Everything below concerns NR1D2. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-02-09. Where a claim depends on a specific study, the study is described rather than over-claimed.
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
Preclinical reports have linked SR9009 to improved endurance and altered energy expenditure in rodents. Such findings have prompted interest in whether REV-ERB activation can influence skeletal muscle metabolism. However, the reported effects depend on dose, route, and experimental model, and replication across laboratories is limited. Human trials have not established comparable outcomes, so claims about exercise performance remain speculative. The absence of controlled human data is a central limitation in interpreting these observations.
The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
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.
=== Proteroglyphous snakes === The effect of the venom of proteroglyphous snakes (sea snakes, kraits, mambas, black snakes, tiger snakes, and death adders) is mainly on the nervous system, respiratory paralysis being quickly produced by bringing the venom into contact with the central nervous mechanism that controls respiration; the pain and local swelling that follow a bite are not usually severe. The bite of all the proteroglyphous elapids, even of the smallest and gentlest, such as the coral snakes, is, so far as known, deadly to humans. However, some mildly venomous elapids remain, such as the hooded snakes (Parasuta), bandy-bandies (Vermicella), etc.
== Organs and tissues affected by IGF-1 == Since many distinct tissue types express the IGF-1 receptor, IGF-1's effects are diverse. It acts as a neurotrophic factor, inducing the survival of neurons. It may catalyse skeletal muscle hypertrophy, by inducing protein synthesis, and by blocking muscle atrophy. It is protective for cartilage cells, and is associated with activation of osteocytes, and thus may be an anabolic factor for bone. Since at high concentrations it is capable of activating the insulin receptor, it can also complement for the effects of insulin. Receptors for IGF-1 are found in vascular smooth muscle, while typical receptors for insulin are not found in vascular smooth muscle.
=== Preclinical === Acne vaccine – immunostimulant ADA-308 – antiandrogen (androgen receptor antagonist) Research programme: acne vulgaris therapeutics - Attillaps Pharmaceuticals – acetylcholinesterase inhibitors
Sources: en.wikipedia.org
Although most species of psilocybin-containing mushrooms bruise blue when handled or damaged due to the oxidization of phenolic compounds, this reaction is not a definitive method of identification or determining a mushroom's potency.
Asparagine endopeptidase (AEP, mammalian legumain, δ-secretase; EC 3.4.22.34) is a proteolytic enzyme from C13 peptidase family which hydrolyses a peptide bond using the thiol group of a cysteine residue as a nucleophile (hence also called cysteine protease). It is also known as asparaginyl endopeptidase, citvac, proteinase B, hemoglobinase, PRSC1 gene product or LGMN (Homo sapiens), vicilin peptidohydrolase and bean endopeptidase. In humans it is encoded by the LGMN gene (previous symbol PRSC1). It hydrolyzes substrates at the C-terminus of asparagine residues. Discovered in 1996 in beans, its homologues have been identified in plants, protozoa, vertebrates, and helminths. The enzyme has been implicated in several human diseases such as cancer, atherosclerosis and inflammation . It can be detected in spleen, liver, brain, testis tissue and heart and the protein is mostly localised to lysosomes and endosomes. It is also interesting that AEP is activated in age-dependent manner.
(i.e. the deviatoric stress in a Newtonian fluid has no normal stress components), and it has a compressibility term in addition to the incompressible case, which is proportional to the shear viscosity:
=== Scientific attempts to quantify the pain of freeze branding === Even though current scientific methodologies cannot adequately distinguish between reflex response and the lay understanding of pain, scientific methods are well suited to comparing two stimuli and making a reasonable assertion as to which is objectively less noxious. Freeze branding has frequently been hailed as a less noxious means of permanently denoting ownership of livestock. Despite this, the claim that freeze branding is inherently less painful than hot branding has been challenged. These challenges provoked scientific studies to determine the matter objectively and they have attempted to measure the pain experienced by animals during and after their branding.
Sources: en.wikipedia.org
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
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.