What Is SR-15099 (SR 2.0)? Comparing It to SR-17018 (SR-17)

Key Points

• SR-15099, also marketed as SR 2.0, is an experimental synthetic opioid compound closely related to SR-17018, commonly called SR-17.
• Both compounds interact with mu-opioid receptors and have demonstrated unusual signaling characteristics in preclinical research, but neither is FDA-approved for treating pain, addiction, or opioid withdrawal.
• Animal research suggests these compounds may produce pain-relieving effects with less respiratory suppression under certain experimental conditions. However, those findings do not establish safety, appropriate dosing, or effectiveness in humans.
• SR-17018 was temporarily placed in federal Schedule I on August 27, 2026. SR-15099 was not specifically named in that order, but it may still be subject to federal controlled-substance analogue provisions or other applicable laws.
• Claims that SR 2.0 can eliminate opioid withdrawal, rapidly reduce tolerance, or replace established addiction medications are not supported by controlled human clinical trials.
• How Brooks helps: Brooks Healing Center provides medically supported detox, residential addiction treatment, individualized medication assessments, and continued recovery care for people struggling with opioid dependence and related substance use.

The market for experimental synthetic opioids continues to evolve. As compounds become restricted, unfamiliar alternatives often begin circulating online, accompanied by claims that they are safer, more effective, or capable of producing benefits that established medications cannot. SR-15099, sometimes referred to as SR 2.0, is one compound attracting attention because of its close relationship to SR-17018.

SR-17018, also known as SR-17, gained attention among researchers for its unusual interaction with opioid receptors. It also became the subject of online discussions about opioid tolerance, withdrawal, and self-directed treatment. Following its placement in federal Schedule I in August 2026, interest in structurally similar compounds such as SR-15099 raised new questions about whether they could produce comparable effects.

However, scientific interest and clinical evidence are not interchangeable. SR-15099 has been studied in laboratory and animal experiments, but those findings do not establish that it is safe for people to consume. Understanding the differences between SR-15099 and SR-17018 is especially important for anyone considering these substances as alternatives to evidence-based medication-assisted treatment.

What Is SR-15099 (SR 2.0)?

An Experimental Synthetic Opioid With a Chemical Structure Similar to SR-17

SR-15099 is a laboratory-developed synthetic opioid that belongs to a group of compounds investigated for their activity at the mu-opioid receptor. This receptor is involved in pain regulation, reward, sedation, physical dependence, and many of the effects associated with traditional opioids such as morphine, oxycodone, heroin, and fentanyl.

SR-15099 is closely related to SR-17018. Structurally, one of the principal differences is that SR-15099 contains a bromine atom where SR-17018 contains a chlorine atom on a particular part of the molecule. Although this is a relatively small chemical modification, even limited structural changes can influence how a compound interacts with receptors, moves through the body, or produces biological effects.

Researchers initially investigated SR-15099 as part of a broader effort to develop opioid medications with potentially improved safety characteristics. A 2017 study published in Cell examined several experimental opioid compounds, including members of the SR series, to investigate whether differences in receptor signaling could help separate pain relief from respiratory suppression.

Importantly, SR-15099 is not a kratom alkaloid, a derivative of 7-hydroxymitragynine, or a naturally occurring botanical compound. It is a synthetic research chemical. Although people discussing kratom and concentrated 7-OH products may encounter SR 2.0 in the same online communities, these substances have different chemical origins and should not be treated as interchangeable.

How Does SR-15099 Work in the Brain?

Understanding Mu-Opioid Receptors, Partial Agonism, and G-Protein Signaling

To understand why SR-15099 attracted scientific attention, it helps to understand the signaling pathways associated with opioid receptors. When an opioid activates the mu-opioid receptor, it can initiate several cellular processes that influence pain perception, breathing, reward, gastrointestinal activity, and the body’s response to repeated opioid exposure.

Two important signaling mechanisms studied in opioid pharmacology involve G proteins and beta-arrestin proteins. Early research suggested that favoring G-protein signaling while limiting beta-arrestin-2 recruitment might help preserve pain relief while reducing certain adverse effects. This concept became known as biased agonism, and it helped guide the development of compounds such as SR-15099 and SR-17018.

