Key Points
- SHR9352 is an experimental synthetic opioid originally investigated as a potential pain medication.
- Researchers developed SHR9352 through chemical research related to oliceridine (TRV130), an opioid medication now FDA-approved for certain acute pain applications.
- A 2017 study reported a mu-opioid receptor signaling EC50 of 0.77 nanomolar, indicating high potency in the specific laboratory assay used.
- SHR9352 was designed to favor G-protein-associated signaling while limiting beta-arrestin recruitment, although this property does not establish human safety.
- SHR9352 and SR-17018 are different synthetic opioids with distinct chemical structures and research histories. No validated human comparison establishes equivalent effects or dosing.
- SHR9352 has not been proven safe or effective for opioid withdrawal, tolerance reduction, pain treatment, or opioid use disorder in humans.
- How Brooks Healing Center helps: Brooks offers opioid addiction treatment using established clinical approaches and FDA-approved medications, including injectable buprenorphine options such as Sublocade and Brixadi when clinically appropriate.
The development of new synthetic opioids has long focused on a difficult medical challenge: producing effective pain relief without the dangerous respiratory effects and dependence concerns associated with traditional opioids. While this research has led to approved medications, numerous experimental compounds remain poorly understood outside laboratory settings.
One example is SHR9352, a synthetic opioid initially described in 2017. Researchers developed the compound to investigate unusually potent mu-opioid receptor activation and its potential to favor certain cellular signaling mechanisms over others.
More recently, SHR9352 has attracted attention in discussions involving SR-17018, another experimental opioid associated with research into pain relief, tolerance, and withdrawal-related effects. The two compounds have some pharmacological similarities, but they differ substantially in chemical structure, research history, and available evidence.
Understanding these differences matters because experimental opioids are sometimes discussed as though they were interchangeable medications or safer substitutes for established treatments. Scientific findings from animal experiments cannot establish that an unapproved substance is appropriate for human consumption.
What Is SHR9352?
An Experimental Synthetic Opioid Developed From Oliceridine-Related Research
SHR9352 is a synthetic compound designed to activate the mu-opioid receptor, commonly abbreviated MOR. These receptors influence pain perception and contribute to several important opioid effects, including sedation, breathing suppression, reward, and physical dependence.
Researchers associated with Shanghai Hengrui Pharmaceutical and Jiangsu Hengrui Medicine first described SHR9352 in a 2017 study published in ACS Omega. The research focused on modifying molecular structures previously investigated during the development of oliceridine, also known as TRV130.
Oliceridine is an opioid medication developed to produce pain relief through preferential G-protein-associated signaling. It was subsequently approved by the FDA for adults with acute pain severe enough to require an intravenous opioid when alternative treatments are inadequate.
SHR9352 emerged from related chemical optimization research but is not the same medication as oliceridine. Its development involved structural modifications intended to increase receptor activity while limiting certain signaling responses.
The resulting compound demonstrated high mu-opioid receptor activity in laboratory experiments and pain-relieving effects in animals. However, SHR9352 has not received FDA approval, and its clinical safety and effectiveness have not been established in humans.
SHR9352 at a Glance
Chemical Classification, Receptor Activity, and Available Research
| Characteristic | SHR9352 |
|---|---|
| Substance classification | Experimental synthetic opioid |
| CAS number | 2095345-71-2 |
| Molecular formula | C28H36N2OS2 |
| Primary biological target | Mu-opioid receptor |
| Research mechanism | G-protein-biased signaling reported in laboratory experiments |
| Related pharmaceutical research | Oliceridine (TRV130) |
| Original research publication | 2017, ACS Omega |
| Reported receptor-signaling EC50 | 0.77 nM in a specific laboratory assay |
| Animal pain research | Demonstrated analgesic activity |
| Human clinical safety | Not established |
| Approved for opioid withdrawal | No |
| Approved for pain treatment | No |
| FDA approval | Not approved |
SHR9352 has several chemical and pharmacological characteristics that distinguish it from conventional opioids. However, its laboratory classification does not establish whether it produces fewer adverse effects, less dependence, or a lower overdose risk in humans.
How Does SHR9352 Work in the Brain?
Mu-Opioid Receptor Activation and G-Protein-Biased Signaling
Opioid receptors are proteins that help regulate communication between cells. When opioid medications activate mu-opioid receptors, they can reduce pain signaling while also influencing breathing, alertness, gastrointestinal function, and reward pathways.
