YK-11 results so far: cells, rats and horses, and no human trial

We found no human trial behind any published YK-11 result. YK-11 is a laboratory-made steroid that scientists have described as a selective androgen receptor modulator, or SARM, and every published result we found comes from cell cultures, from rats and mice, or from doping-control work in horses. This article walks through those studies one by one, groups the measured outcomes and the adverse findings by what was actually measured, and sets the compound beside RAD-140 and LGD-4033.

Key takeaways

• YK-11 is a synthetic steroidal compound that Kanno and colleagues described as a novel steroid compound and reported to be a partial agonist of the androgen receptor in cell experiments (Kanno et al., 2011).
• The key follistatin finding, that YK-11 switched on follistatin in C2C12 myoblast cells while dihydrotestosterone did not, comes from cell culture only (Kanno et al., 2013).
• In the sources we reviewed, animal studies of biological effect are limited to a small number of rodent studies, covering bone repair, inflammation in sepsis and brain chemistry (the brain studies reported adverse changes); the horse studies concern detection only.
• We found no human clinical trial of YK-11 in the sources we reviewed, and no human pharmacokinetic or toxicology data.
• Much of the YK-11 literature that does exist is analytical: how to detect the compound and its metabolites in samples for doping control.
• SARMs were added to the World Anti-Doping Agency (WADA) Prohibited List in 2008 (Thevis and Schänzer, 2018), and a 2024 review notes that none has been approved by the FDA or the European Medicines Agency (Leciejewska et al., 2024).
• Free Muscle sells YK-11 as a research compound for laboratory research use only, to customers aged 18 or over. Nothing here is medical advice.
• The measured outcomes are grouped by endpoint in the results section, the main adverse findings are tabulated in side effects, and the evidence type is set beside RAD-140 and LGD-4033 in the comparison.

What is YK-11?

YK-11 (also written YK11, which is the spelling used in several of the original papers) is a synthetic steroid. Kanno and colleagues described it as a novel steroid compound and gave its chemical name as a long 19-norpregnane derivative. The paper refers to the compound by the short name YK11 (Kanno et al., 2011).

It is usually grouped with SARMs. A SARM is a compound designed to bind the androgen receptor, the protein that testosterone and similar hormones act through, and to activate it in a tissue-dependent way. In the doping-control review by Thevis and Schänzer (2018), most of the SARMs named are non-steroidal, and MK-0773 and YK-11 are given as the steroidal examples. Thevis et al. (2017) call YK-11 a steroidal SARM.

The scientific answer to questions about YK-11 is narrower than the name suggests: it has been studied in test tubes, in a handful of rodent studies and in horses for the purpose of detection. We found no report of it being put through a human trial programme.

For a broader introduction to the class, see our 2026 research guide to SARMs.

How researchers think it works

Partial agonism at the androgen receptor

An agonist switches a receptor on. A partial agonist switches it on, but less completely than the natural signal. In a reporter assay, where cells are engineered to glow when the androgen receptor is active, YK-11 behaved as a partial agonist. It also sped up the movement of the receptor into the cell nucleus (Kanno et al., 2011).

The same group reported that YK-11 did not trigger the interaction between the two ends of the receptor protein (the N/C interaction) and blocked that interaction when dihydrotestosterone was present. The authors proposed this as the reason for the partial behaviour. They also reported that YK-11 behaved as a gene-selective agonist in MDA-MB 453 cells (described in the 2022 paper as a human breast cancer line), with its effect on gene expression relative to an androgen agonist varying with the gene context.

Why genes respond differently

A later paper from the same group of authors looked at why. In MDA-MB-453 cells, dihydrotestosterone and YK-11 produced different patterns of target-gene activity and different patterns of androgen receptor binding at gene enhancer regions. A computer docking model suggested that a bulky group on carbon 17 of YK-11 moved helices 11 and 12 of the receptor, and mutation and two-hybrid experiments suggested that different helper proteins were recruited (Kanno et al., 2022). This is a laboratory model of mechanism, not a measurement in a living animal.