Both compounds have demonstrated a preference for G-protein signaling over beta-arrestin-2 recruitment in laboratory experiments. They have also shown partial agonist characteristics, meaning their ability to activate a receptor can be lower than that of a full agonist under particular experimental conditions.

However, the relationship between biased signaling and opioid safety has become more complicated as additional studies have been published. Researchers have found that a compound’s overall receptor efficacy, the signaling pathways being measured, and the experimental model can all influence the observed effects. It is therefore inaccurate to assume that reduced beta-arrestin-2 activity automatically eliminates opioid-related dangers.

A 2021 study published in the Proceedings of the National Academy of Sciences also found that SR-15099 and SR-17018 demonstrated unusual, potentially noncompetitive interactions with mu-opioid receptors in laboratory assays. These findings may help researchers understand the compounds’ distinctive pharmacology, but they do not establish a predictable safety profile in humans.

SR-17018 (SR-17) vs. SR-15099 (SR 2.0)

Comparing Their Chemical Structures, Research Findings, Potential Risks, and Legal Status

SR-15099 and SR-17018 share important similarities, but they are separate chemical compounds. The nickname SR 2.0 may suggest that SR-15099 is a newer, improved, or more effective version of SR-17. However, that naming convention is marketing terminology rather than evidence that the compound has been clinically improved.

Although both substances have been investigated in experimental opioid research, SR-17018 has received more attention in studies specifically examining morphine tolerance, withdrawal suppression, and repeated administration. SR-15099 has also appeared in receptor-signaling and animal-behavior research, but there is insufficient clinical evidence to establish whether it can reproduce the effects reported for SR-17018 in humans.

One particularly interesting finding appeared in the 2021 receptor-signaling study. In a mouse brainstem assay, SR-17018 produced approximately 48% of the maximum G-protein response generated by a reference opioid agonist called DAMGO, while SR-15099 produced approximately 29%. These values describe responses under specific laboratory conditions and cannot be used to calculate equivalent doses, compare recreational potency, or determine which compound is safer for human consumption.

This distinction matters because consumers frequently interpret chemical similarities or laboratory potency measurements as practical information about strength. In reality, receptor activation is only one aspect of a substance’s effects. Absorption, metabolism, duration of action, interactions with other medications, and individual physiology all influence what happens when an opioid enters the human body.

Is SR-15099 Safer Than Traditional Opioids?

Why Reduced Respiratory Depression in Animal Studies Does Not Prove Human Safety

One of the most frequently misunderstood aspects of SR-15099 research involves respiratory depression. Respiratory depression occurs when opioid activity interferes with the body’s ability to maintain normal breathing, potentially reducing oxygen delivery to vital organs. Severe opioid-induced respiratory depression can result in unconsciousness, brain injury, or death.

The original research into G-protein-biased opioids was partly motivated by the possibility of reducing this dangerous effect while preserving analgesia. In certain animal experiments, compounds within the SR series produced pain-relieving responses with comparatively less respiratory suppression than traditional opioids.

However, reduced respiratory suppression under experimental conditions is not the same as an inability to cause respiratory depression. Animal findings do not establish safe human doses, and researchers have not determined how SR-15099 behaves across the range of circumstances encountered in actual human use.

Potential safety concerns include:

• Excessive sedation or impaired consciousness
• Respiratory depression and possible overdose
• Unpredictable interactions with alcohol, benzodiazepines, and other sedating substances
• Possible physical dependence and withdrawal after repeated exposure
• Unknown long-term neurological and physiological effects
• Unexpected effects caused by unverified product concentrations or additional ingredients
• Possible complications when transitioning between experimental opioids and established treatment medications

These concerns are especially important when a substance is obtained from an unregulated source. Without reliable human pharmacokinetic, toxicological, and clinical data, there is no established basis for predicting what amount of SR-15099 would be safe or how its effects might change when combined with other drugs.

Is SR-15099 Legal After the Federal Ban on SR-17018?

The August 2026 DEA Scheduling Decision and Controlled-Substance Analogue Laws

On August 27, 2026, the Drug Enforcement Administration implemented a temporary Schedule I order covering four synthetic opioids: SR-17018, SR-14968, cychlorphine, and spirochlorphine. This action followed concerns about the public-health risks associated with these compounds and their potential for misuse.

