Captons lack features necessary for activity in the relevant pathways, however. Upon oral administration, captons increase cysteine levels in the blood. Brain levels follow in kind. Increases in cysteine at the expense of cystine in the periphery obviates the absence of cystine transport across the BBB as well as the dependence of brain cells on cystine-glutamate exchange to support intracellular sulfur amino acid pools. Captons, like cysteine, have functionality suitable for the mitigation of oxidative stress, redox-dependent protein aggregation and metal-ion toxicity. Reactive-oxygen species (ROS), for example, react with sulfur-containing molecules, destroying the former and oxidizing the latter. Capton oxidation, specifically, imparts potent neurological agency absent in the administered form of the drug.
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Creation of Captons
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Three phases of the Alzheimer disease. 1. Healthy neuron. 2. Neuron with aggregation of amyloid (yellow). 3. Dead neuron being digested by microglia cells (red).
The sum of activities inherent to captons, in their reduced and oxidized forms, suggest that these compounds might be useful for the treatment of a number of pathologies common among neurological disorders. These include traumatic brain injury (TBI), stroke, epilepsy, amyotrophic lateral sclerosis (ALS), chronic traumatic encephalopathy (CTE), Parkinson's, Alzheimer's and Huntington's diseases. Mercaptor intends to test this proposition.
Protein aggregation is a hallmark of neurodegeneration and part of the neuronal death spiral. Aggregation is a direct result of ROS and an important contributor to the transition from TBI to CTE and ALS. Captons augment free thiol levels in the brain and lower ROS levels at the site of damage, effects anticipated to inhibit aggregation.
Molecules like captons are oxidized in reactions which simultaneously neutralize ROS. Capton oxidation generates products that potentiate inhibitory neurotransmission pathways or, alternatively, inhibit hyperexcitation, depending on the capton chosen. These neurologically active oxidation products are normally excluded by the blood-brain barrier. Oxidation will be favored in damaged areas, where ROS levels are elevated, potentially avoiding nonselective, and unnecessary, global reduction of brain function.
Capton technology was discovered by scientists at Raptor Pharmaceuticals in the late-summer of 2016. On September 12 of that year, it was announced that Raptor, including all of its intellectual property, would soon be acquired by Horizon Pharma, a marketer of approved drugs with no interest in early-stage drug development.
Raptor scientists behind the capton discovery moved to incorporate a new business entity, Mercaptor Discoveries, on September 13, 2016. Mercaptor was created to independently develop captons, if necessary; it was.
Negotiations with Horizon in late 2016 and early 2017 allowed Mercaptor to secure a global, exclusive license to all intellectual property relating to capton technology from the now-defunct Raptor. For all intents and purposes, the license returned the science to its inventors. The group responsible for capton work at Raptor resumed their efforts at Mercaptor in March of 2017, seeking to fully realize on the potential of capton agents as pharmacological therapeutics for brain injury and neurodegeneration.
Mercaptor has developed new chemical entities intended to relieve suffering in both animals and man. Meaningful pharmacological correction of brain dysfunction is the objective. Our drug candidates are called “captons”. Captons are small molecules, selectively reactive and metabolically stable. They are also orally bioavailable and cross the blood-brain barrier. Captons are structurally-similar to a number of known neuroactive agents. These include GABA modulators, cannabinoids, gabapentinoids (which reduce calcium import) and glutamate receptor blockers.