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Reference

Overview of SR-17018

An experimental opioid that started as a 'safer-by-design' research compound and is now being self-administered in unregulated form. Here's what the science says — and where it's still uncertain.

Last reviewed: 2026-05-05Editorial methodology

What it is, in one minute

Quick reference

Compound name
SR-17018
Common short forms
SR-17, SR
CAS number
2134602-45-0
Chemical class
Substituted piperidine benzimidazolone (orphine-class designer opioid)
Receptor target
μ-opioid receptor (MOR), with much lower κ-OR affinity and negligible δ-OR affinity
Functional classification
Atypical biased / partial μ-opioid receptor agonist; non-competitive at MOR
Original publication
Schmid et al., Cell, 2017
Patent
Filed 2016 (Scripps Research / Bohn lab)
Approved medical use
None. Not approved by FDA, EMA, or any national regulator.
First reported in unregulated drug supply
2023
Reported community use cases
Self-administered taper aid for opioid dependence (kratom, nitazenes, fentanyl, methadone, ODSMT, buprenorphine, prescription opioids)
Reversibility
Effects reversible by opioid antagonists (naloxone, naltrexone) in animal models

Why it was made

The μ-opioid receptor turns on at least two cellular signaling cascades when activated. For years, the dominant theory in opioid pharmacology held that one of those cascades — β-arrestin2 recruitment — drove the most dangerous effects of opioids, including respiratory depression, while the other (G-protein signaling) drove pain relief. If that were true, a drug that turned on G-protein signaling without turning on β-arrestin recruitment could relieve pain with a wider safety margin.

SR-17018 was designed to test that hypothesis. In the 2017 paper that introduced it, the authors reported a therapeutic window for SR-17018 of 26–105 (respiratory depression relative to pain relief in mice) — far higher than morphine's 5–21 or fentanyl's 2–5[1].

What follow-up studies found

See Mechanism of action for the molecular detail and Preclinical pharmacology for the breathing data. The short version: SR-17018 has a wider therapeutic window than fentanyl or morphine in some mouse experiments, but it is not free of respiratory depression, and the safety advantage is dose- and route-dependent.

What we know about humans

What does exist is a body of self-reports from online communities (mostly from 2024 forward) describing the use of SR-17018 as a taper aid for people dependent on other opioids — including high-potency synthetic opioids like fentanyl and nitazenes[5]. These reports are useful as descriptive data, but they are unverified, unaudited, and subject to severe selection bias. We cover them in detail in Reported effects in humans.

Where to go from here

  • If you came for the chemistry, head to Chemistry & identity.
  • If you came to understand the biased-agonism story, Mechanism of action covers the original claim and the rebuttals.
  • If you came because you or someone close to you uses this compound, the most important page is Safety considerations.
  • If you came to find out whether it's legal, see Legal status for U.S. and international.
  • If you want every paper we cite in one place, the Bibliography has direct links.

Related reading

Sources cited on this page

  1. [1]Schmid CL, Kennedy NM, Ross NC, Lovell KM, Yue Z, Morgenweck J, Cameron MD, Bannister TD, Bohn LM. Bias factor and therapeutic window correlate to predict safer opioid analgesics · Cell, 171(5):1165–1175.e13 (2017) doi.org/10.1016/j.cell.2017.10.035
  2. [2]Grim TW, Schmid CL, Stahl EL, et al.. A G protein signaling-biased agonist at the μ-opioid receptor reverses morphine tolerance while preventing morphine withdrawal · Neuropsychopharmacology, 45:416–425 (2020) pmc.ncbi.nlm.nih.gov/articles/PMC6901606/
  3. [3]Pantouli F, Grim TW, Schmid CL, et al.. Comparison of morphine, oxycodone and the biased MOR agonist SR-17018 for tolerance and efficacy in mouse models of pain · Neuropharmacology, 185:108439 (2021) pmc.ncbi.nlm.nih.gov/articles/PMC7887086/
  4. [4]Ko M-C et al.. G protein-biased mu opioid receptor agonist SR-17018 has low in vivo efficacy in non-human primates · The Journal of Pain (2023) PubMed searchFull-text DOI verified at editorial review
  5. [5]Kudla L, Bugno R, Podlewska S, et al.. Comparison of an addictive potential of μ-opioid receptor agonists with G protein bias: behavioral and molecular modeling studies · Pharmaceutics, 14(1):55 (2022) pmc.ncbi.nlm.nih.gov/articles/PMC8779292/
  6. [6]SR-17018 — Wikipedia · Wikipedia en.wikipedia.org/wiki/SR-17018Useful index of primary literature