SR-17018 was specifically identified in the order under the chemical name 5,6-dichloro desmethylchlorphine. Its temporary placement in Schedule I means it is subject to federal controlled-substance restrictions, including restrictions on unauthorized manufacture, distribution, and possession.

SR-15099 was not specifically named among the four substances in that order. However, its absence from the list should not be interpreted as confirmation that it is legal to possess, distribute, or consume.

Under federal law, certain substances that are substantially similar in chemical structure and pharmacological effect to Schedule I or II drugs may be treated as controlled-substance analogues when intended for human consumption. Whether those provisions apply to a specific compound or transaction depends on the relevant legal and factual circumstances. Additional state restrictions may also apply.

The DEA’s controlled-substance scheduling guidance specifically explains that a substance does not necessarily have to appear by name on a published list to be subject to federal restrictions.

The official August 27, 2026, scheduling action can be reviewed in the Federal Register.

Can SR-15099 Help With Opioid Withdrawal or Reduce Tolerance?

Separating Experimental Research From Claims About Addiction Treatment

One reason SR-15099 has generated interest is its relationship to research involving SR-17018 and opioid tolerance. Some individuals searching for alternatives to traditional withdrawal management encounter claims that experimental opioid compounds can eliminate withdrawal symptoms or rapidly restore sensitivity to opioids.

Those claims require careful examination because much of the relevant research was performed in animals rather than humans.

A 2020 study published in Neuropsychopharmacology investigated the effects of SR-17018 in mice that had developed tolerance to morphine. Researchers found that substituting SR-17018 could restore certain measures of morphine sensitivity while suppressing withdrawal signs in that experimental model.

These findings generated legitimate scientific interest in the possibility of developing medications that could address opioid dependence differently from existing treatments. However, the study did not demonstrate that SR-17018 could safely treat human opioid withdrawal, and it did not establish SR-15099 as an equivalent substitute.

Later research also demonstrated that SR-17018 could produce tolerance in certain animal pain experiments, despite earlier results showing little tolerance in other tests. This illustrates why findings from one experimental model cannot automatically be applied to every aspect of opioid dependence or long-term exposure.

For SR-15099 specifically, there is no established human clinical protocol demonstrating that it safely prevents opioid withdrawal, reverses tolerance, or treats opioid use disorder. Online experiences cannot substitute for controlled studies because the identity, concentration, previous opioid exposure, and medical histories of the individuals involved are often unknown.

For people struggling with opioid dependence, established medications have substantially stronger clinical evidence. FDA-approved medications for opioid use disorder include buprenorphine, methadone, and naltrexone. These medications are used in different clinical circumstances, and treatment selection depends on the patient’s medical history, current opioid exposure, and recovery needs.

At Brooks Healing Center, medication-assisted treatment is considered as part of an individualized recovery plan rather than relying on unapproved research compounds.

Can SR-15099 Cause Dependence and Withdrawal?

What Is Known About Its Opioid Activity and What Remains Uncertain

Because SR-15099 activates mu-opioid receptors, physical dependence and withdrawal are reasonable clinical concerns. However, there is not enough published human evidence to establish how frequently dependence develops, how long withdrawal lasts, or how its withdrawal profile compares with other opioids.

With established opioid dependence, the body adapts to continued receptor activity. When opioid exposure decreases or stops, symptoms may develop as the nervous system adjusts. Depending on the substance and individual circumstances, opioid withdrawal can involve anxiety, sweating, chills, nausea, diarrhea, muscle aches, restlessness, sleep disruption, and cravings.

These are recognized features of opioid withdrawal generally, not a validated symptom timeline specifically for SR-15099. Its unusual receptor interactions make it particularly inappropriate to assume that withdrawal will follow the same course as a familiar prescription opioid or another research compound.

Someone attempting to discontinue an unidentified or experimental opioid should also consider the possibility of exposure to additional substances. Products obtained through online research-chemical markets may contain unexpected ingredients, and symptoms may reflect more than one compound.

