Stenabolic 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 2026-04-16. Where a claim depends on a specific study, the study is described rather than over-claimed.
Quality control for research materials includes identity confirmation by nuclear magnetic resonance and purity assessment by high-performance liquid chromatography. Mass spectrometry provides molecular weight confirmation and can detect related impurities. Purchasers should request a certificate of analysis that lists lot-specific data. Online products advertised for human use often lack such documentation. Distinguishing legitimate research material from mislabeled or contaminated samples is a recurring challenge in independent testing, and independent laboratories may use orthogonal methods to verify identity.
Detection of SR9009 in biological samples usually relies on liquid chromatography coupled to tandem mass spectrometry. This approach separates the compound from matrix components and identifies it by mass transitions. Because SR9009 can undergo metabolism, laboratories often look for both parent drug and specific metabolites. Sample preparation may involve protein precipitation or solid-phase extraction. Method validation examines sensitivity, carryover, and interference from related substances, and reference standards are required for accurate calibration.
Storage recommendations for SR9009 reference material typically specify a freezer at -20 °C or lower, with protection from moisture and light. Repeated freeze-thaw cycles can degrade small molecules and introduce variability. Stock solutions in dimethyl sulfoxide are often aliquoted to avoid repeated handling. Stability studies may examine degradation under heat, humidity, and light exposure. The compound's thiophene and nitro groups can participate in reactions that alter analytical signals over time, so such changes affect quantitative results.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
| Property | Value | Notes |
|---|---|---|
| Typical storage temperature | -20 °C or lower | Desiccated and protected from light |
| Common analytical method | LC-MS/MS | Detects parent drug and metabolites |
| Solubility class | Lipophilic; soluble in organic solvents | Low aqueous solubility |
| Molecular weight | 437.94 g/mol | Calculated from reported formula |
| Synonyms | SR9009; REV-ERB agonist | Code name used in scientific literature |
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.
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
The amino acids in an α-helix are arranged in a right-handed helical structure where each amino acid residue corresponds to a 100° turn in the helix (i.e., the helix has 3.6 residues per turn), and a translation of 1.5 Å (0.15 nm) along the helical axis. Dunitz describes how Pauling's first article on the theme in fact shows a left-handed helix, the enantiomer of the true structure. Short pieces of left-handed helix sometimes occur with a large content of achiral glycine amino acids, but are unfavorable for the other normal, biological L-amino acids. The pitch of the alpha-helix (the vertical distance between consecutive turns of the helix) is 5.4 Å (0.54 nm), which is the product of 1.5 and 3.6. The most important thing is that the N-H group of one amino acid forms a hydrogen bond with the C=O group of the amino acid four residues earlier; this repeated i + 4 → i hydrogen bonding is the most prominent characteristic of an α-helix. Official international nomenclature specifies two ways of defining α-helices, rule 6.2 in terms of repeating φ, ψ torsion angles (see below) and rule 6.3 in terms of the combined pattern of pitch and hydrogen bonding. The α-helices can be identified in protein structure using several computational methods, such as DSSP (Define Secondary Structure of Protein).
The classic Monod–Wyman–Changeux model (MWC) for cooperativity is generally published in an irreversible form. That is, there are no product terms in the rate equation which can be problematic for those wishing to build metabolic models since there are no product inhibition terms. However, a series of publications by Popova and Sel'kov derived the MWC rate equation for the reversible, multi-substrate, multi-product reaction. The same problem applies to the classic Hill equation which is almost always shown in an irreversible form. Hofmeyr and Cornish-Bowden first published the reversible form of the Hill equation. The equation has since been discussed elsewhere and the model has also been used in a number of kinetic models such as a model of Phosphofructokinase and Glycolytic Oscillations in the Pancreatic β-cells or a model of a glucose-xylose co-utilizing S. cerevisiae strain. The model has also been discussed in modern enzyme kinetics textbooks.
A clinical data management system (CDMS) is a tool used in clinical research to manage the data of a clinical trial. The clinical trial data gathered at the investigator site in the case report form are stored in the CDMS. To reduce the possibility of errors due to human entry, the systems employ various means to verify the data. Systems for clinical data management can be self-contained or part of the functionality of a CTMS. A CTMS with clinical data management functionality can help with the validation of clinical data as well as helps the site employ for other important activities like building patient registries and assist in patient recruitment efforts. The CDMS can be broadly divided into paper-based and electronic data capture systems.