Researchers have investigated whether different compounds can activate the same receptor while producing different downstream cellular responses. Much of this work has centered on G proteins and beta-arrestin proteins.
Early studies suggested that opioid-related pain relief might be more closely associated with G-protein signaling, while some undesirable effects could be influenced by beta-arrestin recruitment. This generated interest in developing substances that preferentially activate one signaling pathway over another.
These compounds are commonly described as G-protein-biased opioid agonists. SHR9352 was investigated as one potential example of this pharmacological approach.
In the original laboratory research, SHR9352 demonstrated potent mu-opioid receptor activity with comparatively limited beta-arrestin recruitment. Researchers interpreted these findings as promising for the development of new analgesic medications.
However, subsequent research has challenged the assumption that reduced beta-arrestin recruitment necessarily prevents dangerous opioid effects. Studies have shown that differences in overall receptor activation, experimental methods, and other receptor interactions can influence how biased agonism is measured.
Consequently, a substance may appear promising in laboratory signaling experiments while still carrying significant risks in humans. G-protein-biased activity does not establish protection against respiratory depression, overdose, or physical dependence.
How Potent Is SHR9352?
Understanding the 0.77 Nanomolar Finding and Its Limitations
One of the most frequently discussed characteristics of SHR9352 is its reported receptor potency. In the original 2017 research, scientists measured an EC50 of 0.77 nanomolar in a laboratory assay evaluating mu-opioid receptor signaling.
EC50 refers to the concentration of a substance needed to produce half of its maximum measured effect under specific experimental conditions. A lower EC50 generally indicates greater potency within that particular assay, but it does not directly establish human drug strength.
For comparison, the researchers reported an EC50 of approximately 7.9 nanomolar for oliceridine in the same type of assay. This suggested that SHR9352 was more potent at producing the measured cellular response under those experimental conditions.
The researchers also evaluated SHR9352 in animal models of pain. They reported analgesic activity in a rat incision model and investigated gastrointestinal effects in mice, observing limited constipation-related effects under certain tested conditions.
These results are scientifically interesting, but several important limitations remain:
- Laboratory potency does not establish the amount required to produce effects in a human.
- Animal pain responses do not directly predict human analgesic effectiveness.
- Reduced constipation-related effects in one experiment do not establish gastrointestinal safety.
- Human respiratory depression and overdose thresholds have not been adequately characterized.
- The relationship between experimental receptor activity and dependence risk remains uncertain.
It would therefore be inaccurate to describe SHR9352 as a specific number of times stronger than fentanyl, morphine, or SR-17018 in humans. The available research does not support a clinically meaningful comparison of that kind.
SHR9352 vs. SR-17018: What Is the Difference?
Comparing Chemical Structures, Receptor Research, and Opioid Withdrawal Findings
Although SHR9352 and SR-17018 have both been investigated for G-protein-biased signaling, they belong to different chemical research families. SHR9352 emerged from work related to oliceridine, while SR-17018 belongs to a separate group of benzimidazolone-derived synthetic opioids.
The distinction is important because compounds that activate the same receptor can have substantially different potency, efficacy, pharmacokinetics, duration of action, and effects on other signaling pathways.
Furthermore, the available studies were not designed to establish equivalent dosing or direct human potency comparisons between these substances.
| Comparison | SHR9352 | SR-17018 |
|---|---|---|
| Classification | Experimental synthetic opioid | Experimental synthetic opioid |
| Chemical research family | Oliceridine-related scaffold | Benzimidazolone-derived opioid |
| Primary receptor | Mu-opioid receptor | Mu-opioid receptor |
| G-protein-biased signaling | Reported in laboratory experiments | Reported in laboratory experiments |
| Original research focus | Potent analgesia and receptor-signaling selectivity | Analgesia, respiratory effects, receptor signaling, and later tolerance studies |
| Animal pain research | Yes | Yes |
| Opioid tolerance research | Limited | Multiple studies involving repeated administration |
| Withdrawal-related research | No established treatment evidence | Experimental findings in morphine-dependent mice |
| Human withdrawal treatment | Not established | Not established |
| FDA-approved medication | No | No |
| Federal scheduling | Not expressly named in the August 2026 SR-17018 order | Temporarily Schedule I effective August 27, 2026 |
| Validated human dose conversion | None | |
Why SR-17018 Has Received More Attention for Opioid Tolerance
SR-17018 has been investigated in several studies involving repeated opioid exposure. One study published in Neuropsychopharmacology reported that substituting SR-17018 for morphine in morphine-dependent mice reduced withdrawal-related signs and influenced experimental measures of morphine tolerance.