YK-11, follistatin and myostatin

The YK-11 myostatin link appears in the wording of some of the papers we reviewed (Lee SJ et al., 2021; Dahleh et al., 2024). Myostatin is described as a negative regulator of muscle mass (Lee SJ et al., 2021). The cell-culture follistatin work (Kanno et al., 2013) and the mouse sepsis study that measured myostatin (Lee SJ et al., 2021) are separate experiments, and no abstract we reviewed shows that follistatin induction by YK-11 accounts for myostatin inhibition or reports a human measurement.

In C2C12 myoblast cells, YK-11 raised the activity of the muscle-differentiation markers MyoD, Myf5 and myogenin more than dihydrotestosterone did. YK-11 also induced follistatin, which dihydrotestosterone did not, and an antibody against follistatin reversed the YK-11 effect on differentiation. The authors concluded that follistatin induction was important to what they called its anabolic effect (Kanno et al., 2013).

The myostatin wording in later papers is the authors' framing. A mouse sepsis study described YK-11 as a myostatin inhibitor (Lee SJ et al., 2021), and a rat paper repeated the idea in its abstract (Dahleh et al., 2024). None of the abstracts we reviewed reports a human measurement of myostatin or follistatin after exposure to YK-11.

Key studies at a glance

The evidence, study by study

To be direct about the central point: no human trial of YK-11 exists in the literature we reviewed. Every YK-11 outcome below describes cells, animals or laboratory samples, in the past tense, and none of it can be assumed to apply to people. The final subsection reports human trials of other compounds, for context only. Where a paper reports a protocol dose, we have not repeated it; the figures are in the linked papers.

Kanno et al., 2011: a novel steroid compound in cell experiments

This study used an androgen-responsive reporter assay and MDA-MB 453 cells. YK-11 activated the androgen receptor only partially, accelerated its movement into the nucleus, and did not induce the N/C interaction. The effect on gene expression relative to a conventional androgen varied with the gene context. The authors suggested it might act as a SARM (PubMed abstract).

Limitations: a single cell line (a breast cancer line per Kanno et al., 2022) and an artificial reporter system. The abstract reports no animal work and no safety assessment.

Kanno et al., 2013: the follistatin finding in C2C12 cells

The researchers treated C2C12 myoblast cells with YK-11 or dihydrotestosterone. The myogenic regulatory factors MyoD, Myf5 and myogenin were induced more strongly with YK-11. Only YK-11 induced follistatin, and an anti-follistatin antibody reversed the YK-11 effect on differentiation. The authors interpreted this as showing follistatin was important to the compound's anabolic effect (PubMed abstract).

Limitations: this was a single cell line grown in a dish. The abstract does not report toxicity, and, as far as the sources we reviewed show, the result has not been independently reproduced in animals or people.

Kanno et al., 2022: why YK-11 behaves differently from dihydrotestosterone

This paper tested the idea that different ligands recruit different partners at the androgen receptor. It combined target-gene measurements, receptor binding at enhancer regions, docking, mutation of a glutamine residue in the receptor and mammalian two-hybrid assays. The patterns differed between YK-11 and dihydrotestosterone, which the authors took as support for differential DNA binding and cofactor recruitment as drivers of gene-selective action (PubMed abstract).

Limitations: a breast cancer cell line and a computational model. It explains mechanism; it says nothing about tolerability.

Yatsu et al., 2018: mouse bone cells

In MC3T3-E1 mouse osteoblast cells, both YK-11 and dihydrotestosterone accelerated proliferation and mineralisation. YK-11-treated cells showed higher osteoprotegerin and osteocalcin, two bone-cell markers, than untreated cells. An androgen receptor antagonist weakened these observations. Phosphorylated Akt rose after YK-11 or dihydrotestosterone, which the authors read as non-genomic signalling through the receptor (PubMed abstract).

