trial was not viewed positive by investors, however a phase 2 study is not typically
powered to significance and the company did find a statistically significant sub group in patients who did not receive SoC background treatment
(memantine). A second, confirmatory study exploring the effects of the 20ug dose in non-memantine patients is planned for 2Q18.

Post Hoc Sub-Group Analysis. In the exploratory endpoint analysis at 15 weeks, the researchers found that among the 20 μg cohort,
mITT patients (n=34) showed a net improvement in SIB of 3.59 (p=0.05), and in completers (n=34) the SIB improvement was 4.09
(p=0.03) over placebo (n=33). During this analysis, the researchers also noticed a large difference between patients who use
memantine as a background therapy vs those who did not. Among patients on memantine, no difference was found at 15 weeks,
however a large difference was found in the non-memantine subgroup. Patients in the mITT cohort (n=14) had an increase of 5.93
(p=0.06) vs. placebo (n=11) and completers (n=14) had an increase of 6.36 vs placebo (n=11).

Memantine Interference. The findings from the subgroup analysis raise the question of whether or not memantine could interfere with
the function of Bryostatin in Alzheimer's patients. The hypothesis is supported by the biological mechanisms of the two drugs.
Memantine is an NMDA channel blocker which prevents activation of the glutamate receptor NMDA that provides symptomatic relief.
18
One of the functions of PKCε is to regulate NMDA receptor function by modulating conductance and receptor traffic. The two functions
cause interference between Bryostatin and Memantine, which in part, may explain the phase 2 results.

Phase 2 Confirmatory Trial. From the Phase 2 data, Neurotrope gained insight into the patient populations to target as well as dosing. Since
powering is not standard for a phase two, some companies proceed to a phase 3 on data that may have been close to significance. However
Neurotrope will be performing a phase 2 trial with the 20μg dose in AD patients who do not take memantine which will be powered for
significance. This will allow them to demonstrate the drug effect and test the observations from the previous trial. This is a smart move in our
view as the sub group can be tested with a larger population and it will not require the capital expenditures necessary to support a larger phase 3
program. The phase 2 trial will enroll 100 patients with moderate to severe AD, defined as a Mini Mental State Exam 2 (MMSE-2) score of 4-15.
The primary endpoint is defined as change in SIB score between baseline and the average of weeks 13 and 15. Patients will be randomized 1:1
to receive Bryostatin 20ug or placebo. Patients on memantine will be excluded unless they have been off drug for 30 days prior to
randomization. The trial should initiate in 2Q18.

Exhibit 5. Bryostatin Addresses Amyloid and Tau Related Neurodegeneration too. Bryostatin impacts Alzheimer's disease from multiple
angles through the activation of PKCε. It triggers cell signaling pathways which enhance synaptogenesis and inhibit apoptosis, while reducing
levels of Aβ and inhibiting Tau protein phosphorylation. These changes result in enhanced spatial learning and long term memory.

16
Ibid.
17
Alkon, Daniel L., et al. “PKC Signaling Deficits: a Mechanistic Hypothesis for the Origins of Alzheimer's Disease.” Trends in Pharmacological Sciences, vol. 28, no. 2, 2007, pp.
51–60.
18
Sen, Abhik, et al. “Protein Kinase C ε (PKCε) Promotes Synaptogenesis through Membrane Accumulation of the Postsynaptic Density Protein PSD-95.” Journal of Biological
Chemistry, vol. 291, no. 32, 2016, pp. 462–476.