People experiencing repeated withdrawal, increasing dependence, or difficulty stopping should seek a professional assessment. Brooks provides information about precipitated withdrawal and medication initiation, including why transitions involving opioid-receptor-active substances should be medically evaluated rather than managed through unverified online instructions.

Why Are Products Marketed as SR 2.0 Appearing Online?

Research-Chemical Marketing, Unverified Product Claims, and Regulatory Changes

When an emerging substance becomes more widely discussed or faces regulatory restrictions, the market surrounding it can change rapidly. Similar compounds may begin appearing under new names, sometimes accompanied by claims that they represent an improved formula or an alternative to a restricted product.

SR 2.0 is an example of how a consumer-facing product name can create expectations that go beyond the available scientific evidence. The name suggests a progression from SR-17, but there is no clinical evidence demonstrating that commercially marketed SR 2.0 products are more effective, safer, or therapeutically superior.

Another concern involves product authenticity. A website may display a molecular structure, a laboratory report, a certificate of analysis, or packaging that appears professional. None of these elements independently establishes that the material delivered to a consumer contains the advertised compound at the stated concentration.

Terms such as “research grade,” “high purity,” and “pharmaceutical grade” are also frequently misunderstood. These claims do not establish FDA approval or demonstrate that a compound has been manufactured, evaluated, and distributed under the standards required for an approved medication.

Even if a material is accurately identified as SR-15099, that would not establish its safety for human use. Chemical identity and clinical safety are separate questions, and both are important when evaluating experimental substances.

What Are the Signs of a Possible SR-15099 Overdose?

Recognizing Opioid Toxicity When the Substance and Its Effects Are Uncertain

There is no well-established human overdose profile specific to SR-15099. However, because the compound has opioid-receptor activity, serious sedation and breathing problems should be treated as potentially life-threatening rather than dismissed because of claims about its experimental safety characteristics.

Possible warning signs of opioid overdose include:

• Unconsciousness or inability to wake the person
• Slow, shallow, irregular, or absent breathing
• Gurgling, choking, or unusual snoring sounds in an unresponsive person
• Blue, gray, or discolored lips and fingernails
• Severe confusion or loss of consciousness
• Very small pupils, although pupil appearance alone cannot confirm or exclude an overdose

If an opioid overdose is suspected, administer naloxone if available, call 911 immediately, and follow emergency-dispatch instructions. Remain with the person until emergency assistance arrives. The Centers for Disease Control and Prevention recommends treating an uncertain situation as a possible overdose rather than delaying emergency care.

Naloxone can reverse many opioid-related effects, but the degree and duration of reversal for SR-15099 in humans have not been established. Laboratory findings involving related compounds should not be interpreted as proof of a predictable response to naloxone in every exposure.

What Should Someone Do If They Are Already Using SR-15099?

Seeking Medical Assessment Without Relying on Unverified Withdrawal Protocols

People who have already used SR-15099 may be uncertain about what they have taken, whether they are physically dependent, or what could happen if they stop. These concerns are especially important when the substance has been used repeatedly or alongside opioids, alcohol, benzodiazepines, or other medications.

A qualified healthcare professional can assess symptoms, current substance use, relevant medical conditions, and the potential need for supervised withdrawal management. It is important to provide as much accurate information as possible about the product, including its name, packaging, source, frequency of use, and any other substances involved.

Because there are no established human withdrawal protocols for SR-15099, self-directed dosing schedules promoted online should not be treated as medical guidance. Attempting to replace one experimental opioid with another may introduce additional uncertainty rather than resolving an existing dependence.

For someone with a history of opioid use disorder, the broader treatment plan also matters. Withdrawal management may address immediate physical symptoms, but recovery treatment can help address cravings, repeated substance use, co-occurring mental health conditions, and the circumstances contributing to continued use.

Opioid Addiction Treatment at Brooks Healing Center

Medical Detox, Residential Treatment, Medication Assessment, and Continued Recovery Support

At Brooks Healing Center, addiction treatment begins with understanding the individual rather than assuming every opioid or opioid-like substance produces the same symptoms. This is particularly important when someone reports using experimental compounds, concentrated 7-OH products, counterfeit medications, or substances whose actual ingredients have not been verified.