Limitations: cells only. Raising a differentiation marker in a dish is not evidence of an effect on bone in a whole organism, and the abstract reports no safety endpoints.

Wang et al., 2025: bone marrow stem cells and a rat skull defect

This group tested YK-11 on bone marrow-derived mesenchymal stem cells (BMSCs) across a range of concentrations. They reported that it promoted osteogenic differentiation, with the effect growing as concentration rose, and that inhibiting the androgen receptor suppressed the effect. In rats with a cranial bone defect, a hydrogel loaded with YK-11 promoted defect repair, again suppressed when the receptor was blocked. The BMP2/Smad pathway was proposed as a mediator (PubMed abstract).

Limitations: the compound was delivered locally in a gel to a skull defect, which differs completely from any oral route. The abstract reports no systemic safety assessment.

Dahleh et al., 2023: oxidative stress in the rat hippocampus

Male Wistar rats were divided into control, YK-11, swimming exercise and exercise-plus-YK-11 groups across a five-week protocol. Molecular docking suggested high affinity for the androgen receptor. In the hippocampus, YK-11 altered the antioxidant system, increased oxidative stress and proteotoxic effects and impaired all of the mitochondrial function markers measured. Exercise alone had a neuroprotective effect. Combining the two prevented changes in some markers, including MnSOD/SOD2 and MTT reduction capacity, but did not reverse the increase in oxidative stress or the mitochondrial respiratory-chain changes (PubMed abstract).

Limitations and adverse findings: adverse findings in rats were increased hippocampal oxidative stress and impaired mitochondrial markers, not fully reversed by exercise. The authors concluded that further research is needed to assess safety and efficacy in humans. Findings in rat brain tissue cannot be translated directly to people.

Dahleh et al., 2024: memory and inflammatory signalling

A second rat study used the same four-group, five-week design. Physiologically based pharmacokinetic modelling suggested YK-11 reached the brain readily. In the hippocampus, YK-11 was associated with impaired consolidation of aversive memory and down-regulation of BDNF/TrkB/CREB signalling, whether or not the animals exercised. It increased the pro-inflammatory cytokines IL-1beta and IL-6 and reduced anti-inflammatory IL-10. Raised p38 MAPK activity and changes in Bax, Bcl-2 and cleaved caspase-3 pointed to an apoptotic cascade. Exercise combined with YK-11 offset some of these changes, such as IL-6, Bcl-2 and cleaved caspase-3 (PubMed abstract).

Limitations and adverse findings: the authors concluded that YK-11 at the anabolic doses they used significantly altered hippocampal neurochemistry and impaired memory consolidation, and said this raised concern about misuse. Rodent memory tests and pharmacokinetic modelling are indirect evidence for human outcomes.

Lee SJ et al., 2021: septic mice

Mice were inoculated with gram-negative bacteria. Muscle myostatin rose alongside follistatin, NF-kappaB, myogenin, MyoD, p-FOXO3a and p-Smad2. When myostatin was inhibited by YK-11, the authors reported lower pro-inflammatory cytokines and organ-damage markers in blood and organs, and lower sepsis mortality (PubMed abstract).

Limitations: this is an acute infection model in mice. The authors suggested potential in sepsis-related muscle wasting, but a single mouse study is a long way from clinical evidence, and the other rodent work above reported harmful changes in brain tissue.

Doping-control papers: detection, not benefit

Thevis and colleagues (2017) synthesised YK-11 with stable-isotope-labelled analogues and mapped how it fragments in a mass spectrometer. The compound protonated readily and lost methanol, acetic acid methyl ester and ketene, and diagnostic ions were identified for the steroid nucleus and the D-ring substituent.

Harding and colleagues (2023) gave YK-11 orally to two horses over a short study. They found the parent compound plus seven phase I metabolites in plasma, and eleven phase I metabolites in urine. In vitro liver incubations produced 79 metabolites with little overlap with what was seen in the animals. The most abundant urinary analytes were a mono-O-demethylated breakdown product and di-O-demethylated YK-11, and two hydroxylated isomers of the breakdown product gave the longest detection time.