Maxim Group LLC 7

 Neurotrope, Inc. (NTRP)

Source: Neurotrope BioScience Corporate Presentation

Exhibit 6. PKC in Alzheimer's and Learning/Memory. PKC is involved in both specific pathological AD pathways as well as those associated
with learning and memory. PKC can be activated by a number of factors including fibroblast growth factor 18 (FGF-18), insulin growth factor
(IGF) and phospholipase C (PLC). PKC can impact Aβ though activation of α-secretase either directly or through MAPK; α-secretase cleaves
APP preventing the formation of amyloid plaques. PKC also inhibits GSK-3β, a factor which is involved in the formation of hyper phosphorylated
Tau, potentially reducing the presence of neurofibrillary tangles. PKC is involved in learning and memory pathways by activation of FNA
transcription by activating the RNA-binding protein ELAV, MAPK, or transcription factors such as NF-ĸB. One issue is that PKC is downregulated
by Aβ, exacerbating Alzheimer's processes and impacting learning and memory.

Source: Alkon, et al. (2007)19

Exhibit 7. PKC Activation Regulates NMDA. One of the pathways by which PKC is activated is through mGluR5 receptor stimulation.
Bryostatin activates PKC and regulates the NMDA receptor in several ways. One example is PKCs phosphorylate the NMDA receptors to
2+
increase conductance. NMDA is responsible for Ca flux, which is thought to play a role in learning and memory. Memantine blocks transport
through NMDA, which interferes with the activity of PKCs.

19
Alkon, Daniel L., et al. “PKC Signaling Deficits: a Mechanistic Hypothesis for the Origins of Alzheimer's Disease.” Trends in Pharmacological Sciences, vol. 28, no. 2, 2007, pp.
51–60.

Maxim Group LLC 8

 Neurotrope, Inc. (NTRP)

Source: Neurotrope BioScience Corporate Presentation

Exhibit 8. Bryostatin Protects Against Amyloid Beta in Rat Models. Rat models treated with Aβ demonstrated reduced synaptic connections
and synaptic activity (Left) but treatment with Bryostatin prevented these effects and demonstrated increased synaptic growth (right).

Source: Neurotrope BioScience Corporate Presentation

Exhibit 9. Phase 2 Data in Moderate – Severe AD. In the first phase 2 trial, patients given Bryostatin at 20 µg experienced improvement in SIB,
while no effect was observed in the 40 mg group. This may be explained by downregulation of PKCε in the 40 mg dose group, whereby too large
of a dose of Bryostatin actually acts as an antagonist for PKCε, rather than the agonistic effect observed with lower doses.

Maxim Group LLC 9

 Neurotrope, Inc. (NTRP)

Source: Neurotrope BioScience Corporate Presentation

Exhibit 10. Memantine Interferes with the Effect of Bryostatin. A key observation from the phase 2 trial data was that memantine seemed to
interfere with the effects of Bryostatin. This is believed to be related to the inhibition of the NMDA transporters caused by memantine, which are
necessary for Bryostatin’s beneficial effects. In patients off-memantine, SIB improvement was observed throughout the observation period,
including at 15 weeks (4 weeks after the last dose), this is consistent with the predicted mechanism of action as synaptic growth would produce
a durable effect on cognitive function. In the on-memantine subgroup, the difference in SIB was negligible. Shown below is the mITT data at 15
weeks.

Source: Neurotrope BioScience Corporate Presentation

Exhibit 11. Phase 2 data at 15 Weeks, Non-Mematine. In the “completers” group that were off-mematine the delta in SIB widened to 6.36,
from 5.93.

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 Neurotrope, Inc. (NTRP)

Source: Neurotrope BioScience Corporate Presentation

Expansion to Other Neurodegenerative Brain Diseases

Universal Memory Therapeutics. With a lack of effective therapeutics, memory disorders are increasingly becoming problem and a global
crisis as lifespans are increasing. Synapses are in large part, responsible for the formation of memory and thus, therapeutic agents which target
the formation of newly matured synapses and restoration of synaptic function could serve as potential “universal” therapeutics for memory
20
disorders. Bryostatin is a potential candidate for such a therapeutic due to the activation of PKCε and BDNF, which enable restoration of
synapses in the Hippocampus, neurotrophin levels, and cognitive function. As such, Neurotrope is exploring multiple indications which could
benefit from Bryostatin with programs in stroke, Fragile X Syndrome and Niemann-Pick Disease type C- the closest to entering the clinic.

