SR9009 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2026-02-03. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved as a medicine in major jurisdictions | Sold as a research chemical; legal status varies |
| Anti-doping status | Prohibited by the World Anti-Doping Agency | Listed under non-approved substances or related category |
| Typical analytical method | LC-MS/MS | Used for detection and confirmation in biological samples |
| Storage temperature | −20 °C or lower for solid | Desiccated and protected from light |
| Common solution solvents | DMSO; ethanol | Aqueous solubility is limited |
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
SR9009 is often grouped with compounds studied for circadian and metabolic regulation rather than with classical anabolic steroids. Its interactions with nuclear receptors differ from those of androgen receptor ligands, and its proposed mechanisms involve transcriptional control rather than direct hormone signaling. Some sources classify it as a metabolic modulator because of observed effects on energy utilization. The distinction matters for regulation and for interpreting research results across different compound classes.
The central pathways of metabolism described above, such as glycolysis and the citric acid cycle, are present in all three domains of living things and were present in the last universal common ancestor. This universal ancestral cell was prokaryotic and probably a methanogen that had extensive amino acid, nucleotide, carbohydrate and lipid metabolism. The retention of these ancient pathways during later evolution may be the result of these reactions having been an optimal solution to their particular metabolic problems, with pathways such as glycolysis and the citric acid cycle producing their end products highly efficiently and in a minimal number of steps. The first pathways of enzyme-based metabolism may have been parts of purine nucleotide metabolism, while previous metabolic pathways were a part of the ancient RNA world. Many models have been proposed to describe the mechanisms by which novel metabolic pathways evolve. These include the sequential addition of novel enzymes to a short ancestral pathway, the duplication and then divergence of entire pathways as well as the recruitment of pre-existing enzymes and their assembly into a novel reaction pathway. The relative importance of these mechanisms is unclear, but genomic studies have shown that enzymes in a pathway are likely to have a shared ancestry, suggesting that many pathways have evolved in a step-by-step fashion with novel functions created from pre-existing steps in the pathway.
== Medical uses == In many countries (e.g., Australia, the United Kingdom, and Russia) it is commonly used for major depressive disorder. Fluvoxamine is also approved in the United States for obsessive–compulsive disorder (OCD), and social anxiety disorder. In Japan, it is also approved to treat OCD, social anxiety disorder, and major depressive disorder. Fluvoxamine is indicated for children and adolescents with OCD. The NICE guidelines in the United Kingdom have, as of 2005, authorized its use for OCD in adults and adolescents of any age and children over the age of 7. There is evidence that fluvoxamine is effective for generalised social anxiety in adults, although, as with other SSRIs, some of the results may be compromised by having been funded by pharmaceutical companies. Of the SSRIs, however, fluvoxamine, paroxetine, and sertraline do appear consistent as viable treatments for generalised social anxiety. Fluvoxamine is also effective for treating a range of anxiety disorders in children and adolescents, including generalized anxiety disorder, social anxiety disorder, panic disorder, and separation anxiety disorder. The drug works long-term, and retains its therapeutic efficacy for at least one year. The average therapeutic dose for fluvoxamine is 100 to 300 mg/day, with 300 mg being the upper daily limit normally recommended. OCD, however, often requires higher doses; doses of up to 450 mg/day may be prescribed in this case.
==== Hospitalized patients ==== Remdesivir was approved for medical use in the United States in October 2020. The US Food and Drug Administration (FDA) approved remdesivir based on the agency's analysis of data from three randomized, controlled clinical trials that included participants hospitalized with mild-to-severe COVID‑19. The FDA granted approval and reissued the revised EUA to Gilead Sciences Inc. The FDA approved remdesivir based primarily on evidence from three clinical trials (NCT04280705, NCT04292899, and NCT04292730) of 2043 hospitalized participants with COVID‑19. The trials were conducted at 226 sites in 17 countries including the United States. In November 2020, the World Health Organization (WHO) updated its guideline on therapeutics for COVID‑19 to include a conditional recommendation against the use of remdesivir, triggered by results from the WHO Solidarity trial. Meanwhile, the Public Health Agency of Canada's COVID‑19 Clinical Pharmacology Task Group recommended that remdesivir only be administered to hospitalized patients as part of a randomized controlled trial due to limited information on risks and benefits. In January 2022, the Canadian component of the WHO Solidarity Trial reported that in-hospital people with COVID‑19 treated with remdesivir had 17% lower relative risk of death (18.7% versus 22.6% death rates) and 47% reduced relative risk for needing oxygen and mechanical ventilation (8.0% versus 15.0%) compared to people receiving standard-of-care treatments.