Located in Normandy, Tennessee, between Nashville and Chattanooga, Brooks provides a continuum of addiction treatment designed to address physical stabilization, substance use, behavioral health concerns, and continuing recovery needs.

Depending on the person’s clinical assessment and recommended level of care, treatment may include:

• Medical Detox: Supervised withdrawal management and stabilization based on the individual’s substance use, symptoms, and medical needs.
• Residential Addiction Treatment: A structured treatment environment focused on recovery, evidence-based therapy, and the factors contributing to continued substance use.
• Medication-Assisted Treatment: Individualized evaluation of appropriate medications for opioid use disorder, including buprenorphine-based treatment options when clinically indicated.
• Partial Hospitalization Program (PHP): Continued structured clinical treatment for individuals who need substantial support beyond residential stabilization.
• Sober Living: Supportive recovery housing and peer connection for eligible individuals continuing their recovery journey.

Brooks also addresses appropriate co-occurring mental health concerns through individualized treatment planning. Therapies such as cognitive behavioral therapy and dialectical behavior therapy may help people develop coping skills, manage cravings, recognize triggers, and strengthen recovery-related behaviors.

Experimental opioid research may eventually contribute to new treatment options, but people struggling with dependence today do not have to rely on unapproved compounds or uncertain internet claims. Evidence-based treatment offers established clinical approaches for managing opioid use disorder while addressing the broader needs involved in recovery.

If you or someone you care about is struggling with opioid dependence, 7-OH use, or an experimental synthetic opioid, Brooks Healing Center can help you explore treatment options. Our admissions team can discuss your circumstances, explain available programs, and help determine the appropriate next step.

CALL NOW: 931-486-8824
Verify Your Insurance

Frequently Asked Questions About SR-15099 (SR 2.0)

Is SR-15099 the same thing as SR-17018?

No. SR-15099 and SR-17018 are distinct synthetic opioid compounds with closely related chemical structures. Both have demonstrated unusual mu-opioid receptor activity in experimental studies, but they cannot be assumed to produce identical effects in humans. Their similarities do not establish equivalent dosing, duration, or safety.

Is SR 2.0 stronger than SR-17?

There is insufficient human evidence to determine whether SR-15099 is stronger than SR-17018 in any clinically meaningful sense. Laboratory studies have measured differences in receptor activity, but those measurements do not establish which compound produces greater sedation, pain relief, withdrawal suppression, or other effects in humans. Claims about one being stronger should not be accepted without appropriate evidence.

Does SR-15099 eliminate opioid withdrawal?

There is no controlled human clinical evidence demonstrating that SR-15099 safely eliminates opioid withdrawal. Although research involving SR-17018 has shown withdrawal-suppressing effects in morphine-dependent mice, those findings cannot automatically be transferred to SR-15099 or to people experiencing opioid withdrawal. Neither compound is an FDA-approved medication for opioid use disorder.

Can SR-15099 lower opioid tolerance?

SR-15099 has not been clinically demonstrated to reduce opioid tolerance in humans. Some animal research involving the related compound SR-17018 has explored changes in morphine tolerance, but results vary according to the experimental model. Attempting to manipulate opioid tolerance with unapproved research chemicals may create additional risks, including overdose if someone subsequently returns to a previously tolerated opioid amount.

Can SR-15099 cause withdrawal symptoms?

Dependence and withdrawal are important concerns because SR-15099 activates opioid receptors. However, there are insufficient published human data to establish its specific withdrawal symptoms, frequency, severity, or duration. Someone who has been using the substance regularly should seek medical guidance rather than assuming a withdrawal timeline based on other opioids.

Is SR-15099 legal in the United States?

SR-15099 was not specifically named in the DEA’s August 27, 2026, temporary scheduling order for SR-17018 and three other synthetic opioids. However, that does not establish that SR-15099 is legal. Federal controlled-substance analogue laws may apply to substances intended for human consumption, and additional state laws or restrictions may be relevant. Its legal status should not be inferred from the fact that a website offers it for sale.

Is SR-15099 related to kratom or 7-OH?