So and colleagues (2025) detected YK-11 in horse mane hair after oral administration, primarily through sweat or sebum rather than the bloodstream. A further report describes detection of YK-11 in a doping control sample (Sobolevsky, Kucherova and Ahrens, 2024); PubMed carries no abstract for it, so we cite only its title.

Limitations: these papers answer a question about detection. They report no efficacy or safety endpoints.

Human trials of other SARMs: context, not YK-11

Trials of other SARMs do not apply to YK-11, since each compound has its own chemistry. We include the two controlled trials in our source set to show what a human programme looks like, and what it found alongside its results.

LGD-4033 (a non-steroidal SARM). Basaria et al. (2013) ran a placebo-controlled study in 76 healthy men aged 21 to 50, who were randomised to placebo or one of three ascending LGD-4033 groups for 21 days, with follow-up for five weeks afterwards. The authors reported that lean body mass rose in a dose-dependent way while fat mass did not change significantly. They also reported dose-dependent suppression of total testosterone, sex hormone-binding globulin, HDL cholesterol and triglycerides, with follicle-stimulating hormone and free testosterone suppressed at the highest dose only. Hormones and lipids returned to baseline after treatment stopped. Haemoglobin, PSA, liver enzymes and QT intervals did not change significantly, and adverse events were similar between groups. The study was short, and the authors called for longer randomised trials.

Enobosarm (a non-steroidal SARM). Dalton et al. (2011) ran a 12-week double-blind, placebo-controlled phase II trial in 120 healthy elderly men and postmenopausal women. Total lean body mass rose in a dose-dependent way (P < 0.001 versus placebo for the comparison the abstract reports), and the abstract reports statistically significant improvements in physical function and insulin resistance (P = 0.013 each, versus placebo, for the comparison the abstract reports). The incidence of adverse events was similar between treatment groups. The trial was 12 weeks long and enrolled a specific population, so it cannot show long-term outcomes.

Safety signals and what regulators and doping laboratories say

Clinical and review literature on the SARM class

A systematic review by Vignali and colleagues included 33 studies (15 case reports or case series and 18 clinical trials), covering 2,136 patients of whom 1,447 had been exposed to a SARM. Among the case reports it identified 15 cases of drug-induced liver injury (DILI), one Achilles tendon rupture, one case of rhabdomyolysis and one of mild reversible liver enzyme elevation; two individuals exposed to a different SARM, GSK2881078, in a clinical trial were also reported to have rhabdomyolysis. Elevated ALT was commonly reported in the trials, averaging 7.1% across them (Vignali et al., 2023). The reviewed compounds were SARMs in general; the abstract does not mention YK-11.

Leciejewska and colleagues found 20 published reports of adverse events since 2020, most described as DILI, with cholestatic or hepatocellular injury and jaundice as the main symptoms. They noted limited data on dosages and purity (Leciejewska et al., 2024).

A systematic review of 72 articles estimated that between 1% and 3% of athletes use SARMs. It reported that most online-sourced products were contaminated with other substances, and that the amounts consumed outside trials were much higher than those studied clinically (Vasireddi et al., 2025). The review labelled its own level of evidence as 4. A case report on a different SARM, RAD-140, described liver injury with jaundice in one patient; it is not about YK-11 (Mohamed et al., 2023).

A word on evidence quality: stories shared on forums or social media are anecdotal reports, and anecdotal reports are not evidence. This article relies only on published studies, regulators and anti-doping bodies.

Product quality and stability

A screening study bought 60 supplements from international vendors in 2020. Twenty contained SARMs at high concentrations, with andarine at 7.2% in one product and GW501516 at 3.49% in another. YK-11 and MK-677 were found undeclared in some products. The authors also noted that YK-11 is easily hydrolysed within a few hours and is unstable enough that its protonated ion was not detected, so identification relied on a sodium adduct and fragmentation (Lee JH et al., 2021). The take-home point is analytical: identifying this compound in a sample needs care.

