Headquartered in Austin, Texas, Ninnion is a pharmaceutical company on a mission to build a fully integrated pharmaceutical psychedelics eco-system leveraging the latest AI drug discovery, development, cGMP manufacturing, commercialization, patient clinics and specialty pharmacy distribution network designed for the next frontier of psychedelic medicine. Focused on the payer-reimbursed market, Ninnion has begun developing a pipeline of next generation psychedelic therapies with a clinical focus on brain injury, chronic pain, inflammation, and addiction disorders. To learn more, visit www.ninnion.com.
Ninnion has begun development of NIN-S119, our proprietary, short-acting substituted tryptamine to treat patients recovering from ischemic stroke. NIN-S119 will be used in conjunction with physical/occupational therapy to potentiate the ability to form new neuronal connections (synapses) and strengthen the connectivity of remaining brain cells engaged during therapy. The ability of the brain to make physical and functional changes is called neuroplasticity.
Neuroplasticity is produced through the processes of neurogenesis (the generation of new brain cells) and synaptogenesis (the formation of new functional connections between brain cells).
NIN-S119 is postulated to enhance stroke recovery through inducing neuroplasticity. This means it induces the formation of new connections between nerve cells, in essence “re-wiring” the brain. Such brain “re-wiring” could prove beneficial for stroke recovery by creating new brain circuitry that could restore function to brain areas damaged by stroke.
NIN-S119 produces its neuroplastic effects by stimulating the serotonin 2A (5-HT2A) receptor. Numerous studies have shown that psychedelic drugs that stimulate the 5-HT2A receptor not only dramatically increase synaptogenesis, but also stimulate neurogenic activity, resulting in increased connectivity between brain cells and the growth of new brain cells.
Stimulation of the 5-HT2A receptor leads to activation of biochemical processes leading to the synthesis and release of Brain-Derived Neurotrophic Factor (BDNF). BDNF is a natural growth factor that stimulates neurogenesis and synaptogenesis. In this manner, NIN-S119 stimulates the brain’s innate ability to heal.
While drugs that produce serotonin 2A receptor agonism can induce “psychedelic” mental states (e.g. LSD, mescaline, DMT, etc.), the doses required to stimulate neuroplasticity are much lower than those required to produce “psychedelic” effects, potentially enabling the use of NIN-S119 in stroke recovery without these psychedelic effects. The lack of psychedelic effects would make NIN-S119 much easier to use clinically, reducing the time and effort of clinical staff, opening the potential for administration by the patient at home
NIN-S119 would be the first drug of its kind in the treatment of stroke, potentially making it eligible for Breakthrough Therapy designation by the FDA, a designation that can accelerate the development timeline. IND-enabling toxicology will be completed and initial clinical trials initiated in 1Q23.