Fragile X syndrome (FXS) is the most common form of inherited intellectual disability in males and also a significant cause of intellectual
disability in females. FXS is a leading mono-genetic (X-linked, mutation in FMR1 gene) cause of mental retardation. The mutation negatively
affects synaptic function, plasticity, and neuronal connections, which results in a spectrum of intellectual disabilities, social anxiety, and memory
problems. FXS affects one in 4,000 males and one in 8,000 females of all races and ethnic groups (National Fragile X Foundation). Delays in
speech and language development are common, as are a variety of physical and behavioral characteristics, including ADD, ADHD, autism, and
autistic behaviors, anxiety, and mood swings. Approximately 7% of women and 18% of men with FXS have seizures. People with FXS are
affected throughout their lives. Currently, there are no known cures or approved therapies for the treatment of FXS. Patients with behavioral and
mental health conditions are treated by medications that treat those conditions, such as anxiety. The FMR1 mutation alters signal processing at
21
synapses in the brain such as metabotropic glutamate receptor (mGluR) signaling. PKCε activation could restore these immature synapses to
full functionality. Preclinical studies in FXR mice have shown that Bryostatin rescues the hippocampus from many of the phenotypes associated
with FXS including decrease in density of presynaptic and postsynaptic membranes, increase in immature synapses, decrease in learning-
22,23
induced mature synapses, and impairment of hippocampus-dependent spatial learning and memory.

Niemann-Pick Type C (NPC) is an ultra-rare, progressive and fatal disease caused by defects in lipid transformation within the cell. Although
there are only 2,000-3,000 cases globally, it is likely the disease is under- and misdiagnosed. There are currently no approved treatments for the
disease in the US. NPC genes (NPC1 and NPC2) code for proteins that act sequentially to release cholesterol into cells. Mutations in either of
these genes cause un-esterified cholesterol and other lipids to become sequestered and impair transport to plasma membrane and endoplasmic
reticulum. Lipid build up in the brain can kill cells and, over time, leads to neurological, systemic, and/or psychiatric problems, generally leading

20
Sun, Miao-Kun, et al. “Towards Universal Therapeutics for Memory Disorders.” Trends in Pharmacological Sciences, vol. 36, no. 6, 2015, pp. 384–394.
21
Lüscher C and Huber KM (2010) Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease. Neuron 65:445–459.
22
Sun, M.-K., et al. “Bryostatin-1 Restores Hippocampal Synapses and Spatial Learning and Memory in Adult Fragile X Mice.” Journal of Pharmacology and Experimental
Therapeutics, vol. 349, no. 3, 2014, pp. 393–401.
23
Sun, M.-K., et al. “Rescue of Synaptic Phenotypes and Spatial Memory in Young Fragile X Mice.” Journal of Pharmacology and Experimental Therapeutics, vol. 357, no. 2, 2016,
pp. 300–310.

Maxim Group LLC 11

 Neurotrope, Inc. (NTRP)

to mortality within the first two decades of life. Bryostatin is currently under preclinical in-vivo testing at Mt. Sinai for its potential ability to correct
the lipid transport defect. Bryostatin was shown to correct the defect during earlier In-vitro studies using NPC cell lines.

Exhibit 12. Synapses in Memory Disorders. Synaptic loss is implicated in the majority of neurodegenerative diseases including Alzheimer's
disease (AD), Ischemic Stroke, Fragile X, Traumatic Brain Injury (TBI), Parkinson’s disease (PD), Huntington’s disease (HD), frontotemporal
dementia (FTD), and Alcohol-associated Dementia. Therapeutics which promote synaptic growth, such as Bryostatin or stem cells, have the
potential to treat the effects of these conditions.

