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WHO WE ARE

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

Our experience and passion for novel drug therapies have enabled us to develop a pipeline that includes various treatment approaches for serious and difficult-to-treat diseases such as Alzheimer’s Disease, Fragile X Syndrome and Niemann-Pick Type C.

SCIENCE

Synaptogenix has targeted Bryostatin-1 due to its high potential and multi-modal efficacy: through protein kinase C (PKCϵ) activation, Bryostatin-1 stimulates synaptic growth factors, amyloid-β degrading enzymes, as well as prevents Tau transformation into neurofibrillary tangles.

Studies have demonstrated that PKCϵ plays a pivotal role in learning and memory. Bryostatin, a small molecule, penetrates the blood-brain barrier and activates PKCϵ, resulting in improved synaptic function, new synapse formation, repair of damaged synapses, and prevention of neuronal death. Synaptogenix’s preclinical work demonstrates improved memory and learning in multiple Alzheimer’s mouse models and several other animal models.

ALZHEIMER’S DISEASE

Alzheimer’s disease is the most common form of dementia, accounting for 60%-80% of all cases. Synaptogenix has conducted the first placebo-controlled, Phase 2 trial of a protein kinase C epsilon (PKCɛ) activator for the treatment of Alzheimer’s, which in preclinical studies induced the growth of new synapses and prevented neuronal death. Recent clinical trial data showed sustained increase in Severe Impairment Battery measures and improvement in cognition, suggesting the drug may treat the progression of AD, rather than just symptoms. A confirmatory trial will commence in 2018.

FRAGILE X SYNDROME

Fragile X syndrome is a genetic disorder that causes developmental delays, intellectual and learning disabilities, anxiety, and autism spectrum disorders. FXS affects 135,000 in the U.S. alone. Bryostatin-1 for Fragile X has been designated as an orphan drug, and in animal models, was shown to restore synaptic networks, rectify memory deficits, and reverse biochemical abnormalities. Synaptogenix preclinical data, in a collaboration with the FRAXA Research Foundation, showed that Bryostatin-1 significantly improves autism spectrum abnormalities. Synaptogenix plans to initiate clinical testing of FXS patients in 2018.

NIEMANN PICK TYPE C

Niemann Pick Type C is both a debilitating and lethal disease, affecting about 35,000 children per year. Synaptogenix is working with world renowned experts at the Icahn School of Medicine, Mt. Sinai to develop its lead compound, Bryostatin-1, as a potential treatment for the excessive accumulation of cholesterol and other lipids in the viscera and brain resulting in cell death and to neuologic symptoms, including difficulty in swallowing and speaking, loss of coordination, seizures, and progressive dementia. There is no FDA approved treatment for Niemann-Pick Type C.

LINKS TO PUBLICATIONS
Key PublicationsDownload
AAIC Abstract July 26, 2021
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

PIPELINE

Synaptogenix is building a sustainable pipeline of treatments in major areas of unmet need.

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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CONTACT US

CORPORATE ADDRESS

New York Office

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

INVESTOR RELATIONS
Neil Cataldi

E-mail: ncataldi@synaptogen.com

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