The increasing predominance of the divalent state well before the actinide series concludes is attributed to the relativistic stabilization of the 5f electrons, which increases with increasing atomic number: an effect of this is that nobelium is predominantly divalent instead of trivalent, unlike all the other lanthanides and actinides. In 1986, nobelium metal was estimated to have an enthalpy of sublimation between 126 kJ/mol, a value close to the values for einsteinium, fermium, and mendelevium and supporting the theory that nobelium would form a divalent metal. Like the other divalent late actinides (except the once again trivalent lawrencium), metallic nobelium should assume a face-centered cubic crystal structure. Divalent nobelium metal should have a metallic radius of around 197 pm. Nobelium's melting point has been predicted to be 800 °C, the same value as that estimated for the neighboring element mendelevium. Its density is predicted to be around 9.9 ± 0.4 g/cm3.
== Interactions == When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats. It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans, 5-HTP has never been clinically associated with serotonin syndrome – although a case report suggests 5-HTP can precipitate mania when added to an MAOI. When combined with carbidopa (as a treatment for symptoms of Parkinson's disease), 5-HTP causes nausea and vomiting; however, this can be alleviated via administration of granisetron. Cases of scleroderma-like illness have been reported in patients using carbidopa and 5-HTP. Oral 5-HTP results in an increase in urinary 5-HIAA, a serotonin metabolite, indicating that 5-HTP is peripherally metabolized to serotonin, which is then metabolized. This might cause false positive results in tests looking for carcinoid syndrome. Due to the conversion of 5-HTP into serotonin by the liver, there could be a risk of heart valve disease from serotonin's effect on the heart, as based on preclinical findings. However, 5-HTP has not been associated with cardiac toxicity in humans. It has been suggested that 5-HTP may cause eosinophilia-myalgia syndrome (EMS), a serious condition which results in extreme muscle tenderness, myalgia, and blood abnormalities. However, there is evidence to show that EMS was likely caused by a contaminant in certain 5-HTP supplements.
Sources: en.wikipedia.org
Congressman Gabe Vasquez official U.S. House website Gabe Vasquez for Congress campaign website Biography at the Biographical Directory of the United States Congress Financial information (federal office) at the Federal Election Commission Legislation sponsored at the Library of Congress Profile at Vote Smart Appearances on C-SPAN
=== Biosynthesis === Glutamine synthesis from glutamate and ammonia is catalyzed by the enzyme glutamine synthetase. The majority of glutamine production occurs in muscle tissue, accounting for about 90% of all glutamine synthesized. Glutamine is also released, in small amounts, by the lungs and brain. Although the liver is capable of glutamine synthesis, its role in glutamine metabolism is more regulatory than productive, as the liver takes up glutamine derived from the gut via the hepatic portal system.
=== Dendrimers === Dendrimers are polymeric macromolecules with a branched network similar to a tree structure. Generally, they are spherical and homogeneous. Surface charge and molecule chemistry can play crucial role with drug interaction and release. Poly(amidoamine) (PAMAM) dendrimers are the most commonly used system. A study investigated potential application of dendrimer-based formulation of haloperidol. Intranasal administration showed improved targeting, and solubility as well as high concentrations in the brain. Drugs can be loaded in dendrimers through formulation and nanoconstruct.
Palmitoyl tetrapeptide-7 (Pal-GQPR) is a tetrapeptide that is derived from an amino acid sequence Gly-Gln-Pro-Arg found in the immune system modulator immunoglobulin G, conjugated with a lipophilic palmitoyl chain to enhance skin absorption. Even though it is not derived from connective tissue proteins, it is commonly grouped with the matrikine peptides as it has similar effects in the body in promoting synthesis of collagen, and is claimed to produce anti-aging and anti-wrinkle effects. It also has an additional antiinflammatory action due to inhibition of interleukin 6 production and is used in skin creams.
Sources: en.wikipedia.org
Liquid chromatography-tandem mass spectrometry is a common approach. It can detect the parent compound and its metabolites in biological matrices.
Research samples are typically kept frozen, desiccated, and protected from light. Stock solutions are often aliquoted to reduce freeze-thaw cycles.
High-performance liquid chromatography and nuclear magnetic resonance are standard for purity and identity. Mass spectrometry confirms molecular weight.
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.