24
Source: Sun, et al. (2015).

Bryologs. Bryostatin is a large complex marine-derived compound which requires a large amount of biomass to extract a small amount. Even
with synthetic processes for production, the complexity of the compound makes it less than ideal for manufacturing. Bryologs are synthetic
structural derivatives of Bryostatin which would allow for accelerated synthesis. Stanford researchers have developed a large family of Bryologs
which are licensed to Neurotrope for development. Besides the advantage of improved production, Bryologs offer the ability to manage the IP
lifecycle as the periods of exclusivity could be staggered for different compounds. These Bryologs could advance to clinical development for
additional neurodegenerative diseases such as ischemic stroke, Fragile X Syndrome, traumatic brain injury and AD.

24
Sun, Miao-Kun, et al. “Towards Universal Therapeutics for Memory Disorders.” Trends in Pharmacological Sciences, vol. 36, no. 6, 2015, pp. 384–394.

Maxim Group LLC 12

 Neurotrope, Inc. (NTRP)

MODELING ASSUMPTIONS

1. We assume that Bryostatin launches in the US in 2023 and the EU in 2024.

2. We assume a Population increase of 3% for year for Americans and Europeans over 60 due to on an aging population with longer life
expectancies.
3. We assume that Alzheimer's maintains a prevalence of 10% of the population over 60 in the US and 7.5% in the EU.
4. We assume that only 25% of individuals with AD are diagnosed as having disease.
5. We assume pricing of $10K in the US and $7.5K in the EU with a y/y price increase of 2%.
6. We assume that EU commercialization will occur through a licensing agreement and Neurotrope receives a 15% royalty.
7. A risk adjustment of 50% is applied base on stage of development and risk associated with AD drug development.

Exhibit 13. Bryostatin Alzheimer's Disease Market Model (U.S.)

Bryostatin in Alzheimer's Disease (US) 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E 2026E 2027E 2028E
US Population over 60 52,884,046 54,387,865 55,934,447 57,525,008 59,160,798 60,843,103 62,573,247 64,352,590 66,182,530 68,064,507 70,000,000
Population Increase 3% 3% 3% 3% 3% 3% 3% 3% 3% 3% 3%
Prevalence of Alzheimers (10%) 5,288,405 5,438,787 5,593,445 5,752,501 5,916,080 6,084,310 6,257,325 6,435,259 6,618,253 6,806,451 7,000,000
Diagnosed with Alzheimer's (25%) 1,322,101 1,359,697 1,398,361 1,438,125 1,479,020 1,521,078 1,564,331 1,608,815 1,654,563 1,701,613 1,750,000
Market Share 1.5% 3.0% 4.0% 4.5% 5.0% 5.50%
Total Patients Treated 22,816 46,930 64,353 74,455 85,081 96,250
Cost of Treatment $ 10,000 $ 10,200 $ 10,404 $ 10,612 $ 10,824 $ 11,041
Increase in Cost 2% 2% 2% 2% 2% 2%
Revenue ('000) $ 228,162 $ 478,685 $ 669,524 $ 790,126 $ 920,940 $ 1,062,678
Risk adjustment 50% 50% 50% 50% 50% 50%
Total Revenue ('000) $ 114,081 $ 239,343 $ 334,762 $ 395,063 $ 460,470 $ 531,339
Source: Maxim Estimates

Exhibit 14. Bryostatin Alzheimer's Disease Market Model (EU)