Sources: en.wikipedia.org
== Therapeutic research and use == Antimicrobial peptides have been used as therapeutic agents; their use is generally limited to intravenous administration or topical applications due to their short half-lives. As of January 2018 the following antimicrobial peptides were in clinical use:
=== Pharmacodynamics === Prazosin is an α1-blocker that acts as a non-selective inverse agonist at α1-adrenergic receptors, including of the α1A-, α1B-, and α1D-adrenergic receptor subtypes. It binds to these receptors with affinity (Ki) values of 0.13 to 1.0 nM for the α1Α-adrenergic receptor, 0.06 to 0.62 nM for the α1B-adrenergic receptor, and 0.06 to 0.38 nM for the α1D-adrenergic receptor. It has much lower affinity for the α2-adrenergic receptors (Ki = 210–5,012 nM for the α2A-adrenergic receptor, 13–676 nM for the α2B-adrenergic receptor, and 10–257 nM for the α2C-adrenergic receptor). The α1-adrenergic receptors are found in vascular smooth muscle, where they are responsible for the vasoconstrictive action of norepinephrine. They are also found throughout the central nervous system. α1-Adrenergic receptors have additionally been found on immune cells, where catecholamine binding can stimulate and enhance cytokine production.
Certain drugs that have been introduced for uses other than analgesics are also used in pain management. Both first-generation (such as amitriptyline) and newer antidepressants (such as duloxetine) are used alongside NSAIDs and opioids for pain involving nerve damage and similar problems. Other agents directly potentiate the effects of analgesics, such as using hydroxyzine, promethazine, carisoprodol, or tripelennamine to increase the pain-killing ability of a given dose of opioid analgesic. Adjuvant analgesics, also called atypical analgesics, include orphenadrine, mexiletine, pregabalin, gabapentin, cyclobenzaprine, hyoscine (scopolamine), and other drugs possessing anticonvulsant, anticholinergic, and/or antispasmodic properties, as well as many other drugs with CNS actions. These drugs are used along with analgesics to modulate and/or modify the action of opioids when used against pain, especially of neuropathic origin. Dextromethorphan has been noted to slow the development of and reverse tolerance to opioids, as well as to exert additional analgesia by acting upon NMDA receptors, as does ketamine. Some analgesics such as methadone and ketobemidone and perhaps piritramide have intrinsic NMDA action. The anticonvulsant carbamazepine is used to treat neuropathic pain. Similarly, the gabapentinoids gabapentin and pregabalin are prescribed for neuropathic pain, and phenibut is available without prescription. Gabapentinoids work as α2δ-subunit blockers of voltage-gated calcium channels, and tend to have other mechanisms of action as well.
== Early life and education == McGuire was born in Fayetteville, Arkansas, and grew up and graduated high school in Mountain Home, Arkansas. He earned a Bachelor of Arts in chemistry, summa cum laude and with Distinction from Hendrix College in Conway, Arkansas. He received his Doctor of Medicine from the Johns Hopkins University School of Medicine, where he was elected to the Alpha Omega Alpha Honor Medical Society. He completed his internship and residency in internal medicine at the University of Texas Southwestern Medical Center, followed by cardiology fellowship training at Duke University School of Medicine. He was a research fellow at the Duke Clinical Research Institute, where he was Chief Fellow from 1999 to 2000, and earned a Master of Health Sciences degree in clinical research.
Sources: en.wikipedia.org
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.
Laboratories typically use LC-MS/MS to detect SR9009 and related compounds in urine or blood. The method is sensitive but depends on sample collection timing. Confirmatory analysis follows quality-control procedures.
Solid material is generally kept cold, dry, and protected from light. Solutions are often stored in sealed containers at low temperature. Stability beyond recommended periods is not well documented.
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.