Non-Opioid-Based Anti-Inflammatory Medication

Technology #15887

Compounds Modulate Inflammatory Responses in Human Cells and Reduce Pain Response in Mice

This therapeutic compound reduces inflammation without opioid-based pharmacology, offering pain relief without the threat of addiction and showing potential for neurocognition processes. Inflammation is associated with a number of disease states and physiologic symptoms, including pain. Currently, opioid-based pain relievers and anti-inflammatory medications are under intense scrutiny because of their health-related problems, including abuse and addiction. Out of the 20 million Americans with substance abuse problems, 2 million are associated with prescription pain relievers. Almost 50,000 overdoses occur every year, with 30,000 related to abuse of opioids, making drug overdose the number one cause of accidental death in the United States. Researchers at the University of Florida have discovered an opioid-free compound with the ability to modulate the intrinsic factors which produce inflammation, resulting in a reduction of pain in the nervous system. This compound offers exciting modalities for pain relief and inflammation, given its opioid-free pharmaceutical properties and chemical composition.


Opioid-free compound to reduce inflammation and pain


  • Selectively stabilizes nicotinic receptors, modulating inflammatory responses in human cells and reducing pain response in mice
  • Uses completely different pharmacology to reduce inflammation and pain, enabling relief without threat of addiction


This series of quaternary ammonium compounds demonstrates the ability to selectively stabilize signaling states of alpha7-type nicotinic acetylcholine receptors, which have been shown to mediate cholinergic anti-inflammatory pathway. The reduction of inflammation has the effect of reducing pain responses in the nervous system. While the alpha7 nicotinic can signal through the ion-channel active state, such activation is transient and has not been linked to activation of the cholinergic anti-inflammatory pathway. Rather activation of the cholinergic anti-inflammatory pathway appears to arise from the induction of nonconducting states associated with desensitization of the ion channel function. Compounds that selectively desensitize, without facilitating significant channel activation are termed “silent agonists.” The variations of the N-alkyl groups and other substituents associated with these compounds can promote selective entry into desensitized states associated with anti-inflammatory responses. These silent agonists are prevalent in this technology and offer control of inflammation-related phenomena through selective induction of desensitized states of inflammation receptors.