Everything below concerns REV-ERB. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-03-01. Numbers and descriptions here follow the published literature rather than marketing material.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule nuclear receptor ligand |
| Appearance | Off-white to pale yellow solid | Typical for research-grade powder |
| Solubility class | Soluble in DMSO; low water solubility | Common stock solutions use organic solvent |
| Typical stock solvent | Dimethyl sulfoxide | Used for laboratory assays |
| Common analytical method | HPLC with UV or mass detection | Used for identity and purity checks |
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.
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
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 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.
Due to the recent development of many designer drugs, laws banning or regulating their use have not been developed yet, and in recent cases novel drugs have appeared directly in response to legislative action, to replace a similar compound that had recently been banned. Many of the chemicals fall under the various drug analogue legislations in certain countries, but most countries have no general analogue act or equivalent legislation and so novel compounds may fall outside of the law after only minor structural modifications. In the United States, the Controlled Substances Act was amended by the Controlled Substance Analogue Enforcement of 1986, which attempted to ban designer drugs pre-emptively by making it illegal to manufacture, sell, or possess chemicals that were substantially similar in chemistry and pharmacology to Schedule I or Schedule II drugs. Other countries have dealt with the issue differently. In some, the new drugs are banned as they become a concern, as in Germany, Canada, the United Kingdom, and Sweden. In Sweden, the police and customs may also seize drugs that are not on the list of drugs covered by the anti-drug laws if the police suspect that the purpose of the holding is related to drug abuse. Following a decision by a prosecutor, the police may destroy the seized drugs. In Ireland, the Criminal Justice (Psychoactive Substances) Act 2010 bans substances based on their psychoactive effect, and was introduced as a catch-all to address the time lag between new substances appearing and their being banned individually.
=== Florists' attitudes === Many traditional retail florists have a deep-rooted disdain for modern wire services. This comes from the perception that companies such as FTD, 1800flowers, From You Flowers and Teleflora take floral orders away from the local business and extract excessive commission. FTD was formerly a co-op, owned by its member florists. In 1994 the board of directors made the decision to sell the co-op to Perry Capital. The revenue from the sale was disbursed amongst the member florists, more senior florists being paid substantially more than the more junior florists. At this point FTD became a for-profit company.
=== Thermal conductivity === Thermal transport in graphene is a burgeoning area of research, particularly for its potential applications in thermal management. Most experimental measurements have posted large uncertainties in the results of thermal conductivity due to the limitations of the instruments used. Following predictions for graphene and related carbon nanotubes, early measurements of the thermal conductivity of suspended graphene reported an exceptionally large thermal conductivity up to 5300 W⋅m−1⋅K−1, compared with the thermal conductivity of pyrolytic graphite of approximately 2000 W⋅m−1⋅K−1 at room temperature. However, later studies primarily on more scalable but more defected graphene derived by Chemical Vapor Deposition have been unable to reproduce such high thermal conductivity measurements, producing a wide range of thermal conductivities between 1500 – 2500 W⋅m−1⋅K−1 for suspended single-layer graphene. The large range in the reported thermal conductivity can be caused by large measurement uncertainties as well as variations in the graphene quality and processing conditions. In addition, it is known that when single-layer graphene is supported on an amorphous material, the thermal conductivity is reduced to about 500 – 600 W⋅m−1⋅K−1 at room temperature as a result of scattering of graphene lattice waves by the substrate, and can be even lower for few-layer graphene encased in amorphous oxide.
Thyroglobulin (Tg) acts as a substrate for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), as well as the storage of the inactive forms of thyroid hormone and iodine within the follicular lumen of a thyroid follicle. Newly synthesized thyroid hormones (T3 and T4) exist as prohormonal modified tyrosine residues of thyroglobulin, which comprise the colloid within the follicle. When stimulated by thyroid stimulating hormone (TSH), the colloid of the follicular lumen is endocytosed into the surrounding thyroid follicular epithelial cells. When endosomes fuse with lysosomes in these cells, Tg is subsequently cleaved by proteases to release thyroglobulin from its T3 and T4 attachments. Because of the hydrophobic nature of T3 and T4, they are able to then diffuse across the lysosomal membrane and into the cytoplasm. The active forms of thyroid hormone (T3 and T4), are then released into circulation where they are either unbound or attached to plasma proteins. Iodine is recycled back into the follicular lumen where it can continue to serve as a substrate for thyroid hormone synthesis, while the non-modified residues of Tg reenter cellular metabolic pathways.