Bryostatin in Alzheimer's Disease (EU) 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E 2026E 2027E 2028E
EU Population over 60 102,489,282 105,403,683 108,400,958 111,483,465 114,653,626 117,913,935 121,266,954 124,715,320 128,261,744 131,909,015 135,660,000
Population Increase 3% 3% 3% 3% 3% 3% 3% 3% 3% 3% 3%
Prevalence of Alzheimers (7.5%) 7,686,696 7,905,276 8,130,072 8,361,260 8,599,022 8,843,545 9,095,022 9,353,649 9,619,631 9,893,176 10,174,500
Diagnosed with Alzheimer's (25%) 1,921,674 1,976,319 2,032,518 2,090,315 2,149,755 2,210,886 2,273,755 2,338,412 2,404,908 2,473,294 2,543,625
Market Penetration 2.0% 4.0% 5.0% 6.0% 6.5%
Total Patients Treated 45,475 93,536 120,245 148,398 165,336
Cost of Treatment $ 7,500 $ 7,650 $ 7,803 $ 7,959 $ 8,118
Increase in Cost 2% 2% 2% 2% 2%

Partner Revenue ('000) $ 341,063 $ 715,554 $ 938,275 $ 1,181,106 $ 1,342,234

Royalty Percentage 15% 15% 15% 15% 15%

Total revenue ('000) $ 51,159 $ 107,333 $ 140,741 $ 177,166 $ 201,335
Risk adjustment 50% 50% 50% 50% 50%
Total Revenue ('000) $ 25,580 $ 53,667 $ 70,371 $ 88,583 $ 100,668
Source: Maxim Estimates

Maxim Group LLC 13

 Neurotrope, Inc. (NTRP)

VALUATION
We model commercialization of Bryostatin for Alzheimer's disease in the US in 2023 and in the EU in 2024. A risk adjustment is applied to the
therapeuctic models based on stage of development and clinical trial risk. A 30% discount is then applied to the Free Cash Flow, Discounted
EPS, and Sum-of-the-Parts Models, which are equally weighted to derive a 12-month price target of $16.

Exhibit 15. Free Cash Flow Model

Average 16

Price Target 14
Year 2018

DCF Valuation Using FCF (mln):

2016 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028
units ('000) 2016A 2017A 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E 2026E 2027E 2028E
EBIT (12,924) (12,615) (14,802) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 330,683 383,664 428,935
Tax Rate 0% 0% 0% 0% 0% 0% 0% 0% 0% 0% 5% 8% 10%
EBIT (1-t) (12,924) (12,615) (14,802) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 314,149 352,971 386,042
CapEx (3) (4) - - - - - - - - - - -
Depreciation 7 4 3 3 6 6 7 7 7 8 8 9 9
Change in NWC
FCF (12,920) (12,615) (14,799) (20,662) (24,614) (25,765) (28,480) 50,536 162,929 263,604 314,157 352,980 386,051

PV of FCF (21,835) (16,399) (14,799) (15,894) (14,565) (11,727) (9,972) 13,611 33,755 42,010 38,512 33,286 28,003

Discount Rate 30%

Long Term Growth Rate 1%

Terminal Cash Flow 1,344,522

Terminal Value YE2027 97,529

NPV 219,749
NPV-Debt
Shares out ('000) 15,480 2028E
NPV Per Share 14
Source: Maxim estimates

Exhibit 16. Discounted-EPS Model

Current Year 2018
Discount Rate and Earnings Multiple Varies, Year is Constant
Year of EPS 2028
Earnings Multiple 10 18.09 5% 10% 15% 20% 25% 30%
Discount Factor 30% Earnings 0 0 0 0 0 0 0
Selected Year EPS 24.94 Multiple 5 76.55 48.07 30.82 20.14 13.39 9.04
NPV 18 10 153.10 96.15 61.64 40.28 26.78 18.09
Source: Maxim estimates 15 229.65 144.22 92.47 60.42 40.17 27.13
20 306.20 192.30 123.29 80.55 53.56 36.18
25 382.75 240.37 154.11 100.69 66.94 45.22
30 459.30 288.45 184.93 120.83 80.33 54.27
35 535.85 336.52 215.76 140.97 93.72 63.31

