circadian clock 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.
Updated 2026-05-08. Numbers and descriptions here follow the published literature rather than marketing material.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Derived from published structure. |
| Molecular weight | 437.94 g/mol | Calculated value. |
| Appearance | White to off-white solid | Typical for purified research samples. |
| Solubility | DMSO, ethanol; low in water | Class: poorly water-soluble. |
| Typical storage | -20 °C, desiccated, protected from light | Limits degradation. |
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.
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.
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.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
The French censor cut some violent scenes and made the director change the end of his movie which was seen as "too pessimistic". Léo Joannon's film Fort du Fou (Fort of the Mad) /Outpost in Indochina was released in 1963. Another film was The 317th Platoon (La 317ème Section) was released in 1964, it was directed by Indochina War (and siege of Dien Bien Phu) veteran Pierre Schoendoerffer. Schoendoerffer has since become a media specialist about the Indochina War and has focused his production on realistic war movies. He was cameraman for the army ("Cinematographic Service of the Armies", SCA) during his duty time; moreover, as he had covered the Vietnam War he released The Anderson Platoon, which won the Academy Award for Documentary Feature. Graham Greene's novel The Quiet American takes place during this war. In 2011, Vietnamese software developer Emobi Games released a first-person-shooter called 7554. Named after the date 07-05-54 (7 May 1954) which marks the end of the decisive Battle of Dien Bien Phu, it commemorates the First Indochina War from the Vietnamese point of view. The 2017 film by Olivier Lorelle, Ciel Rouge, starring Cyril Descours and Audrey Giacomini, is set during the early part of the First Indochina War.
=== The theory of protein crystallization === Protein crystallization is governed by the same physics that governs the formation of inorganic crystals. For crystallization to occur spontaneously, the crystal state must be favored thermodynamically. This is described by the Gibbs free energy (∆G), defined as ∆G = ∆H- T∆S, which captures how the enthalpy change of a process, ∆H, trades off with the corresponding change in entropy, ∆S. Entropy, roughly, describes the disorder of a system. Highly ordered states, such as protein crystals, are disfavored thermodynamically compared to more disordered states, such as solutions of proteins in solvent, because the transition to a more ordered state would decrease the total entropy of the system (negative ∆S). For crystals to form spontaneously, the ∆G of crystal formation must be negative. In other words, the entropic penalty must be paid by a corresponding decrease in the total energy of the system (∆H). Familiar inorganic crystals such as sodium chloride spontaneously form at ambient conditions because the crystal state decreases the total energy of the system. However, crystallization of some proteins under ambient conditions would both decrease the entropy (negative ∆S) and increase the total energy (positive ∆H) of the system, and thus does not occur spontaneously. To achieve crystallization of such proteins conditions are modified to make crystal formation energetically favorable. This is often accomplished by creation of a supersaturated solution of the sample.
=== Importance === Calciseptine has been shown to specifically inhibit the L-type voltage-gated Ca2+ channels and was the first natural polypeptide discovered with this property. Specific polypeptide inhibitors of voltage-sensitive channels are important tools in research, and were already known for voltage-sensitive Na+ channels, both voltage-sensitive and Ca2+-activated K+ channels, and for N-type Ca2+-channels. Before calciseptine was sequenced and shown to be a specific L-type calcium channel inhibitor, no specific polypeptide inhibitors were known for this type of voltage-gated channels. Specific blockers of the L-type channel were small organic molecules like 1,4-dihydropyridines. It was suggested that polypeptide inhibitors could be found in snake venoms. Calciseptine confirmed this as it was shown to not only block the L-type channels specifically, but also to do this in exactly the same spot as the 1,4-dihydropyridines. After calciseptine, other polypeptides specifically blocking the L-type channels were found as well: FS2, C10S2C2 and S4C8.
Sources: en.wikipedia.org
=== Helix structure === In 1948, Pauling discovered that many proteins included helical (see alpha helix) shapes. Pauling had deduced this structure from X-ray patterns and from attempts to physically model the structures. (Pauling was also later to suggest an incorrect three chain helical DNA structure based on Astbury's data.) Even in the initial diffraction data from DNA by Maurice Wilkins, it was evident that the structure involved helices. But this insight was only a beginning. There remained the questions of how many strands came together, whether this number was the same for every helix, whether the bases pointed toward the helical axis or away, and ultimately what were the explicit angles and coordinates of all the bonds and atoms. Such questions motivated the modeling efforts of Watson and Crick.
== Early life and education == Hagedorn was born in Copenhagen. His father was the captain of a coaster adapted for use as a folk high school ship where aspiring sailors received training in navigation as well as other subjects. Hagedorn attended Hesselager Latin School on Funen. In 1916, he began to study medicine at the University of Copenhagen. During his studies, he worked as an assistant for Carl Julius Salomonsen. He also assisted Christian Bohr.
Fully annexed localities (Auteuil, Batignolles-Monceau, Belleville, Bercy, Charonne, Grenelle, La Chapelle, La Villette, Montmartre, Passy, and Vaugirard): Everything disappeared along with the registers of the Parisian arrondissements—both originals and duplicates. Partially annexed localities (Aubervilliers, Bagnolet, Clichy, Gentilly, Ivry, Montrouge, Neuilly, Pantin, Le Pré-Saint-Gervais, Saint-Mandé, Saint-Ouen, and Vanves) or non-annexed areas (the rest of what is today known as the Petite Couronne): The originals, having been preserved locally, are still accessible in municipal archives unless transferred to the Departmental Archives of Hauts-de-Seine, Seine-Saint-Denis, or Val-de-Marne. The duplicates, however, were destroyed, except for the decennial tables covering 1793–1859.
Sources: en.wikipedia.org
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.
No. SR9009 targets the nuclear receptors REV-ERBα and REV-ERBβ, not the androgen receptor. This mechanism differs from selective androgen receptor modulators and from exercise mimetics that act on PPARδ.
Published evidence is mainly preclinical, using cell cultures and animal models. Controlled human trials are not well documented in the public literature. Claims about human performance or health effects therefore remain unsupported by robust clinical data.
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.