KNX100 is Kinoxis Therapeutics’ lead clinical candidate, a first-in-class, short-acting small-molecule inhibitor of ALOX15 being developed for the treatment of agitation and aggression associated with dementia.
By targeting neuroinflammatory pathways in the central nervous system, KNX100 is designed to modulate the neural circuits that drive agitation and aggression without the sedation and safety limitations associated with current atypical antipsychotic therapies.
The compound has demonstrated robust activity across multiple preclinical models of agitation and aggression and has shown a favorable safety and tolerability profile in clinical studies. KNX100 is currently being evaluated in a Phase 2 clinical trial in patients with agitation associated with dementia, with the goal of providing a safer and more effective treatment option for this significant unmet medical need.
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KNX101 is a second-generation, long-acting small-molecule inhibitor of ALOX15 being developed for the treatment of acute and chronic pain.
The compound is designed to interrupt both the initiation and amplification of glia-driven pain signaling that underlies many chronic pain conditions. Preclinical studies indicate that inhibition of ALOX15 can reduce neuropathic and inflammatory pain phenotypes by preventing activation of lipid–ROS pathways that sensitize pain circuits.
As part of Kinoxis’ differentiated ALOX15 inhibitor platform, KNX101 is advancing through IND-enabling studies with the goal of delivering a novel, non-opioid therapy for patients suffering from acute and chronic pain.
The KNX200 series comprises a set of novel small molecules engineered to act as partial agonists of the oxytocin receptor.
These compounds are designed to fine-tune oxytocin-mediated signaling within neural circuits involved in stress adaptation, emotional regulation, and nociception.
By providing controlled receptor engagement, the KNX200 series aims to restore physiological signaling balance while minimizing the overstimulation and peripheral effects often associated with full receptor agonists.
