NR1D1 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 2026-02-07. 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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
| 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 |
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
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.
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.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
A lotus seed or lotus nut is the seed of plants in the genus Nelumbo, particularly the species Nelumbo nucifera. The seeds are used in Asian cuisine and traditional medicine. Mostly sold in dried, shelled form, the seeds are rich in protein, B vitamins, and dietary minerals.
The thymus (pl.: thymuses or thymi) is a specialized primary lymphoid organ of the immune system. Within the thymus, T cells mature. T cells are critical to the adaptive immune system, where the body adapts to specific foreign invaders. The thymus is located in the upper front part of the chest, in the anterior superior mediastinum, behind the sternum, and in front of the heart. It is made up of two lobes, each consisting of a central medulla and an outer cortex, surrounded by a capsule. The thymus holds immature T cells called thymocytes. Lining cells (epithelial cells) help the thymocytes develop. T cells that successfully develop react appropriately with MHC immune receptors of the body (called positive selection) and not against proteins of the body (called negative selection). The thymus is largest and most active during the neonatal and pre-adolescent periods. By the early teens, the thymus begins to decrease in size and activity and its tissue is gradually replaced by fatty tissue. Nevertheless, some T cell development continues throughout adult life. Thymus abnormalities can result in autoimmune diseases, such as autoimmune polyendocrine syndrome type 1 and myasthenia gravis, and can also decrease the total number of T cells. These are often associated with cancer of thymus tissue, called thymoma, or tissues arising from immature lymphocytes, such as T cells, called lymphoma. Removal of the thymus is called a thymectomy.
== Pharmacology == Volufralin works by increasing expression of the melanocortin MC4 receptor and of its endogenous agonist in the brain. In relation to this, its mechanism of action differs from that of earlier direct melanocortin receptor agonists like bremelanotide. As such, the drug is described as a potential first-in-class medication. Volufralin produces non-acute long-lasting pro-erectile effects in rodents and humans, with short-term dosing resulting in gradually increasing improvement that is then sustained for weeks despite cessation of dosing. The pro-erectile effects of volufralin can be reversed by a melanocortin MC4 receptor antagonist in rodents.
Sources: en.wikipedia.org
== Engineering of 4S pathway enzymes == The desulfurization rate for the wild-type 4S pathway enzymes is low when compared to the rate that needs to be achieved for a viable application in the industrial sector. An increase of 500-fold on the overall rate of the pathway is the required improvement for an efficient application of this biodesulfurization method. Directed evolution, rational design or a combination of both strategies are some of the approaches that have been applied to tackle the lack of catalytic efficiency and stability of the 4S enzymes. The 4S pathway best improvement to date was obtained by a directed evolution approach in which Rhodococcus strains were transformed with a plasmid encoding a modified dsz operon (which encodes for DszA, DszB and DszC). After 40 subculturing events in a medium in which DBT was the sole sulfur source, the modified Rhodococcus strains presented a 35-fold improvement. The strong feedback inhibition of DszC was also tackled by a combination of directed evolution and rational design approach to desensitize DszC to the 4S pathway product, HBP. The bacterial strain expressing the DszC A101K mutant showed higher activity relative to the wild-type strain. Additionally docking of HBP to the protein revealed that HBP forms a π-interaction with Trp327, thus inhibiting DszC. The A101K/W327C (AKWC) double mutant revealed to be desensitized to low HBP concentrations and the bacterial strain expressing the AKWC DszC was 14-fold more efficient than the wild-type strain.
Jesse Bloom (Jay Duplass) is an independent billionaire investor who profited heavily from the COVID-19 pandemic. He owns the hedge fund Crotona Capital and becomes a mentor and tenuous ally to Harper, who admires his maverick investment philosophy. In series 2, Harper meets Jesse while living in a hotel and working remotely, and begins courting him as a Pierpoint client. Jesse first becomes central to Pierpoint’s business through a $3.3 billion block trade in healthcare startup Rican: when anchor investor Felim Bichan withdraws after Harper misses a client meeting, Harper sells the shares to Jesse at the last moment. Acting on Harper’s advice and against Eric’s instructions, Jesse later buys out FutureDawn Partners’ stake in Rican, securing a controlling interest that Eric had promised to Felim. Jesse employs Gus Sackey to tutor his estranged son Leo, and Gus and Leo begin a relationship. Later, on Harper’s recommendation, Jesse enters a short position in brick-and-mortar pharmacy chain FastAide, routed through another bank rather than Pierpoint; when the trade turns against him, he visits Pierpoint to confront Harper, and later abandons a scheduled public speaking appearance after receiving a call from Leo. When Gus leaks to Harper that the government is allowing Amazon to acquire FastAide, Harper alerts Jesse. Jesse then goes on television to publicly criticize the acquisition, reviving regulatory scrutiny and protecting his short position. Gus is fired for the leak but later hired by Jesse as an assistant.