Exhibit 17. Sum-of-the-Parts Model

Discount Peak Sales
LT Gr Yrs to Mkt % Success Term Value
Neurotrope BioScience Rate (MM's)
Bryostatin Alzheimer's (US) 1% 30% 5 70% $483 $1,666
NPV $12.17
Bryostatin Alzheimer's (EU Royalty) 1% 30% 6 50% $101 $347
NPV $1.39
Pipeline 1% 30% 6 50% $50 $172
NPV $1
Net Margin 60%
MM Shrs OS (2028E) 15
Total $14
Source: Maxim estimates

Maxim Group LLC 14

 Neurotrope, Inc. (NTRP)
Neurotrope Bioscience .: Income Statement ($000)
.: YE December 31 2017A 1Q18A 2Q18E 3Q18E 4Q18E 2018E 2019E 2020E 2021E 2022E 2023E 2024E 2025E 2026E 2027E 2028E
Revenue:

Bryostatin in Severe Alzheimer's Disease (US) 114,081 239,343 334,762 395,063 437,447 483,035

Net revenue - - - - - - - - - - 114,081 239,343 334,762 395,063 437,447 483,035

Collaborative revenue: -
-
Bryostatin in Alzheimer's (EU Royalty) - - - - - - - - - - - 25,580 53,667 70,371 88,583 100,668
- - - - - - - - - - - -
Total Collaborative Revenue - - - - - - - - - - - 25,580 53,667 70,371 88,583 100,668
Total Revenue - - - - - - - - - - 114,081 264,922 388,429 465,434 526,029 583,703
Expenses:
Costs of Goods Sold - - - - - - - - - - 34,224 71,803 93,733 102,716 109,362 120,759
%COGS 30% 30% 28% 26% 25% 25%
Research and Development 4,549 89 1,560 1,690 1,755 6,500 12,000 15,600 16,380 16,708 17,042 17,383 17,730 18,085 18,447 18,815
%R&D
Selling, General and Administrative 5,456 1,122 1,384 1,500 1,557 5,768 6,056 6,359 6,677 9,011 9,461 9,935 10,431 10,953 11,500 12,075
%SG&A
-
Research and Development, Related Party 215 113
General and Administrative, Related Party 39 13
Stock Based Compensation, Related Party 155 113
Stock Based Compensation 2,288 563 614 665 691 2,558 2,609 2,661 2,714 2,769 2,824 2,881 2,938 2,997 3,057 3,118
Total Expenses 12,702 2,013 3,558 3,855 4,003 14,826 20,665 24,620 25,771 28,487 63,552 102,000 124,833 134,751 142,365 154,768
Operating Income (Loss) (12,702) (2,013) (3,558) (3,855) (4,003) (14,826) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 330,683 383,664 428,935
- - - - - - - - - - - -
- - - - - - - - - - - -
Loss on Disposal of Fixed Assets (34) - - - - - - - - - - -
Gain on Lease settlement 54 - - - - - - - - - - -
Interest income 68 24 24 - - - - - - - - - -
- - - - - - - - - - - -
Total Other Income 87 24 - - - 24 - - - - - - - - - -
Pretax Income (12,615) (1,989) (3,558) (3,855) (4,003) (14,802) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 330,683 383,664 428,935

Taxes on income - - - - - - - - - - - - - 16,534 30,693 42,894

Tax Rate 5% 8% 10%
GAAP Net Income (Loss) (12,615) (1,989) (3,558) (3,855) (4,003) (14,802) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 314,149 352,971 386,042

Total comprehensive loss (12,615) (1,989) (3,558) (3,855) (4,003) (14,802) (20,665) (24,620) (25,771) (28,487) 50,529 162,922 263,596 314,149 352,971 386,042