Other research found that SR-17018 retained analgesic effects after repeated administration in certain animal pain models but produced tolerance in another. These findings demonstrate that its effects can vary depending on the experimental conditions.
More recent research published in 2024 also investigated whether SR-17018 interacts with mu-opioid receptors through mechanisms not fully explained by conventional receptor-binding models.
These studies have expanded scientific understanding of SR-17018, but they do not establish that the compound safely treats opioid dependence in humans. They also do not justify assuming that SHR9352 produces equivalent results.
Does SHR9352 Work the Same Way as SR-17018?
Both compounds interact with mu-opioid receptors, but this similarity alone is insufficient to conclude that they work identically. Their chemical structures are different, and researchers have investigated distinct aspects of their pharmacological activity.
SHR9352 has been characterized primarily through its early potency, receptor-signaling, and animal analgesia findings. SR-17018 has a broader published research history involving tolerance, repeated exposure, and distinctive receptor interactions.
Without appropriate comparative studies, differences between the substances cannot be translated into claims about stronger effects, safer use, or improved opioid withdrawal treatment.
Is SHR9352 Safer Than Traditional Opioids?
Why Experimental Receptor Signaling Does Not Eliminate Overdose Concerns
The original development of SHR9352 was motivated by the possibility of producing powerful pain relief with fewer adverse effects. However, the available data do not establish that SHR9352 is safe for human use.
An important comparison comes from oliceridine, the approved opioid medication associated with the research framework that informed SHR9352’s development. Despite its unusual receptor-signaling properties, oliceridine carries FDA warnings about addiction, misuse, and potentially fatal respiratory depression.
This demonstrates why G-protein-biased signaling should not be interpreted as proof that an opioid cannot suppress breathing or create other serious adverse effects.
Potential concerns involving an inadequately studied mu-opioid receptor agonist include:
- Respiratory depression and overdose.
- Excessive sedation or impaired consciousness.
- Possible tolerance and physical dependence.
- Withdrawal following repeated exposure.
- Drug interactions involving alcohol, benzodiazepines, and other sedatives.
- Unpredictable effects caused by uncertain product composition.
- Unknown long-term effects on physical and mental health.
The specific frequency and severity of these risks with SHR9352 have not been established through adequate human clinical studies. This uncertainty is itself an important safety concern, particularly when research chemicals are obtained outside regulated medical or laboratory settings.
Can SHR9352 Treat Opioid Withdrawal or Reduce Tolerance?
Why SHR9352 Is Not an Approved Medication for Opioid Dependence
There is no established human clinical evidence demonstrating that SHR9352 safely treats opioid withdrawal, reverses tolerance, or improves outcomes for people with opioid use disorder.
Its original research focused on analgesic effects and receptor-signaling characteristics rather than evaluating addiction treatment. Findings involving other experimental compounds, including SR-17018, cannot establish therapeutic benefits for SHR9352.
Some individuals seek experimental opioids because they hope to avoid withdrawal from prescription opioids, fentanyl, or other substances. However, replacing one opioid-active substance with another unapproved research chemical can introduce new uncertainties while potentially continuing physical dependence.
Withdrawal management is also not simply a matter of activating opioid receptors. Appropriate treatment requires consideration of the patient’s substance exposure, withdrawal symptoms, medical history, co-occurring conditions, other medications, and risk of returning to opioid use.
FDA-approved medications such as buprenorphine and methadone have extensive evidence supporting their use in opioid use disorder. Naltrexone is another approved option for appropriately selected patients after adequate opioid clearance.
For someone considering SHR9352 because of withdrawal concerns, professional medical assessment provides a more evidence-based approach than relying on unverified claims about research chemicals.
Can SHR9352 Cause Dependence, Withdrawal, or Overdose?
Understanding Potential Opioid Risks When Human Research Is Limited
SHR9352 activates the mu-opioid receptor, making opioid-related adverse effects a legitimate concern. However, available research does not establish its human dependence potential, withdrawal timeline, or overdose threshold.
The absence of published human outcomes should not be interpreted as evidence that those outcomes cannot occur. A compound can demonstrate promising preclinical characteristics while still requiring extensive testing before its clinical risks are understood.
Another concern involves products sold under experimental chemical names. Without independent analytical confirmation, consumers may not know whether a substance contains the claimed compound or additional opioid-active ingredients.
