REV-ERB agonist comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2026-01-22. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small molecule | Studied as a REV-ERB agonist |
| Molecular formula | C20H24ClN3O4S | Reported for the neutral compound |
| Appearance | Off-white to pale yellow solid | Typical research-grade material |
| Solubility | Sparingly soluble in water | Soluble in solvents such as DMSO |
| Common synonyms | SR9009; Stenabolic | Stenabolic is an informal alias |
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
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.
SR9009 is a synthetic small molecule developed as a REV-ERB agonist. It binds to REV-ERBα and REV-ERBβ, nuclear receptors that help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, the compound alters lipid and glucose handling and influences skeletal muscle oxidative capacity. Its exact effects in humans remain largely uncharacterized because controlled clinical trials have not been reported. The molecule is frequently described in preclinical literature as a metabolic modulator.
=== Toll Holdings === In 1985, Little, along with businessmen Peter Rowsthorn as well as Rowsthorn's son, Mark Rowsthorn, and Lyall McLachlan, led a management buyout team which purchased Toll Holdings which in 1993 listed on the Australian Securities Exchange. Little and his team developed Toll from an 18-truck operation worth $1.5 million, into a $3.8 billion international organisation with 45,000 employees and operations in 50 countries. As a result of his involvement in Toll Holdings, Little has become one of Australia's richest men. Little subsequently further developed his ability to acquire new businesses, buying many between 1989 and 2000. He then began taking over two companies a year until 1997, when Toll paid $145 million for eight TNT businesses. In 2000, it paid $120 million for rival Finemore Holdings. Little also oversaw Toll's investments in technology, wine, rail freight and cargo shipping.
=== Vedolizumab === Vedolizumab is very similar to natalizumab in that it is a humanized IgG monoclonal antibody, but vedolizumab is an IgG1 that specifically blocks the alpha 4 beta 7 integrin that is located primarily on cells in the gastrointestinal tract. It is promoted as being gut specific due to the localization of alpha 4 beta 7 integrin in the gastrointestinal tract and was the first biologic to be made specifically for inflammatory bowel disease.
It is also possible to translate either by hand (for short sequences) or by computer (after first programming one appropriately, see section below); this allows biologists and chemists to draw out the primary amino acid sequence of the encoded protein on paper. First, convert each template DNA base to its RNA complement (note that the complement of A is now U), as shown below. Note that the template strand of the DNA is the one the RNA is polymerized against; the other DNA strand would be the same as the RNA, but with thymine instead of uracil.
Sources: en.wikipedia.org
==== Corneal retention and permeability in topical drug delivery to the eye ==== The majority of ocular therapeutic agents are administered to the eye via the topical route. Cornea is one of the main barriers for drug diffusion because of its highly impermeable nature. Its continuous irrigation with a tear fluid also results in poor retention of the therapeutic agents on the ocular surface. Poor permeability of the cornea and quick wash out of therapeutic agents from ocular surface result in very low bioavailability of the drugs administered via topical route (typically less than 5%). Poor retention of formulations on ocular surfaces could potentially be improved with the use of mucoadhesive polymers. Drug permeability through the cornea could be facilitated with addition of penetration enhancers into topical formulations.
==== Soil fungi ==== Putrescine production in plants can also be promoted by fungi in the soil. Piriformospora indica (P. indica) is one such fungus, found to promote putrescine production in Arabidopsis and common garden tomato plants. In a 2022 study it was shown that the presence of this fungus had a promotional effect on the growth of the root structure of plants. After gas chromatography testing, putrescine was found in higher amounts in these root structures. Plants that had been inoculated with P. indica had presented an excess of arginine decarboxylase. This is used in the process of making putrescine in plant cells. One of the downstream effects of putrescine in root cells is the production of auxin. That same study found that putrescine added as a fertilizer showed the same results as if it was inoculated with the fungus, which was also shown in Arabidopsis and barley. The evolutionary foundations of this connection and putrescine are still unclear.
== Clinical development == The precursor molecule to BOLD-100, KP1339 was tested in a Phase 1 monotherapy clinical trial in heavily pretreated patients with advanced cancers. In this dose escalation study, KP1339 was administered to 46 patients with doses ranging from 20 mg/m2 to 780 mg/m2. KP1339 was well tolerated, with the treatment-emergent adverse events occurring in >20% of patients being nausea, fatigue, vomiting, anaemia and dehydration. These adverse events were mainly grade 2 or lower. In the 38 efficacy-evaluable patients, nine patients achieved stable disease and 1 patient had a durable partial response. 625 mg/m2 was determined to be the recommended Phase 2 dose. BOLD-100 is being tested in a Phase 1b/2a clinical trial in combination with the chemotherapy regimen FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin) for the treatment of gastrointestinal cancers, including gastric, pancreatic, colon and bile duct cancer. This trial includes a dose escalation phase followed by a cohort expansion with 117 patients enrolled. Interim data presented at ASCO GI in January 2024 showed that BOLD-100 + FOLFOX was active and well-tolerated treatment in a heavily pre-treated Stage IV mCRC study population with 36 patients. Progression Free Survival, Overall Survival, and Objective Response Rate demonstrate significant clinical benefit and improvement over the currently available therapies, with minimal treatment emergent neuropathy or significant toxicities.
Another case was that of Ismil bin Kadar, who was initially sentenced to death for a 2005 robbery-murder case in Boon Lay, but eventually acquitted of the crime as the Court of Appeal found that based on the evidence, Ismil was not involved in the case and that it was solely his younger brother Muhammad bin Kadar who was responsible for the robbery and murder; Muhammad was subsequently executed in April 2015. Successful clemency applications are thought to be even rarer. Since 1965, the presidential clemency has been granted seven times to death row inmates, whose sentences were all commuted to life imprisonment (not counting the clemency pleas of the underaged offenders serving TPP). The most recent case was in August 2025, when convicted drug trafficker Tristan Tan Yi Rui was granted clemency by President Tharman Shanmugaratnam, who commuted Tan's death sentence to life imprisonment. Prior to Tan's pardon, the last presidential clemency to be granted was in April 1998, when President Ong Teng Cheong pardoned a 19-year-old death row inmate and convicted murderer Mathavakannan Kalimuthu, commuting his death sentence to life imprisonment. Previously, other than the Court of Appeal, offenders were allowed to file criminal or civil appeals to the Privy Council in London, where the judges could hear their appeals once they exhausted all avenues of appeal in Singapore. This avenue of appeal was fully abolished for all criminal and civil matters in April 1994. One case in which an appeal to the Privy Council was successful was the case of murderer Mohamed Yasin bin Hussin.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.
No. SR9009 is frequently mislabeled as a SARM in online discussions, but it does not target androgen receptors. Its known mechanism involves REV-ERB nuclear receptors and circadian-metabolic gene regulation.
Human clinical data are very limited. There is no approved human use, and safety and efficacy in people are not established. Most evidence comes from preclinical models, so effects observed in animals may not apply to humans.
It is usually detected by LC-MS or HPLC-UV against a reference standard. In biological matrices, metabolite targeting can improve detection. No universal immunoassay is widely available.