SR-15099 is not derived from the kratom plant and is not another name for 7-hydroxymitragynine. It is a synthetic opioid research compound developed through laboratory chemistry. Both SR-15099 and 7-OH interact with opioid receptors, which helps explain why they may appear in similar online discussions, but their chemical structures and available research differ considerably.

Can naloxone reverse an SR-15099 overdose?

There is insufficient human evidence to establish exactly how SR-15099 responds to naloxone during an overdose. However, its opioid-receptor activity makes naloxone an appropriate emergency measure when opioid toxicity is suspected. Give naloxone if available, call 911, and follow emergency instructions. Do not delay treatment because a product was advertised as having reduced respiratory effects.

Will SR-15099 show up on a drug test?

Routine drug screening panels do not necessarily test specifically for every emerging synthetic opioid. Detecting an unusual compound may require specialized laboratory methods, and a negative routine screen does not establish that a product contains no opioid-active substances. Individuals seeking medical care should disclose suspected SR-15099 use even if routine testing does not identify the compound.

Does Brooks Healing Center treat dependence involving experimental synthetic opioids?

Brooks Healing Center provides individualized addiction treatment for opioid use disorder and related substance-use concerns. Individuals reporting use of experimental synthetic opioids can contact admissions for an assessment of their symptoms, medical needs, and available treatment options. Recommendations are based on the individual clinical situation rather than an established SR-15099-specific detox protocol.

Related Resources

Learn More About Emerging Opioid Compounds, Withdrawal, and Drug Safety

• What Is SR-17018? A Look at the Experimental Opioid Compound
• 7-OH Withdrawal: Symptoms, Duration, and What Actually Helps
• What Is Precipitated Withdrawal? Buprenorphine Induction Facts and Treatment Options
• Mitragynine Pseudoindoxyl vs. 7-Hydroxymitragynine: What’s the Difference?
• DEA 7-OH Scheduling Updates and What They Mean for Consumers

Related Treatment Pages

Explore Opioid Addiction Treatment and Recovery Programs at Brooks

• Opioid Addiction Treatment in Tennessee
• Fentanyl Addiction Treatment and Detox
• Kratom and 7-OH Addiction Treatment
• Medical Detox in Tennessee
• Residential Addiction Treatment
• Medication-Assisted Treatment for Opioid Use Disorder
• Partial Hospitalization Program

Sources and References

Peer-Reviewed Research and Government Publications (APA Format)

1. Acevedo-Canabal, A., Grim, T. W., Schmid, C. L., McFague, N., Stahl, E. L., Kennedy, N. M., Bannister, T. D., & Bohn, L. M. (2023). Hyperactivity in mice induced by opioid agonists with partial intrinsic efficacy and biased agonism administered alone and in combination with morphine. Biomolecules, 13(6), 935.
   https://www.mdpi.com/2218-273X/13/6/935
2. Centers for Disease Control and Prevention. (2024). 5 things to know about naloxone.
   https://www.cdc.gov/overdose-prevention/reversing-overdose/about-naloxone.html
3. 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, 91, 55252–55258.
   https://www.federalregister.gov/d/2026-17531
4. Drug Enforcement Administration. (n.d.). Controlled substance schedules. U.S. Department of Justice.
   https://www.deadiversion.usdoj.gov/schedules/schedules.html
5. 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://pmc.ncbi.nlm.nih.gov/articles/PMC6901606/
6. 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://www.sciencedirect.com/science/article/pii/S0028390820305074
7. 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/
8. Stahl, E. L., Schmid, C. L., Acevedo-Canabal, A., Read, C., Grim, T. W., Kennedy, N. M., Bannister, T. D., & Bohn, L. M. (2021). G protein signaling–biased mu opioid receptor agonists that produce sustained G protein activation are noncompetitive agonists. Proceedings of the National Academy of Sciences, 118(48), e2102178118.
   https://pmc.ncbi.nlm.nih.gov/articles/PMC8640941/
9. 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

Medical disclaimer: This article is provided for educational purposes and does not establish the safety or effectiveness of SR-15099 or SR-17018 for human use. Neither compound is an FDA-approved medication for addiction treatment. Individuals experiencing substance-related medical emergencies should call 911.