His rare non-comedic film roles include two collaborations with Andre Gregory and Louis Malle: the semi-autobiographical dialogue My Dinner with Andre, and a combined production-and-backstage-drama of Uncle Vanya titled Vanya on 42nd Street. Shawn quite often appears on television, where he has appeared in many genres and series. He has had recurring roles as the Grand Nagus Zek on Star Trek: Deep Space Nine, Stuart Best on Murphy Brown, Jeff Engels on The Cosby Show, Dr. Howard Stiles on Crossing Jordan, Arnie Ross on Taxi, Charles Lester on both The Good Wife and The Good Fight, a reprisal of his role as Mr. Hall on Clueless (based on the film), and Father Frank Ignatius on Evil. He appeared in the 1985 music video for Chaka Khan's "This Is My Night". On February 4, 2010, Shawn appeared as Alan Rubin on The Daily Show with Jon Stewart. A Master Builder opened in New York City in June 2014. In 2018, he joined the cast of Young Sheldon in the recurring role of Meemaw's boyfriend and Sheldon's physics professor, Dr. John Sturgis. Shawn starred in Woody Allen's 2020 film Rifkin's Festival, set in San Sebastián, Spain. Shawn was honored in 2005 with the PEN/Laura Pels International Foundation for Theater Award as a Master American Dramatist.
Sources: en.wikipedia.org
The first performance in Los Angeles in 1954 was introduced with a tribute to Thomas from Aldous Huxley. Thomas spent the last nine or ten days of his third tour in New York mostly in the company of Reitell, with whom he had an affair. During this time, Thomas fractured his arm falling down a flight of stairs when drunk. Reitell's doctor, Milton Feltenstein, put his arm in plaster and treated him for gout and gastritis. After returning home, Thomas worked on Under Milk Wood in Laugharne. Aeronwy, his daughter, noticed that his health had "visibly deteriorated...I could hear his racking cough. Every morning he had a prolonged coughing attack...The coughing was nothing new but it seemed worse than before." She also noted that the blackouts that Thomas was experiencing were "a constant source of comment" amongst his Laugharne friends. Thomas sent the original manuscript to Douglas Cleverdon on 15 October 1953. It was copied and returned to Thomas, who lost it in a pub in London and required a duplicate to take to America. Thomas flew to the States on 19 October 1953 for what would be his final tour. He died in New York before the BBC could record Under Milk Wood. Richard Burton starred in the first broadcast in 1954, and was joined by Elizabeth Taylor in a subsequent film. In 1954, the play won the Prix Italia for literary or dramatic programmes.
Key improvements made after the Union with Ireland Act 1800 (39 & 40 Geo. 3. c. 67) included the illumination of the South Stack Lighthouse in 1809, the construction of a built-up harbour in 1810, and the addition of a substantial breakwater between 1848 and 1873. Although mail service through Holyhead was temporarily suspended in 1838 in favour of rail transport through Liverpool, the development of the north Wales coastal railway in 1850 led to its reinstatement.
==== Proteins ==== Proteins often have groups present on their surfaces that can be ionized or deionized depending on pH, making it relatively easy to change the surface charge of a protein. This has particularly important ramifications on the activity of proteins that function as enzymes or membrane channels, mainly, that the protein's active site must have the right surface charge in order to be able to bind a specific substrate.
== Further reading == D. R. Nässel (2002). "Neuropeptides in the nervous system of Drosophila and other insects: multiple roles as neuromodulators and neurohormones". Progress in Neurobiology. 68 (1): 1–84. doi:10.1016/S0301-0082(02)00057-6. PMID 12427481. S2CID 24447517.
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 a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.