Anti-doping and regulators

SARMs were added to the WADA Prohibited List in 2008, and the review by Thevis and Schänzer (2018) notes that none had received full clinical approval, with YK-11 among the steroidal SARMs covered. A 2024 review notes that none has been approved by the FDA or the European Medicines Agency (Leciejewska et al., 2024).

What the research does not tell us

The evidence hierarchy

One way to read the literature is as a ladder from laboratory studies, through animal studies, to human randomised trials and systematic reviews of them (our framing, not a statement from any cited paper). In the sources we reviewed, the YK-11 ladder has rungs only at the bottom: cell lines, a few rodent experiments and detection chemistry. We found nothing on the human rungs.

Route and formulation

The YK-11 literature is in vitro work (C2C12 myoblasts, MDA-MB 453 and MC3T3-E1 cells), rodent studies and doping-control analysis of urine, plasma and hair. We found no oral bioavailability or human pharmacokinetic data in the sources we reviewed. Results from cell culture, a local gel in a rat skull or analytical samples from horses therefore cannot be assumed to apply to an oral capsule in any species.

Known gaps

• We found no human clinical trial of YK-11 in the sources we reviewed.
• We found no human pharmacokinetic or toxicology data in the sources we reviewed.
• The follistatin finding rests on cell-culture work, and no independent replication in animals or people was found in our sources.
• Rodent studies that did look at the brain reported adverse changes, and nothing in our sources tells us whether those changes would occur in other species.
• Doping-control papers establish how to detect the compound, not whether it is beneficial or harmful.
• Findings on other SARMs, such as LGD-4033 or enobosarm, do not transfer to YK-11.

YK-11 results grouped by what was measured

Grouped by outcome rather than by paper, the YK-11 results in our sources fall into six sets of measurements. None was made in a human being. Where a paper states the protocol dose, that figure is in the linked paper and is not repeated here.

Receptor behaviour (cell lines). In an androgen-responsive luciferase reporter assay, YK-11 switched the androgen receptor on only partially, accelerated its movement into the nucleus and did not induce the N/C interaction; in MDA-MB 453 cells its effect on individual genes varied with the gene context (Kanno et al., 2011). A follow-up in the same cell line observed different enhancer-recruitment patterns from dihydrotestosterone, and mutation and two-hybrid experiments suggested different cofactor recruitment (Kanno et al., 2022).

Muscle-cell markers and follistatin (C2C12 cells). The YK-11 follistatin C2C12 experiment measured key myogenic regulatory factors, including MyoD, Myf5 and myogenin, which rose more with YK-11 than with dihydrotestosterone, plus follistatin, which rose with YK-11 alone; an antibody against follistatin cancelled the differentiation effect (Kanno et al., 2013).

Bone endpoints (mouse osteoblast cells, bone marrow stem cells and a rat skull defect). MC3T3-E1 osteoblasts proliferated and mineralised faster, expressed more osteoprotegerin and osteocalcin, and carried more phosphorylated Akt (Yatsu et al., 2018). In the YK-11 bone study, marrow stem cells differentiated towards bone in a concentration-dependent manner, a YK-11-loaded hydrogel promoted repair of a cranial defect, and inhibiting the receptor suppressed both effects (Wang et al., 2025).

Infection (mice). In mice inoculated with gram-negative bacteria, inhibition of myostatin by YK-11 was reported to lower pro-inflammatory cytokines, organ-damage markers and the death rate from sepsis (Lee SJ et al., 2021).

Metabolites and detection (horses and laboratory samples). The YK-11 horse metabolites study counted the parent compound plus seven phase I metabolites in plasma and eleven in urine from two horses, against 79 metabolites generated by liver incubations in vitro (Harding et al., 2023). A later study found the compound in mane hair, incorporated mainly via sweat or sebum (So et al., 2025).

