Synaptogenix |
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Pioneers of
Restorative
Therapeutics

Executive Summary

OUR MISSION

Discovering restorative, novel therapeutics for patients with life altering neurodegenerative diseases and developmental disorders.

 

  • Clinically meaningful restoration of cognitive function
  • Regeneration of cerebral connections
  • Two Phase II pilot study trials completed
  • Biomarkers track cognitive improvement
  • Extensive toxicity safety profile
  • Partnerships with National Cancer Institute, National Institute of Health, and National Institute of Aging
WHO WE ARE
  • Management team has 30+ years of experience with the development of Bryostatin and Platform Drugs
  • Pilot Phase II studies met pre-specified endpoints
  • Greater than $200M of funding from the Blanchette Rockefeller Neurosciences Institute and the National Institutes of Health (NIH)
  • Successful translation of decades of pre-clinical work to the clinic
  • Working on indications:
    • Alzheimer’s disease
    • Fragile X Syndrome / Autism
    • Multiple Sclerosis
    • Parkinson’s Disease
    • Traumatic Brain Injury
    • Stroke
What are Synapses?
(And Why Are They So Important?)
  • Synapses are tiny connectors that permit a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron. Trillions of synapses form networks in the brain.
  • When abundant and working correctly, synapses allow neurons to communicate with each other effectively.This means our nervous system is performing well and with sharp cognitive functioning (i.e. reasoning, attention, memory, and language).
  • Fewer or defective synapses means less connectivity in the brain, a weaker nervous system, and ultimately impaired cognition.1

1. Terry RD, Masliah E, Salmon DP, et al. Synapse Loss is the Major Correlate of Cognitive Impairment Ann Neurol. 1991 Oct; 30 (4): 572-80.

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Synaptic loss is the major pathologic correlate of Alzheimer’s disease and other dementias, and has been shown to occur in very early stages of such diseases.2

2. Scheff SW, Price DA. Alzheimer’s disease-related alterations in synaptic density: neocortex and hippocampus. J Alzheimers Dis. 2006;9 (3 Suppl): 101-15.

Bryostatin: Promotes Neuronal Health &
Synaptic Regeneration

Treated Without Bryostatin

Treated With Bryostatin

*Image courtesy of Daniel L. Alkon, MD.

