Delix Therapeutics recently published results of a study on the mechanism that causes psychoplastogens and serotonin to differentially activate the 5-HT2A receptor.

The paper, developed in collaboration with Researchers at UC Davisprovides unprecedented insight into the long-standing question of why serotonin does not stimulate growth of cortical neurons.

How? While both psychedelic substances and serotonin stimulate 5-HT2A receptors, psychedelics work by activating the intracellular receptor population, a difference that would ultimately be responsible for new dendrite growth (aka neuroplasticity).

The study results show that 5-HT2A receptors located primarily in cells, mediate the psychoplastogenic effects of psychedelics. As Serotonin cannot activate this receptor population Because their polar chemical nature prevents them from going beyond the surface and penetrating cell membranes, the results could explain why serotonin-based therapeutics like SSRIs (common antidepressants) have different effects than psychedelics and other psychoplastogenic therapeutics.

“There seems to be a lot of tipping over about what we should believe to be true about how these drugs work,” says a neuroscientist at Cornell University Alex Kun says. The general thought used to be that psychedelics “act on receptors that are on the cell surface”.

The discovery could thus aid in the development of drugs that treat patients more effectively with fewer risks and side effects, including Delix’s ongoing work on a library of now over 2,000 psychedelic-inspired, non-hallucinogenic therapeutics that promote rapid and sustained neuroplasticity in the brain .

The company will be testing the first of these novel compounds in the clinical phase in 2023 with the aim of expanding patient access to novel, safe, fast-acting and long-lasting medicines for a range of mental disorders.

“Cortical atrophy is a central feature of so many neuropsychiatric and neurodegenerative…