Adverse results in the same literature. The two rat brain studies are the only YK-11 experiments in our sources that reported adverse effects of YK-11 itself, and both found them. The first recorded increased hippocampal oxidative stress, proteotoxic effects and impairment of every mitochondrial function marker measured (Dahleh et al., 2023). The second recorded impaired consolidation of aversive memory, reduced BDNF/TrkB/CREB signalling, higher IL-1beta and IL-6, lower IL-10 and activation of an apoptotic pathway (Dahleh et al., 2024). In the 2023 study, swimming exercise offset some mitochondrial markers but not the increased oxidative stress or the respiratory-chain changes; in the 2024 study it offset IL-6, Bcl-2 and cleaved caspase-3 changes but not the impaired memory consolidation.

What is missing. There are no YK-11 results from a human trial, no human pharmacokinetic or toxicology data and no long-term animal toxicology in the sources we reviewed. A reading from a dish, a gel placed in a rat skull or a horse urine sample cannot be assumed to apply to an oral capsule in any species, and nothing in this section is a statement about what the compound would do in a person.

YK-11 side effects reported in the research

This table collects the main adverse findings in our sources: the two YK-11 rat studies, the class-level reviews of SARMs, and the human trial and case-report data on other SARMs, which are included only because no YK-11 human data exist. Each row names the population and design so that no finding is read as a statement about people in general.

Case reports can show that an injury followed exposure to a product closely enough for clinicians to suspect a link, and they can describe the pattern of injury, as the liver biopsy in the RAD-140 report did. They cannot show how often an event occurs, because there is no denominator, and they rarely establish what the product contained: Leciejewska et al. (2024) noted limited data on dosages and purity, and Vasireddi et al. (2025) found that most SARM products bought online had been shown to be contaminated with other substances. For YK-11 itself, our sources contain no human case report with an abstract; the Sobolevsky 2024 letter is titled as a detection in a doping control sample and PubMed carries no abstract, so we cannot say more about it.

The gaps are therefore wide. There are no human pharmacokinetic or toxicology data for YK-11, no systematic adverse-event data for the compound itself, and the animal harm data come from two rat brain studies by one research group. Those authors said that their findings highlight the need for further research on safety and efficacy in humans (Dahleh et al., 2023) and that they challenge the common perception that SARMs have minimal side effects (Dahleh et al., 2024). Nothing in this section describes what would happen to any individual, and none of it is medical advice.

YK-11 vs RAD-140 vs LGD-4033: how they differ

Our sources contain no head-to-head trial of any two of these compounds, in animals or in people, so this section compares the type of evidence each one has rather than the size of any effect, and it does not rank them.

Three differences stand out. The first is chemistry: YK-11 is the steroidal member of the trio, while RAD-140 and LGD-4033 are non-steroidal molecules designed to bind the same receptor. The second is the kind of evidence each compound has. RAD-140 and LGD-4033 each have at least one human study in our sources; YK-11 has none. That is a statement about how much is known, not about what the compounds do, and the two human studies are not comparable with each other either: the RAD-140 study enrolled heavily pretreated cancer patients and the LGD-4033 study enrolled healthy men aged 21 to 50, so their adverse-event figures describe different populations and neither tells us anything about YK-11. The third is that, at class level, the anti-doping and approval position is the same for all three in the sources we cite: the same 2008 WADA listing and the same absence of FDA or EMA approval. The UK legislation linked in the next section names none of them.

For the detail on the other two compounds, including their own case-report literature, see the RAD-140 and LGD-4033 articles linked in the last row of the table, where each compound's evidence is summarised on its own terms. This is general information, not legal advice.

Legal and anti-doping status in brief

This section summarises verified statements only. This is general information, not legal advice.