GAAP-EPS (1.64) (0.25) (0.45) (0.49) (0.51) (1.87) (1.89) (1.89) (1.71) (1.88) 3.33 10.69 17.23 20.46 22.89 24.94
GAAP-EPS (Dil) (1.64) (0.25) (0.45) (0.49) (0.51) (1.87) (1.89) (1.89) (1.71) (1.88) 3.33 10.69 17.23 20.46 22.89 24.94
Wgtd Avg Shrs (Bas) - '000s 7,709 7,903 7,910 7,918 7,926 7,914 10,951 12,995 15,053 15,113 15,173 15,234 15,295 15,356 15,418 15,480
Wgtd Avg Shrs (Dil) - '000s 7,709 7,903 7,910 7,918 7,926 7,914 10,951 12,995 15,053 15,113 15,173 15,234 15,295 15,356 15,418 15,480
Source: Company reports and Maxim

Maxim Group LLC 15

 Neurotrope, Inc. (NTRP)

DISCLOSURES

Neurotrope, Inc. Rating History as of 05/15/2018

powered by: BlueMatrix

$35
$30
$25
$20
$15
$10
$5
$0
Jul 15 Oct 15 Jan 16 Apr 16 Jul 16 Oct 16 Jan 17 Apr 17 Jul 17 Oct 17 Jan 18 Apr 18

Closing Price Target Price

Maxim Group LLC Ratings Distribution As of: 05/15/18

% of Rating for which Firm
% of Coverage Provided Banking Services
Universe with Rating in the Last 12 months
Fundamental metrics and/or identifiable catalysts exist such that we
Buy 79% 36%
expect the stock to outperform its relevant index over the next 12 months.
Fundamental metrics are currently at, or approaching, industry averages.
Hold Therefore, we expect this stock to neither outperform nor underperform 19% 19%
its relevant index over the next 12 months.
Fundamental metrics and/or identifiable catalysts exist such that we
Sell expect the stock to underperform its relevant index over the next 12 2% 25%
months.
*See valuation section for company specific relevant indices

I, Caroline Palomeque, attest that the views expressed in this research report accurately reflect my personal views about the subject security and
issuer. Furthermore, no part of my compensation was, is, or will be directly or indirectly related to the specific recommendation or views expressed
in this research report.

I, Jason McCarthy, Ph.D., attest that the views expressed in this research report accurately reflect my personal views about the subject security and
issuer. Furthermore, no part of my compensation was, is, or will be directly or indirectly related to the specific recommendation or views expressed
in this research report.

The research analyst(s) primarily responsible for the preparation of this research report have received compensation based upon various factors,
including the firm’s total revenues, a portion of which is generated by investment banking activities.

Maxim Group makes a market in Neurotrope, Inc.

Maxim Group expects to receive or intends to seek compensation for investment banking services from Neurotrope, Inc. in the next
3 months.

NTRP: For Neurotrope we use the BTK (Biotechnology Index) as the relevant index
Valuation Methods
NTRP: We model bryostatin commercialization in the US in 2023 and the EU in 2024. A 50% risk adjustment is applied to the therapeutic models
for the US and the EU based on stage of development and time to commercialization. A 30% discount (vs 15% for an emerging growth company

Maxim Group LLC 16

 Neurotrope, Inc. (NTRP)
and 10% for a well-established company) is applied to the Free Cash Flow, Discounted EPS, and Sum-of-the-Parts Models, which are equally
weighted to derive a 12-month price target.
Price Target and Investment Risks
NTRP: Aside from general market and other economic risks, risks particular to our price target and rating for Neurotrope include: (1) the regulatory
and clinical risk associated with product development, (2); the ability to access additional capital and the very high likelihood that company will
need to raise additional capital, the terms of which may not be favorable based on the outcome of clinical data and other factors; (3) the rate
and degree of progress of product development; (4) the rate of regulatory approval and timelines to potential commercialization of products. (5)
Changes to reimbursement levels for future marketed tests and panels. (6) the level of success achieved in clinical trials; (7) the requirements
for marketing authorization from regulatory bodies in the United States and other countries; (8) the liquidity and market volatility of the company’s
equity securities; (9) regulatory and manufacturing requirements and uncertainties; (10) Product and technology developments by competitors; (11)
Inability, if product(s) is approved to gain adequate market share; (12) Potential to continue to operate is an “ongoing concern” as per the company’s
auditors based on several factors including the risk that if the company cannot raise sufficient capital to execute the business plan the company
may have to liquidate and investors lose their investment; which could negatively impact the company.