LINKS TO PUBLICATIONS
Key PublicationsDownload
Activation of Protein Kinase C Isozymes for the Treatment of Dementias
Pharmacology of protein kinase C activators: Cognition-enhancing and antidementic therapeutics
Miao-Kun Sun, Daniel L. Alkon
PKC ε Activation Prevents Synaptic Loss, Aβ Elevation, and Cognitive Deficits in Alzheimer’s Disease Transgenic Mice
Jarin Hongpaisan, Miao-Kun Sun, and Daniel L. Alkon
PKC signaling deficits: a mechanistic hypothesis for the origins of Alzheimer’s disease
Daniel L. Alkon, Miao-Kun Sun and Thomas J. Nelson
Neuroprotective versus tumorigenic protein kinase C activators
T.J. Nelson and D.L. Alkon
PKC signaling deficits: a mechanistic hypothesis for the origins of Alzheimer’s disease
Daniel L. Alkon, Miao-Kun Sun and Thomas J. Nelson
Adduct formation in liquid chromatography-triple quadrupole mass spectrometric measurement of bryostatin 1
Thomas J. Nelson, Abhik Sen, Daniel L. Alkon, Miao-Kun Sun
PKCε Promotes HuD-Mediated Neprilysin mRNA Stability and Enhances Neprilysin-Induced Ab Degradation in Brain Neurons
Chol Seung Lim, Daniel L. Alkon
Bryostatin-1 Restores Hippocampal Synapses and Spatial Learning and Memory in Adult Fragile X Mice
Miao-Kun Sun, Jarin Hongpaisan, Chol Seung Lim, and Daniel L. Alkon
PKC activation during training restores mushroom spine synapses and memory in the aged rat
Jarin Hongpaisan, Changqing Xu, Abhik Sen, Thomas J. Nelson, Daniel L. Alkon
Synergistic effects of chronic bryostatin-1 and α-tocopherol on spatial learning and memory in rats
Miao-Kun Sun, Daniel L. Alkon
Postischemic PKC activation rescues retrograde and anterograde long-term memory
Miao-Kun Sun, Jarin Hongpaisan, and Daniel L. Alkon
Neuroprotective versus tumorigenic protein kinase C activators
T.J. Nelson and D.L. Alkon
Reduction of β-Amyloid Levels by Novel Protein Kinase Cε Activators
Thomas J. Nelson, Changhai Cui, Yuan Luo, and Daniel L. Alkon
A cellular model of Alzheimer’s disease therapeutic efficacy: PKC activation reverses Aβ-induced biomarker abnormality on cultured fibroblasts
Tapan K. Khana, Thomas J. Nelson, Vishal A. Verma, Paul A. Wender, and Daniel L. Alkon
Synergistic effects of chronic bryostatin-1 and α-tocopherol on spatial learning and memory in rats
Miao-Kun Sun, Daniel L. Alkon
Analysis of long-term cognitive-enhancing effects of bryostatin-1 on the rabbit (Oryctolagus cuniculus) nictitating membrane response
Desheng Wang, Deya S. Darwish, Bernard G. Schreurs, and Daniel L. Alkon
PKC signaling deficits: a mechanistic hypothesis for the origins of Alzheimer’s disease
Daniel L. Alkon, Miao-Kun Sun and Thomas J. Nelson
Protein synthesis required for long-term memory is induced by PKC activation on days before associative learning
Daniel L. Alkon, Herman Epstein, Alan Kuzirian, M. Catherine Bennett, and Thomas J. Nelson
Therapeutic effects of PKC activators in Alzheimer’s disease transgenic mice
Discrimination Learning Alters the Distribution of Protein Kinase C in the Hippocampus of Rats
James L. Olds, Stephanie Golski, Donna L. McPhie, David OKon, Mot-timer Mishkin and Daniel L. Alkonl
Classical conditioning induces long-term translocation of protein kinase C in rabbit hippocampal CAl cells (memory storage/membrane-associated protein kinase)
BARRY BANK, ANN DEWEER, ALAN M. KuZIRIAN, HOWARD RASMUSSEN, AND DANIEL L. ALKON
A cellular model of Alzheimer's disease therapeutic efficacy: PKC activation reverses
Aβ-induced biomarker abnormality on cultured fibroblasts
Tapan K. Khan, Thomas J. Nelson, Vishal A. Verma, Paul A. Wender, Daniel L. Alkon
The maddening saga of how an Alzheimer’s ‘cabal’ thwarted progress toward a cure for decades
PKC epsilon Promotes Synaptogenesis through Membrane Accumulation of the Postsynaptic Density Protein PSD-95 J Biol Chem. 5;291(32):16462-76, 2016 Abhik Sen, Jarin Hongpaisan, Desheng Wang, Thomas J. Nelson and Daniel L. Alkon
Rescue of Synaptic Phenotypes and Spatial Memory in Young Fragile X Mice. J. Pharmacol. Exp. Ther. 357: 300-310, 2016Miao-Kun Sun, Jarin Hongpaisan, and Daniel L. Alkon
ApoE4 and Aβ Oligomers Reduce BDNF Expression via HDAC Nuclear Translocation Neuroscience 35(19): 7538-7551; doi: 10.1523 /JNEUROSCI. 0260-15.2015 Abhik Sen, Thomas J. Nelson and Daniel L. Alkon
Apolipoprotein E3 (ApoE3) but Not ApoE4 Protects against Synaptic Loss through Increased Expression of Protein Kinase Cε. J Biol Chem 287(19), 15947-15948, 2012. Sen A, Alkon DL, Nelson TJ
PKCε Activation Prevents Synaptic Loss, Aβ Elevation, and Cognitive Deficits in Alzheimer's Disease Transgenic Mice, Journal of Neuroscience, 31(2):630–643, 2011. Hongpaisan, J., Sun, MK, Alkon DL
Postischemic PKC activation rescues retrograde and anterograde long-term memory. (Proc Nat. Acad. Sci. USA) 106 (34): 14676–14680, 2009. Sun, MK, Hongpaisan, J, Alkon, DL
A structural basis for enhancement of long-term associative memory in single dendritic spines regulated by PKC. Proc Natl Acad Sci USA 104 (49): 19571-19576, 2007. Hongpaisan J, and Alkon DL
Towards universal therapeutics for memory disorders. Trends in Pharmacological Sciences, June 2015, Vol. 36, No. 6. Miao-Kun Sun, Thomas J. Nelson, and Daniel L. Alkon
PKC activator therapeutic for mild traumatic brain injury in mice. Neurobiology of Disease 41 (2011) 329–337. Ofer Zohar, Rotem Lavy, Xiaomei Zi, Thomas J. Nelson, Jarin Hongpaisan, Chaim G. Pick, D.L. Alkon
Program Goals Achieved:
NIH Supported Phase II Clinical Trial Enhancements

“Namenda is now an exclusion criteria”

Bryostatin works through NMDA Receptors

NIH Grant Supported Full Trial;


Six months and 2x doses, to allow for full Bryostatin effect, Eliminate Placebo effect

We are now using patients who have moderate and moderately severe AD patients


Eliminates Variability with Most Severe AD patients

TEAM

Synaptogenix is led by an experienced team with deep expertise in neurodegenerative disorders and successful track records in both drug discovery and development.

Alan Tuchman, M.D.
Chief Executive Officer

Daniel Alkon, M.D.
President & Chief Science Officer

Robert Weinstein
Chief Financial Officer

Elaine Grenier
Executive Director, Clinical Ops

Alan Tuchman, M.D.

Chief Executive Officer & CMO

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Daniel Alkon, M.D.

President & Chief Science Officer

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Joshua Silverman

Chairman

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William Singer

Vice Chairman

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Jonathan Schechter.

Director

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Bruce Bernstein

Director

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George Perry, Ph.D.

Director

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Martin R. Farlow

(Chairman) MS

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Paul Coleman, PhD

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Daniel F. Hanley Jr. MD

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Marwan Sabbagh, MD

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Lee Jen Wei, PhD

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Summary

Synaptogenix is a clinical-stage biotech company leveraging Bryostatin-1 and its analogues to discover and develop targeted, novel regenerative therapeutics for neurodegenerative diseases and developmental disorders.

Our experience and passion for novel drug therapies have enabled us to develop a pipeline that includes synaptogenic treatment approaches for serious and difficult-to-treat diseases such as Alzheimer’s disease, Fragile X Syndrome, MS, Parkinsons, Traumatic Brain Injury, Stroke, and Autism Spectrum Disorders.

CONTACT US

Investor Relations
Brett Maas, Hayden IR
(646)-536-7331
Brett@Haydenir.com

CONTACT US

CORPORATE ADDRESS

New York Office

1185 Avenue of the Americas, 3rd Floor
New York, NY 10036
(973) 242-0005

INVESTOR RELATIONS
Brett Maas

E-mail: Brett@Haydenir.com

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