• WADA. SARMs as a class were added to the WADA Prohibited List in 2008 (Thevis and Schänzer, 2018), and that review covers YK-11 among the steroidal SARMs.
• Approval. A 2024 review notes that none has been approved by the FDA or the European Medicines Agency (Leciejewska et al., 2024).
• Legislation. The Human Medicines Regulations 2012 define a "medicinal product" in regulation 2(1), and regulation 46 restricts the sale or supply of unauthorised medicinal products. Article 6 of Regulation (EU) 2015/2283, as it applies in Great Britain, provides in the linked text that only authorised novel foods may be placed on the market in Great Britain. None of these pages names YK-11, so how they apply to any particular product is a legal question we do not answer.

Free Muscle sells its research compounds for laboratory research use only, to customers aged 18 or over, and not for human consumption.

Full breakdown with sources: Is YK-11 legal in the UK?

About the Free Muscle YK-11 listings

Free Muscle sells research compounds and gym apparel online at freemuscle.co.uk. The compound discussed here is listed as a YK-11 research compound listing. Related research compounds are listed in the SARMs collection.

• Batch testing. Every Free Muscle batch of research compounds is assayed for identity and purity by Janoshik Analytical, an independent laboratory. The Certificate of Analysis for a batch is sent on request: email the batch number printed on the label together with the product name. Details are on the lab tests page. If you are new to these documents, read how to read a certificate of analysis, and see what Janoshik Analytical is.
• Delivery. UK delivery is free and tracked, in plain packaging. Standard UK delivery takes 2 to 5 working days, and orders placed before 2pm UK time Monday to Friday are processed the same working day (shipping information).
• Returns. Unopened items in their original packaging can be returned within 30 days (30-day guarantee). Apparel returns are covered by the refund policy.

Research compounds sold by Free Muscle are supplied for laboratory research use only and are not for human consumption. They are not authorised as medicines by the MHRA, EMA or FDA, are not food supplements, and are sold only to adults aged 18 or over. Nothing on this page is medical or dosing advice.

Frequently asked questions

What is YK-11 in simple terms?

It is a synthetic steroid that laboratory researchers have described as a partial agonist of the androgen receptor and, by extension, a SARM (Kanno et al., 2011). It has been studied in cell cultures and a few rodent experiments, and it has been analysed in horses for doping-control purposes.

Is YK11 the same thing as YK-11?

Papers use both spellings. Kanno et al. and several later papers write YK11, and the doping-control papers write YK-11; the Dahleh et al. (2023) abstract gives the same chemical name that Kanno et al. (2011) use for YK11.

Is YK-11 a steroid or a SARM?

Both labels are used. It has a steroid backbone, and the authors proposed it might act as a SARM (Kanno et al., 2011). In the review by Thevis and Schänzer (2018), most of the SARMs named are non-steroidal, and MK-0773 and YK-11 are given as the steroidal examples.

Does YK-11 block myostatin?

Papers use that wording, but one cell-culture finding is that YK-11 raised follistatin in C2C12 myoblast cells (Kanno et al., 2013). A mouse sepsis study also describes it as a myostatin inhibitor (Lee SJ et al., 2021). No human data on either protein were found.

Have there been human trials of YK-11?

No human clinical trial of YK-11 appears in the literature we reviewed, and we found no human pharmacokinetic or toxicology data in those sources. The human trials in this article concern LGD-4033 and enobosarm, which are different compounds.

How do anti-doping laboratories detect YK-11?

Doping-control approaches for SARMs predominantly rely on chromatography hyphenated to mass spectrometry (Thevis and Schänzer, 2018). Published work has mapped the fragmentation of the parent compound (Thevis et al., 2017), identified metabolites in horse urine and plasma (Harding et al., 2023) and found it in horse hair (So et al., 2025).

Has any regulator approved YK-11 as a medicine?

The reviews we cite say that no SARM has received full clinical approval (Thevis and Schänzer, 2018) or FDA/EMA approval (Leciejewska et al., 2024). We found no approval of YK-11.