Sources: en.wikipedia.org
=== Normal tissue and immune expression === ITGA1 (integrin subunit alpha 1; CD49a/VLA1) is expressed across multiple tissue and cellular compartments. When it comes to cells, ITGA1 is expressed in multiple cell types such as epithelial cells, endothelial cells, stromal cells, and immune cells. Among immune cells, ITGA1 is specifically expressed on decidual natural killer (dNK) cells more than peripheral blood NK (pNK) cells. This tissue-specific expression contributes to the specialized functional properties of dNK cells previously stated (regulation of adhesion, migration, and immune activity at the maternal-fetal interface). Reduced expression of CD49 has been observed in dNK cells of patients with recurrent spontaneous abortion, which indicates a disease-associated dysregulation of ITGA1 expression. The molecular regulation of ITGA1 expression within immune cells involves non-coding RNA mechanisms. In human dNK cells, the long non-coding RNA: Inc-49a has been identified as a positive regulator of CD49a expression, influencing CD49a-dependent immune cell migration, adhesion, and cytotoxic regulation.
Propranolol is classified as a competitive non-cardioselective sympatholytic beta blocker that crosses the blood–brain barrier. It is lipid soluble and also has sodium channel-blocking effects. Propranolol is a non-selective β-adrenergic receptor antagonist, or beta blocker; that is, it blocks the action of epinephrine (adrenaline) and norepinephrine (noradrenaline) at both β1- and β2-adrenergic receptors. It has little intrinsic sympathomimetic activity, but has strong membrane stabilizing activity (only at high blood concentrations, e.g. overdose). Propranolol can cross the blood–brain barrier and exert effects in the central nervous system in addition to its peripheral activity. In addition to blockade of adrenergic receptors, propranolol has very weak inhibitory effects on the norepinephrine transporter and/or weakly stimulates norepinephrine release (i.e., the concentration of norepinephrine is increased in the synapse). Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenoceptor activation, with the α1-adrenoceptor being particularly important for effects observed in animal models. Therefore, it can be looked upon as a weak indirect α1-adrenoceptor agonist in addition to potent β-adrenoceptor antagonist. In addition to its effects on the adrenergic system, there is evidence that indicates that propranolol may act as a relatively weak antagonist of certain serotonin receptors, namely the 5-HT1A, 5-HT1B, and 5-HT2B receptors.
=== Cold War === The Soviet biological weapons program began a program focusing on botulinum toxin from 1951 at the Ministry of Defence's Scientific-Research Institute of Hygiene in Sverdlovsk Oblast. The United States biological weapons program possessed botulinum toxin before it was disbanded in 1969. The Iraqi biological weapons program began developing botulinum toxin at its Al Hakum production plant from 1989, the basis for which it originally received among a range of agents from the American Type Culture Collection in 1988.
Soy sauce allergy not caused by soy or wheat allergy is rare. Most varieties of soy sauce contain wheat, to which some people have a medical intolerance. However, protein hydrolysis (fermentation or industrial) breaks down gluten, so some soy sauces may end up tolerable to gluten-intolerant individuals with no detectable gluten left. Japanese tamari soy sauce is traditionally wheat-free, and some tamari available commercially today is wheat- and gluten-free. Acid-hydrolyzed vegetable protein is non-allergenic due to the completeness of protein breakdown.
== The Holocaust == On 6 March 1943, Eva and her parents were transported to the Theresienstadt Ghetto in Terezín, where her father was separated from her and her mother. In Terezín, she worked in agriculture, so she was able to go into the ghetto and managed to make contact with her father. In December 1943, she and her mother were transferred to the Auschwitz concentration camp, where she stayed until June 1944. After six months of horrible conditions at Auschwitz, Eva and her mother were unexpectedly recognized as able to work and were relocated to the Dessauer Ufer camp of the Neuengamme concentration camp in Hamburg, where she experienced better conditions. Her final transport was without her mother to Bergen-Belsen concentration camp in April 1945, which was liberated the same month.
Sources: en.wikipedia.org
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.
It binds REV-ERB alpha and REV-ERB beta and changes the expression of genes tied to metabolism and circadian rhythm. These changes can affect mitochondria and energy use in animal models. The exact chain from receptor binding to physiological outcome is still being mapped.
No reliable human trials show that SR9009 improves athletic performance. Some rodent studies report endurance changes, but these results are not proof of human benefit. Its use in sport is prohibited, and quality and safety data are lacking.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.