Copyright 2017 © Mercaptor Discoveries

Research activities

​Mercaptor has a number of capton molecules under development. Initial studies are intended to test these molecules in seizure and traumatic brain injury (TBI).  Additional studies in stroke and amyotrophic lateral sclerosis are planned. Other indications anticipated to benefit from capton technology include: chronic traumatic encephalopathy (CTE), alcohol withdrawal, chemobrain, Alzheimer’s disease, Parkinson’s disease, and epilepsy in animal companions.

Mercaptor develops drugs to treat damage, dysfunction and degeneration in the brain. Our molecules, called captons, are designed to reduce acute and progressive pathologies initiated by neuronal injury. Captons combine three complementary neuroprotective activities into a single small-molecule agent. 

The approach is investigational and without precedent.  It also promises significant improvements in the performance of a variety of drugs. If capton dosage is metered and delimited by the pathogenic species it is designed to treat, interference in healthy tissue function will be minimized.


A seizure is characterized by abnormally-synchronous electrophysiological activity occurring across large areas of the brain. Seizures engender significant energy expenditure to restore ion imbalances in neurons subject to extreme work-loads.  Consequent ATP depletion upregulates mitochondrial activity.  These effects are common to seizures elicited by congenital, structural, environmental and chemical-based stimuli, including cholinesterase inhibition.  Extended intervals of mitochondrial activation result in persistently elevated levels of reactive-oxygen species (ROS), overwhelming endogenous antioxidant capacity.  Loss-of-control over ion concentrations inside and outside the cell leads to calcium toxicity in the endoplasmic reticulum (ER) and mitochondria.  Cell death follows.  Mercaptor has designed captons to normalize both ROS and neuronal hyperexcitation.  Captons also are uniquely suitable to minimize damage left in the wake of seizure events.



Traumatic Brain Injury (TBI)

TBI is characterized by an acute injury to brain tissue, often resulting from blunt or torqueing forces that impact, twist and stretch neurons, often through their vulnerable axonal processes. These effects can lead to damage by direct physical disruption of cell membranes. Among the many species released into the extracellular space when neuronal integrity is breached, glutamate is particularly pathogenic.  Excess glutamate causes persistent opening of glutamate-gated ion channels, hyperexcitation and loss of ion gradient control. These events and their sequelae are commonly defined as glutamate excitotoxicity.  The delicate balance between glutamate (excitatory) and GABA (inhibitory) neurotransmission becomes skewed by the damage.  Continuous excitation by glutamate obliges a neuron to consume significantly more energy to maintain membrane voltage potentials. Energy depletion is countered by increased mitochondrial activity and its consequence, elevated levels of ROS.  Elevated intracellular calcium adds additional strain on mitochondria and the ER, which sacrificially sequester calcium in favor of the cytoplasm. Mitochondrial failure from excessive ROS and calcium levels leads to apoptosis of the neuron, releasing more glutamate into the extracellular space and perpetuation of the damage.  This cataclysm of runaway neurotransmission has been termed a glutamate storm. Propagation of damage from the initial insult may continue for years, turning acute injury into progressive neurodegeneration.  As previously noted, captons represent potentially valuable tools in efforts to minimize the effects of TBI.


Blood-vessel occlusion may cause areas of the brain to become hypoxic.  Responding homeostatically, affected cells downregulate antioxidant systems. Damage can be significant if the primary occlusion is removed, allowing oxygen-rich blood to return to the area.  Such an event is called reperfusion. Reperfusion of neurons with down-regulated antioxidant reserves causes oxidative stress.  Neurons that die during reperfusion then release their contents into the extracellular space.  Pathogenic factors include glutamate, which leads to excitotoxicity and additional neuronal death.

Amyotrophic lateral sclerosis (ALS)

Unlike TBI and stroke, amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease targeting motor neurons. ALS is linked to a few well-defined genetic lesions, but is predominantly sporadic in nature, likely triggered by repetitive insult of injury.  Injury to some neurons leads to glutamatergic excitotoxicity, with glutamate hyperexcitation, ROS, calcium dyshomeostasis and redox-dependent protein aggregates as common features.  Captons to the rescue!

​​​​​​​​​​​​​​​ ​"We understand the importance that

luck plays in scientific

discovery. For that reason we leave ourselves open to unconventional hypothesis."

 -Todd, CSO and Co-founder

​“We have spent 11 years following our data, and it has led us to this discovery. We ask questions based on the data and follow the evidence wherever it leads us.”

- Sara, CEO and Co-founder

Depiction of neuronal activity inside brain. When injured by a degenerative disease or blunt trauma, this firing goes out of control. Mainly triggered by a glutamate storm causing further damage to neighboring cells, leading to progression of the disease.