If someone becomes unresponsive or develops slow, irregular, or absent breathing after taking an opioid or suspected opioid, call 911 immediately. Administer naloxone if available, follow emergency dispatcher instructions, and remain with the person until emergency responders arrive.
Naloxone is an established emergency medication for suspected opioid overdose. Although clinical studies specifically evaluating its effectiveness against SHR9352 are lacking, uncertainty about the exact opioid should not delay emergency response.
FDA-Approved Alternatives to Experimental Opioids Like SHR9352
How Medication-Assisted Treatment Supports Opioid Addiction Recovery
Although SHR9352 is not an approved medication, established treatments are available for individuals experiencing opioid use disorder. The FDA has approved three medications for this condition: buprenorphine, methadone, and naltrexone.
These medications work through different mechanisms and have distinct clinical applications. Treatment decisions depend on individual needs, including current opioid exposure, withdrawal symptoms, medical history, and recovery goals.
At Brooks Healing Center, our Medication-Assisted Treatment (MAT) program incorporates FDA-approved medications alongside counseling, behavioral therapies, and recovery support when clinically appropriate.
Available options include buprenorphine-based medications, including extended-release injectable formulations such as Sublocade and Brixadi.
| Medication | FDA Status | Clinical Purpose |
|---|---|---|
| SHR9352 | Not approved | Experimental research compound with no established addiction-treatment indication |
| SR-17018 | Not approved | Experimental synthetic opioid; federally Schedule I |
| Sublocade | Approved | Monthly extended-release injectable buprenorphine for opioid use disorder |
| Brixadi | Approved | Weekly or monthly extended-release injectable buprenorphine for opioid use disorder |
| Buprenorphine/naloxone | Approved | Reduces withdrawal symptoms and cravings as part of OUD treatment |
| Methadone | Approved | Long-acting opioid agonist used in appropriately certified opioid treatment programs |
| Naltrexone | Approved | Opioid antagonist used after appropriate opioid clearance |
Sublocade: Monthly Injectable Buprenorphine for Opioid Use Disorder
Sublocade is an FDA-approved extended-release buprenorphine injection administered monthly by a qualified healthcare professional. It provides sustained medication delivery to help reduce opioid cravings and withdrawal symptoms.
For eligible patients, Sublocade may reduce the need to manage daily buprenorphine dosing during maintenance treatment. Its use requires appropriate medical evaluation, initiation procedures, and ongoing clinical supervision.
At Brooks Healing Center, Sublocade can be incorporated into individualized MAT plans alongside structured addiction treatment, counseling, and recovery planning.
Brixadi: Weekly and Monthly Injectable Buprenorphine Options
Brixadi is another FDA-approved extended-release buprenorphine medication. Unlike Sublocade, it offers both weekly and monthly formulations, providing additional flexibility for medical providers.
Brixadi can help manage cravings and withdrawal symptoms in eligible individuals with opioid use disorder. The appropriate formulation and initiation approach depend on medical assessment and the medication’s prescribing requirements.
Both Sublocade and Brixadi contain buprenorphine, but their delivery systems and administration schedules differ. Neither should be considered universally preferable, and the choice depends on the patient’s clinical circumstances.
Medication-Assisted Treatment Across Different Levels of Care
At Brooks Healing Center, MAT is not exclusively associated with one level of treatment. Medication support may be integrated into medical detox, residential addiction treatment, or appropriate continuing care depending on clinical needs.
For individuals experiencing opioid withdrawal, medication can help provide physiological stabilization. During continued treatment, behavioral interventions and recovery planning address the broader patterns contributing to substance use.
Brooks does not dispense methadone onsite or operate an opioid treatment program. When clinically appropriate, care may be coordinated with outside methadone providers.
Unlike experimental compounds such as SHR9352 and SR-17018, established medications for opioid use disorder have defined prescribing requirements and extensive clinical evidence supporting their appropriate use.
Synthetic Opioid Addiction Treatment in Tennessee
Medical Detox, Residential Treatment, and Continued Recovery at Brooks Healing Center
People struggling with opioid dependence may encounter many different substances, including prescription opioids, heroin, fentanyl, concentrated kratom-derived products, and unfamiliar synthetic compounds. Treatment needs depend on more than the name of the substance involved.
