SR-17018: what it is, how it works, and what's known.

SR-17018 is a synthetic opioid first described by scientists at the Scripps Research Institute in 2017. It activates the μ-opioid receptor — the same receptor as morphine and fentanyl — but with unusual, only partial activity. It has not been approved for any medical use, and there are no completed human clinical trials.

SR-17018 is not specifically scheduled in many countries, but unscheduled is not the same as legal. In the United States, federal prosecutors can treat it as a Schedule I substance under the Federal Analogue Act when it is intended for human consumption. Germany controls it under the NpSG (since 2025). The UK Psychoactive Substances Act 2016 likely applies. This is not legal advice; verify in your jurisdiction.

There is no clinically validated dose for SR-17018 — no human trials have been completed. We document community-reported dose ranges descriptively on the protocols page, with strong disclaimers. They are not recommendations.

In mice, the half-life is approximately 6–8 hours, with a brain-to-plasma ratio of about 3:1. Self-reports describe an effective duration of 6–12 hours per oral dose in humans, but no formal human pharmacokinetic profile has been published.

Yes. Despite SR-17018's non-competitive binding kinetics, orthosteric antagonists — naloxone (Narcan), naltrexone, cyprodime — fully reverse SR-17018-mediated μ-opioid receptor activation in cellular and animal studies. Because SR-17018's duration of action can be long, repeat doses of naloxone may be needed.

Yes, at higher doses — particularly with oral administration. The 'no respiratory depression' claim from the original 2017 paper has not held up cleanly. The original work used intraperitoneal dosing in mice; oral dosing (the only route used in humans) does produce significant respiratory depression in mice. SR-17018 has a wider therapeutic window than morphine or fentanyl in mouse parenteral assays, but it is not free of breathing risk.

Yes. SR-17018 produces dependence in mice, with a clear withdrawal syndrome on discontinuation (Kudla et al., 2022). Self-reports describe post-acute withdrawal-like symptoms after stopping. The compound is not free of dependence liability.

Both are partial μ-opioid receptor agonists with low intrinsic efficacy. Buprenorphine is FDA-approved for opioid use disorder, has decades of clinical data, and is dose-controlled. SR-17018 has none of these things. SR-17018's binding kinetics are markedly different — non-competitive and slowly reversible, rather than competitive — but the clinical comparison strongly favors buprenorphine for any actual treatment context.