Pioneering Science
Intracellular Magnesium in Synaptic Terminal:
Critical Regulator of Synaptic Density and Plasticity
Neurocentria discovered-
Elevation of intracellular magnesium is critical for prevention of synapse loss via:
Improvement of mitochondria function and elevation of
ATP production
Prevention and attenuation of neuroinflammation via
normalization of
NF-kB signaling
Reduction of probability of
neurotransmitter release, venting synaptic hyperexcitability
Reduction of Amyloid β deposition
Novel Mechanism of Action - New class of therapies
Unique Products Increasing Synapse Density and Plasticity for Treating CNS Disorders
•Small molecule: L-Threonate Magnesium Salt (L-TAMS, NRCT-101)
•Elevates Mg2+ and L-Threonate in the CSF
•Only known compound that effectively increases Mg2+ in the synaptic terminal
•Increases synaptic density and plasticity
•Improves cognition and emotional regulation
Pioneering Clinical Programs
ADHD
The Burden:
• ~17 million people in the US have ADHD
• Only 10% are treated
• Heavy burden on patients and families;
ADHD affects performance and mood, and causes
difficulties in workplace environments and
challenges with family life
Current treatments:
• Do not improve quality of life and executive function
• Stimulants – impose significant side-effects
Non-stimulants – insufficient efficacy
• Act on monoaminergic synapses, a target developed
decades ago
Neurocentria's Path Forward:
• Pathophysiology of ADHD involves dysfunction of
glutamatergic synapses in the prefrontal cortex (PFC)
• NRCT-101SR improves glutamatergic synapse function in
PFC to address ADHD (novel drug class)
No novel treatments are under investigation
Depression
The Burden:
• 13% of adults in the US (34M) are treated
with antidepressants
• Heavy burden on patients and their families: persistent
sadness, loss of interest, difficulties with sleep, decreased
energy level, cognitive impairment and suicidal thoughts
• Cause: currently, the leading hypothesis is that imbalance
of monoamines such as serotonin is the cause for
depression, hence SSRIs are massively prescribed.
This hypothesis has been recently questioned.
Neurocentria's Path Forward:
• Recent studies suggest that the pathophysiology of
MDD involves synapse loss in the prefrontal cortex (PFC).
Our research suggests that the synapse loss during
depression is caused by reduction of
intracellular magnesium.
• The API of NRCT-101SR is an endogenous molecule,
naturally present in the brain and regulates
magnesium in synapses
• NRCT-101SR increases glutamatergic synapse density and
improves synaptic plasticity in the PFC to normalize
emotional regulation and address cognitive dysfunction
(novel drug class)
Alzheimer's Disease
The Burden:
• ~30 million people worldwide and ~6 million in the US
suffer from AD, expected to double by 2050
• Heavy burden on patients, families, care givers and the
health system
• No cure available; the established drugs address
symptoms only
• Recently approved drugs aiming to treat the pathology
have only modest effects and bear risk for
serious side-effects
• High failure rate of AD drug development suggests that
AD may not be treatable at advanced stages
Neurocentria's Path Forward:
• Synapse loss is hallmark of AD; NRCT-101SR
prevents synapse loss
• Clinical data shows NRCT-101SR improves cognition
and mood in older adults and those with early AD
• Best therapeutic approach is prevention or early treatment;
NRCT-101SR has shown an excellent safety profile,
making it a good candidate for preventional treatment
Pipeline