RISK RATINGS

Risk ratings take into account both fundamental criteria and price volatility.
Speculative – Fundamental Criteria: This is a risk rating assigned to early-stage companies with minimal to no revenues, lack of earnings, balance
sheet concerns, and/or a short operating history. Accordingly, fundamental risk is expected to be significantly above the industry. Price Volatility:
Because of the inherent fundamental criteria of the companies falling within this risk category, the price volatility is expected to be significant with the
possibility that the investment could eventually be worthless. Speculative stocks may not be suitable for a significant class of individual investors.
High – Fundamental Criteria: This is a risk rating assigned to companies having below-average revenue and earnings visibility, negative cash
flow, and low market cap or public float. Accordingly, fundamental risk is expected to be above the industry. Price Volatility: The price volatility of
companies falling within this category is expected to be above the industry. High-risk stocks may not be suitable for a significant class of individual
investors.
Medium – Fundamental Criteria: This is a risk rating assigned to companies that may have average revenue and earnings visibility, positive cash
flow, and is fairly liquid. Accordingly, both price volatility and fundamental risk are expected to approximate the industry average.
Low – Fundamental Criteria: This is a risk rating assigned to companies that may have above-average revenue and earnings visibility, positive
cash flow, and is fairly liquid. Accordingly, both price volatility and fundamental risk are expected to be below the industry.

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Past performance should not be taken as an indication or guarantee of future performance, and no representation or warranty, express or implied, is
made regarding future performance. Information, opinions and estimates contained in this report reflect a judgment at its original date of publication
by Maxim and are subject to change without notice. The price, value of and income from any of the securities mentioned in this report can fall as
well as rise. The value of securities is subject to exchange rate fluctuation that may have a positive or adverse effect on the price or income of such
securities. Investors in securities such as ADRs, the values of which are influenced by currency volatility, effectively assume this risk. Securities
recommended, offered or sold by Maxim: (1) are not insured by the Federal Deposit Insurance Company; (2) are not deposits or other obligations
of any insured depository institution; and (3) are subject to investment risks, including the possible loss of principal invested. Indeed, in the case
of some investments, the potential losses may exceed the amount of initial investment and, in such circumstances, you may be required to pay
more money to support these losses.

ADDITIONAL INFORMATION IS AVAILABLE UPON REQUEST

Maxim Group LLC 17

 Corporate Headquarters
The Chrysler Building
405 Lexington Ave., 2nd FL
New York, NY 10174
Tel: 212-895-3500

Capital Markets/Syndicate: 212-895-3695 Global Equity Trading: 212-895-3623

Corporate Finance: 212-895-3811
Corporate Services: 212-895-3631
Equity/Options Trading: 212-895-3790
Equity Research: 212-895-3736
Fixed Income Trading: 212-895-3875
Institutional Sales: 212-895-3873
Institutional Sales Trading: 212-895-3873
Port./Transition Trading: 212-895-3567
Prime Brokerage: 212-895-3723
Wealth Management: 212-895-3624

Woodbury, Long Island Red Bank, New Jersey

20 Crossways Park Drive North 246 Maple Avenue
Suite 304 Red Bank, NJ 07701
Woodbury, NY 11797 Tel: 732-784-1900
Tel: 516-393-8300

West Palm Beach, Florida San Rafael, California

105 South Narcissus Avenue 4040 Civic Center Drive
Suite 222 Suite 200
West Palm Beach, FL 33401 San Rafael, CA 94903
Tel: 561-508-4433 Tel: 212-895-3670