Chronic post-surgical pain is a significantly incapacitating and under-evaluated condition impacting several millions of people worldwide each year. It lasts from few weeks until more than a year after the initial insult and is induced in approximately 10% of all surgeries. Despite considerable efforts to develop new treatments, opioids are prescribed to 80% of patients worldwide postoperatively. Opioids side effect are well described, and opioid-induced hyperalgesia (OIH) and tolerance are well known for worsening post-operative pain. Additionally, untreated OIH increases the risk of developing persistent postsurgical pain and delays hospital discharge. Opioids consumption for post-operative pain has contributed substantially to the current opioid crisis.

In this context, there is an urgent need to prevent patients from chronification of post-operative pain. A new treatment preventing pain chronification and hyperalgesia will have a tremendous effect and help overcome the current opioid crisis.

Program description

NPFFR antagonist

  • Discovery
  • Candidate
  • Preclinical
  • Phase I

Domain’s NPFFR antagonist program, originating from the university of Strasbourg in France, is currently in lead optimization phase. Animal proof-of-concept studies as well as evaluations through the Addiction Treatment Discovery Program at the National Institute for Drug Abuse (ATDP-NIDA) have shown that NPFFR antagonist holds strong potential to become a disease-modifying treatment to combat opioid crisis and pain chronification.

We are developing a first-in-class small molecule antagonists of NPFF receptor to address multiple aspects of pain chronification and hyperalgesia.

This program is at the end of lead op

Additional resources

DT095597 a New NPFFR1 Antagonist Devoid of Addictive Properties to Fight Opioid Crisis

This poster presents the characterization of a proprietary NPFF receptor antagonist as a game-changer and a promising therapeutic strategy to fight the current opioid crisis.

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Other programs


mGluR4/7/8 PAM


mGluR3 PAM