Hypocretin blocker approach to safer opioid relief
Official title: Maintaining opioid analgesia and preventing addiction with hypocretin antagonism
Funded at University of California Los Angeles · NIH-11325692 · Data updated 2026-11-12
A study exploring a new way to give strong pain relief with opioids while lowering the risk of addiction by targeting hypocretin signals.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California Los Angeles NIH-funded |
| Lab location | 1 site (Los Angeles, United States) |
| Project start | August 1, 2023 |
| Project end | May 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $561,974 |
| NIH project number | 5R01DA058639-04 |
| Project ID | NIH-11325692 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are adults with severe, chronic pain who may require opioid therapy and are concerned about addiction risk.
✕Less likely to help
Patients not using opioids or those without addiction risk factors may not benefit from this approach.
What this research studies
This project looks at how blocking hypocretin signals could allow physicians to use opioids more safely for severe pain. Researchers will examine how antagonizing hypocretin affects pain relief and addictive tendencies in models that relate to human pain and addiction pathways. The work builds on prior findings that hypocretin neurons change with long-term opioid use and addiction, aiming to translate those insights toward better, safer pain management in people who need strong analgesia.
Why it matters
Potential benefit: If successful, this approach could lead to opioid pain relief that carries a lower risk of addiction for patients who require strong pain control.
How similar studies have gone: Previous animal and human studies show hypocretin changes with addiction, suggesting the approach is plausible but still early.
Where this research is happening
-
University of California Los Angeles
Los Angeles, United States Active
Researchers
- Principal investigator: Siegel, Jerome M — University of California Los Angeles
- Study coordinator: Siegel, Jerome M
Related research
Other NIH-funded projects on the same topics.
-
Using hypocretin antagonism to manage pain and reduce addiction risk
This study is exploring a new way to help people with severe pain using opioids while trying to reduce the chances of becoming addicted, by looking at how certain brain cells called hypocretin neurons affect pain and addiction.
-
Understanding how brain circuits affect pain relief and addiction from opioids
This study is looking at how certain brain pathways affect the pain relief and addictive qualities of opioids, using mice to help find ways to manage pain better without the risk of becoming addicted.
-
Immune and nerve signals behind acupuncture relief for sickle cell pain
This NIH grant explores how acupuncture helps reduce pain and opioid use for people with sickle cell disease.
-
Reducing Addiction Risk in High Schools Through Better Prevention Infrastructure
Aims to build a sustainable, school-based system to prevent opioid and other drug use among high school students, especially those at higher risk.
-
HEAL Data Platform to share addiction-related data across programs
A platform project to make HEAL data from many programs easier to find and use, helping researchers and clinicians access information about addiction in children and youth.
-
Cognitively-enhanced tDCS to reduce cocaine craving
A study to test whether real brain stimulation together with learning strategies can lessen craving in people with cocaine use disorder.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.