Discovery is in our nature
Pioneering the Next Generation of Neuropsychiatric Medicines
Küleon is a drug discovery company leveraging proprietary, AI-based technology to identify novel serotonergic drugs for the targeted treatment of various neuropsychiatric diseases and disorders.
Küleon | About Us
A GPCR Focus
Küleon is advancing its patented library of highly selective compounds targeting specific G protein-coupled receptors (GPCRs). GPCRs have been proven to be the most successful class of druggable targets in the human genome and make up 50-60% of all druggable targets in the body. Küleon is focused primarily on developing small molecule therapeutics for diseases and disorders that can be modulated through serotonin GPCRs found in the prefrontal cortex of the brain. Selective modulation of certain serotonin receptor subtypes can be leveraged to treat a variety of neuropsychiatric diseases and disorders, including pain, inflammation, depression, schizophrenia, obesity, addiction, and neurodegeneration.
Latest From The Blog
Küleon Receives Another Favorable PCT Search Report and Written Opinion from WIPO.
Küleon Receives Favorable PCT Search Report and Written Opinion from WIPO.
Küleon’s first Patent Application is Published.
Küleon | Our Approach
Selective Agonists
The serotonin 5-HT2C G-protein coupled receptor (GPCR) is a validated target for treating psychotic and addictive disorders, but selectively targeting 5-HT2C has proven to be a significant challenge. However, many 5-HT2C receptor agonists are plagued by unacceptable off-target effects due to the high level of homology shared amongst all 15 serotonin receptor subtypes. Küleon has solved these critical technical limitations. Through our work, we have identified several novel and patentable compound classes that are not only selective for 5-HT2C, but exhibit a unique 5-HT2C Gq-mediated signaling bias that can enhance the drug’s long-term therapeutic effect.
ADVANTAGES OF THIS OPPORTUNITY
The Opportunity Ahead
Most “selective” 5-HT2C receptor agonists exhibit detrimental off-target activation of 5-HT2A (hallucinations) and 5-HT2B (cardiotoxicity). Further, recent evidence suggests that existing 5-HT2C agonists lack “functional selectivity” by activating both Gq signaling (mediating the putative therapeutic effect) and calmodulin-β-arrestin intracellular signaling, leading to receptor internalization and attenuation of signal, which limits therapeutic functionality. Indeed, a robust positive correlation for magnitude of β–arrestin recruitment has been identified as the primary reason for a significant number of patients developing a tolerance to the therapeutic effects of 5-HT2C drugs in humans. Thus, identifying 5-HT2C agonists biasing Gq-mediated signaling offers a tremendous improvement in long-term therapeutic benefits and a potential reduction of side effects.