How does Free Muscle confirm what is in a batch?

Each batch of research compounds is assayed for identity and purity by Janoshik Analytical, an independent laboratory, and the Certificate of Analysis is sent on request when you email the batch number and product name. See the lab tests page for details.

What YK-11 results have been published?

Every published YK-11 result we found comes from cells, rodents or horses. The measured outcomes are receptor activity and gene patterns in cell lines (Kanno et al., 2011), follistatin and myogenic markers in C2C12 cells (Kanno et al., 2013), bone-cell markers and rat skull-defect repair (Wang et al., 2025), inflammatory markers and death rate in septic mice (Lee SJ et al., 2021), metabolites in horse plasma, urine and hair (Harding et al., 2023) and adverse brain changes in rats (Dahleh et al., 2024). The results section groups them by endpoint.

What side effects of YK-11 have been reported?

In rats, the reported adverse effects were increased hippocampal oxidative stress, impaired mitochondrial function markers, impaired memory consolidation and raised inflammatory cytokines (Dahleh et al., 2023; Dahleh et al., 2024). No human adverse-event data specific to YK-11 exist in our sources. The class-level reviews describe case reports of liver injury, tendon rupture and rhabdomyolysis for SARMs in general (Vignali et al., 2023). The side effects table lists the main findings with their populations.

What does YK-11 do, according to the studies?

In the studies, it partially activated the androgen receptor in cell lines (Kanno et al., 2011), induced follistatin in C2C12 myoblasts (Kanno et al., 2013), raised bone-cell markers in mouse osteoblasts (Yatsu et al., 2018), promoted repair of a skull defect in rats when delivered in a gel (Wang et al., 2025), lowered the death rate in septic mice (Lee SJ et al., 2021), and produced oxidative stress (Dahleh et al., 2023) and memory impairment (Dahleh et al., 2024) in the rat hippocampus. What it does in a person has not been measured in any published trial we found, so the honest answer stops at the animal and cell data.

How does YK-11 compare with RAD-140?

They differ in chemistry and in evidence. YK-11 is steroidal and has no human study in our sources; RAD-140 is non-steroidal (Miller et al., 2011) and has a first-in-human phase 1 study in 22 women with metastatic breast cancer in which raised liver enzymes were the most frequent adverse events (LoRusso et al., 2022). There is no head-to-head trial, so no comparison of effect is possible. See the comparison section, which links our RAD-140 article.

Is YK-11 legal in the UK?

The sources we can cite do not give a yes or no. The reviews say that no SARM has FDA or EMA approval (Leciejewska et al., 2024), and the Human Medicines Regulations 2012 and the retained novel foods regulation are linked in the legal section above; none of those pages names YK-11. Our YK-11 UK guide goes through the legislation, the anti-doping position and what a research use only label means. This is general information, not legal advice.

Does YK-11 show up in anti-doping tests?

Doping-control laboratories test for SARMs in blood and urine, and the mass-spectrometric signature of YK-11 was characterised for that purpose (Thevis et al., 2017). Equine studies identified the metabolites with the longest detection time (Harding et al., 2023), and a 2024 letter is titled as reporting detection of YK-11 in a doping control sample (Sobolevsky et al., 2024). Anyone subject to anti-doping rules should read the current WADA Prohibited List and their own anti-doping body's guidance directly.

Does this article give doses or protocols for YK-11?

No. This article deliberately leaves out the protocol doses used in the cell and animal studies; those figures are in the linked papers. The compound is sold for laboratory research use only, to customers aged 18 or over, and it is not for human consumption. Nothing on the site or in this article is medical advice.

Related reading

• Short overview: YK-11: a steroidal compound sold as a SARM, what is actually known

Sources

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23. Human Medicines Regulations 2012 (SI 2012/1916): regulation 2; regulation 46. Regulation (EU) 2015/2283 (as it applies in Great Britain),Article 6.