Brooks Healing Center provides individualized addiction treatment in Normandy, Tennessee, between Nashville and Chattanooga. Clinical planning considers the person’s medical history, withdrawal symptoms, substance use patterns, mental health needs, and appropriate level of care.
Depending on individual assessment, treatment options may include:
- Medical Detox: Supervised withdrawal management, clinical assessment, and stabilization.
- Residential Treatment: Structured addiction treatment, individual counseling, group therapy, and relapse-prevention support.
- Medication-Assisted Treatment: FDA-approved medications incorporated into individualized treatment plans when clinically appropriate.
- Partial Hospitalization Program: Continued structured clinical treatment for individuals who no longer require residential care.
- Continuing Recovery Support: Aftercare planning, peer support, and recovery-focused housing options.
Brooks also provides specialized resources addressing opioid addiction treatment, fentanyl addiction, and kratom and concentrated 7-OH dependence.
For someone who has used an unfamiliar research chemical, providing the clinical team with information about the product, packaging, frequency of use, and other substances taken may help inform medical assessment and treatment planning.
Get Help for Opioid Dependence at Brooks Healing Center
Explore FDA-Approved Medications and Individualized Recovery Programs
SHR9352 illustrates the continuing scientific interest in developing new opioid medications. However, promising receptor-signaling findings and animal experiments are not equivalent to evidence that a substance is safe for human consumption or appropriate for treating addiction.
Brooks Healing Center provides evidence-based opioid addiction treatment with access to FDA-approved MAT options, including Sublocade and Brixadi when clinically appropriate. Our admissions team can explain available programs, discuss individual treatment needs, and help verify insurance benefits.
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Frequently Asked Questions About SHR9352
Potency, Opioid Withdrawal, and FDA-Approved Treatment
Is SHR9352 a Synthetic Opioid?
Yes. SHR9352 is a synthetic research compound that activates mu-opioid receptors. It was originally developed for experimental pain research and is not an FDA-approved medication.
Is SHR9352 Stronger Than Fentanyl?
There is insufficient human evidence to make a reliable potency comparison between SHR9352 and fentanyl. SHR9352 demonstrated high potency in a laboratory receptor-signaling assay, but those findings do not establish equivalent human doses, effects, or overdose thresholds.
Is SHR9352 the Same as SR-17018?
No. SHR9352 and SR-17018 are chemically different experimental opioids. They have been investigated for some similar receptor-signaling characteristics, but there is no established clinical evidence demonstrating that they produce equivalent effects or can safely substitute for one another.
Can SHR9352 Reduce Opioid Tolerance?
There is no established human evidence demonstrating that SHR9352 safely reduces opioid tolerance. Research involving SR-17018 and morphine tolerance in mice cannot establish equivalent effects for SHR9352. Its original research primarily investigated analgesia and receptor signaling.
Can SHR9352 Treat Opioid Withdrawal?
No approved clinical application for SHR9352 exists, and it has not been proven safe or effective for opioid withdrawal. Individuals seeking treatment for opioid dependence should discuss established medication options with a qualified healthcare professional.
Is SHR9352 Related to Oliceridine?
Yes. SHR9352 was developed through chemical research involving structural modifications related to oliceridine, also known as TRV130. However, SHR9352 is a separate compound and does not share oliceridine’s FDA approval or established clinical prescribing information.
Is SHR9352 Federally Controlled?
SHR9352 was not expressly named in the DEA’s August 27, 2026 scheduling order covering SR-17018 and several other synthetic opioids. That does not establish that SHR9352 is legal. Controlled-substance analogue provisions and other applicable federal or state laws may affect its status.
Does Brooks Healing Center Offer FDA-Approved Alternatives to SHR9352?
Yes. Brooks offers Medication-Assisted Treatment using FDA-approved medications when clinically appropriate. Available options for eligible patients with opioid use disorder include extended-release buprenorphine injections such as Sublocade and Brixadi, alongside counseling and recovery support.
Can Brixadi or Sublocade Help Someone With Fentanyl Use Disorder?
Both Brixadi and Sublocade are FDA-approved medications for opioid use disorder, including cases involving fentanyl. However, fentanyl exposure can complicate the timing of buprenorphine initiation. Medication selection and initiation should be guided by qualified medical providers. Learn more about fentanyl addiction treatment at Brooks Healing Center.
Related Resources
Further Reading About Experimental Opioids and Emerging Substances
- What Is SR-15099 (SR 2.0)? Comparing It to SR-17018
- What Is SR-17018? A Look at the Experimental Opioid Compound
- MGM-15: Understanding an Emerging Synthetic Opioid
- MGM-16 vs. MGM-15: Understanding Kratom-Derived Opioids
- Mitragynine Pseudoindoxyl vs. 7-Hydroxymitragynine
- 7-OH Withdrawal: Symptoms, Duration, and What Helps
Related Treatment Pages
Opioid Dependence Treatment and FDA-Approved Medication Options
- Medication-Assisted Treatment (MAT)
- Sublocade Injection Treatment
- Brixadi Injection Treatment
- Opioid Addiction Treatment
- Fentanyl Addiction Treatment
- Kratom and 7-OH Addiction Treatment
- Medical Detox
- Residential Addiction Treatment
- Partial Hospitalization Program
References
Peer-Reviewed Research and Government Sources (APA Format)
Drug Enforcement Administration. (2026, August 27). Schedules of controlled substances: Temporary placement of 5,6-dichloro brorphine, 5,6-dichloro desmethylchlorphine, N-propionitrile chlorphine, and spirochlorphine in Schedule I of the Controlled Substances Act. Federal Register. https://www.govinfo.gov/content/pkg/FR-2026-08-27/pdf/2026-17531.pdf
Gillis, A., Gondin, A. B., Kliewer, A., Sanchez, J., Lim, H. D., Alamein, C., Manandhar, P., Santiago, M., Fritzwanker, S., Schmiedel, F., Katte, T. A., Reekie, T., Grimsey, N. L., Kassiou, M., Kellam, B., Krasel, C., Halls, M. L., Connor, M., Lane, J. R., . . . Canals, M. (2020). Low intrinsic efficacy for G protein activation can explain the improved side effect profiles of new opioid agonists. Science Signaling, 13(625), eaaz3140. https://pubmed.ncbi.nlm.nih.gov/32234959/
Grim, T. W., Schmid, C. L., Stahl, E. L., Pantouli, F., Ho, J.-H., Acevedo-Canabal, A., Kennedy, N. M., Cameron, M. D., Bannister, T. D., & Bohn, L. M. (2020). A G protein signaling-biased agonist at the μ-opioid receptor reverses morphine tolerance while preventing morphine withdrawal. Neuropsychopharmacology, 45, 416–425. https://pubmed.ncbi.nlm.nih.gov/31443104/
Li, X., He, W., Chen, Y., Yang, G., Wan, H., Zhang, L., Hu, Q., Feng, J., Zhang, Z., He, F., Bai, C., Zhang, L., You, L., & Tao, W. (2017). Discovery of SHR9352: A highly potent G protein-biased μ-opioid receptor agonist. ACS Omega, 2(12), 9261–9267. https://pubmed.ncbi.nlm.nih.gov/31457439/
Pantouli, F., Grim, T. W., Schmid, C. L., Acevedo-Canabal, A., Kennedy, N. M., Cameron, M. D., Bannister, T. D., & Bohn, L. M. (2021). Comparison of morphine, oxycodone and the biased MOR agonist SR-17018 for tolerance and efficacy in mouse models of pain. Neuropharmacology, 185, 108439. https://pubmed.ncbi.nlm.nih.gov/33345829/
Schmid, C. L., Kennedy, N. M., Ross, N. C., Lovell, K. M., Yue, Z., Morgenweck, J., Cameron, M. D., Bannister, T. D., & Bohn, L. M. (2017). Bias factor and therapeutic window correlate to predict safer opioid analgesics. Cell, 171(5), 1165–1175.e13. https://pmc.ncbi.nlm.nih.gov/articles/PMC5731250/
Singleton, S., Dieterle, C., Walker, D. J., Runeberg, T., Oswald, A. S., Rosenqvist, G., Robertson, L., McCarthy, T., Sarkar, S., Baptista-Hon, D., & Hales, T. G. (2024). Activation of μ receptors by SR-17018 through a distinctive mechanism. Neuropharmacology, 258, 110093. https://pubmed.ncbi.nlm.nih.gov/39067665/
U.S. Food and Drug Administration. (n.d.). Information about medications for opioid use disorder (MOUD). https://www.fda.gov/drugs/food-and-drug-administration-overdose-prevention-framework/information-about-medications-opioid-use-disorder-moud
U.S. National Library of Medicine. (2025, December 31). Olinvyk (oliceridine) injection: Prescribing information. DailyMed. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ce167984-8b9d-40b7-84ce-d0f33fff1eaa
