YK-11 is a synthetic steroid, sold as a SARM, that has never been tested in any human or animal study of its effects.
Amounts reported for YK-11 are listed under Reported protocols, each with its source and study kind. No amount ladder is inferred from them. This is educational source context, not a protocol or recommendation.
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Human study rows are described per source under Reported protocols; they belong to their trial populations and are not a general amount.
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What published studies and recent community write-ups report about amounts, timing and course length. 2 clinical, 2 preclinical and 1 community-reported rows, each linked to its source. These are descriptions of what others report, not instructions, and nothing here is medical advice.
| Context | Dose | Frequency | Route | Course | Source |
|---|---|---|---|---|---|
| Clinical2 rows | |||||
| The only recorded human administration, an excretion study for doping controlAn elimination study using 6-fold deuterated material, run to identify urinary markers | Single dose of 6-fold deuterated YK11; the amount administered is not stated in the abstract | Single administration | Not stated in the abstract | Urine collected over more than 48 hoursNot applicable | Drug Testing and Analysis2018 |
| Fourteen deuterated urinary metabolites were found, comprising unconjugated, glucuronidated and sulfated forms. No intact compound appeared in urine at all, which tells you the orthoester group on the D-ring is extensively broken down in the body. Unconjugated metabolites disappeared within 24 hours while conjugated ones stayed detectable beyond 48 hours. The paper also records that the compound was identified in a seized black market product, and describes it as an experimental drug candidate not approved for humans. This study measured detection windows, not effect or safety. | |||||
| Reported adverse events for this classAdverse event database entries and case reports for compounds sold as SARMs | Self-reported amounts from unverified consumer products; a survey of 2,269 young male gym users found 2.7% reported SARM use, and this compound was one of the names used to query the adverse event database | Not stated | Oral, as a product bought online | Not stated | European Journal of Clinical Pharmacology2023 |
| This review searched the regulator's adverse event database using the names of each SARM, this one included, and found reports of liver injury alongside visual impairment, cerebrovascular events, abnormal hormone levels and testicular changes. No case series specific to this compound exists, which reflects how little is documented rather than an absence of risk. | |||||
| Preclinical2 rows | |||||
| Muscle cell differentiation, the study the field rests onC2C12 mouse myoblasts in differentiation medium with 2% horse serum, three replicates per condition | 500 nanomolar, against 500 nanomolar dihydrotestosterone and a vehicle control; across a 1 to 500 nanomolar range it needed 100 nanomolar or more to act | Continuous exposure in culture | In vitro | 4 to 7 daysNot applicable | Biological and Pharmaceutical Bulletin2013 |
| Myosin heavy chain protein rose by day 7 under both this compound and dihydrotestosterone, while Myf5 and myogenin transcripts rose further under this compound at day 4. The androgen receptor blocker hydroxyflutamide at 10 micromolar suppressed the effect, confirming it runs through the receptor. Follistatin was induced by this compound but not by dihydrotestosterone, and an anti-follistatin antibody reversed the differentiation, which is the basis of every claim made for it. This is a mouse cell line at a fixed concentration in a dish, not a dose in an organism. | |||||
| Receptor pharmacology, the original descriptionAndrogen response element luciferase reporter assays and MDA-MB-453 human breast cancer cells | Concentrations are reported in the 2011 paper's figures rather than its abstract | Single exposure | In vitro | Not stated | Biological and Pharmaceutical Bulletin2011 |
| This is where the compound was first characterised. It accelerated nuclear translocation of the androgen receptor but did not induce the amino-to-carboxyl terminal interaction, and it prevented dihydrotestosterone from inducing it, which explains its partial agonist behaviour. Its effect varied by gene, so the authors proposed it was a selective androgen receptor modulator. Nothing here concerns muscle, dose or safety. | |||||
| Community-reported1 row | |||||
| The myostatin inhibitor description, checked against sources | Follistatin was induced at 500 nanomolar in one 2013 cell experiment; no published study has measured myostatin under this compound at any dose | Not stated | Described online as an oral myostatin inhibitor | Not stated | Community resource2026 |
| This editorial ledger traced the myostatin claim to its origin and found there is no measurement behind it. What the 2013 paper measured was follistatin induction in mouse myoblasts, and follistatin does bind myostatin among other TGF-beta family members, so the description is an inference from that one observation. Three later papers repeat it in their titles and introductions, which spreads it without testing it. | |||||
The muscle result ran 4 to 7 days in mouse cell culture at a fixed 500 nanomolar concentration. There is no animal study of growth, no toxicology study and no dose-ranging work of any kind, so there is nothing to translate into a schedule for a person.
A single deuterated dose was given so that laboratories could learn what to look for. The compound itself never appeared intact in urine, and its metabolites stayed detectable for more than two days. That is the sum of what has been observed in a person.
Product pages describe weekly milligram amounts, cycle lengths and recovery protocols for this compound. None of those numbers derives from a study, because no study has given it to a person or an animal to measure an effect.
Plus 1 community resource (a dosing guide, forum thread or vendor write-up), reported above but not linked.
YK-11 is a synthetic steroid, sold as a SARM, that has never been tested in any human or animal study of its effects. It is built on a 19-norpregnadiene core and activates the androgen receptor only partially, because it does not induce the amino-to-carboxyl terminal interaction that full agonists need. Everything claimed for its effect on muscle traces to mouse cell culture, chiefly a 2013 experiment in which it induced follistatin and drove myotube differentiation further than dihydrotestosterone did, and the only recorded human administration was a urine excretion study run to build a doping test after the compound turned up in a seized black market product.
These themes describe recurring questions in published research. They are not claims of effectiveness or recommendations for use.
Androgen receptor modulators, myostatin pathways and exercise-mimetic research.
Myosin heavy chain protein rose by day 7 under both this compound and dihydrotestosterone, while Myf5 and myogenin transcripts rose further under this compound at day 4. The androgen receptor blocker hydroxyflutamide.
This is where the compound was first characterised. It accelerated nuclear translocation of the androgen receptor but did not induce the amino-to-carboxyl terminal interaction, and it prevented dihydrotestosterone from.
Fourteen deuterated urinary metabolites were found, comprising unconjugated, glucuronidated and sulfated forms. No intact compound appeared in urine at all, which tells you the orthoester group on the D-ring is.
This editorial ledger traced the myostatin claim to its origin and found there is no measurement behind it. What the 2013 paper measured was follistatin induction in mouse myoblasts, and follistatin does bind myostatin.
This review searched the regulator's adverse event database using the names of each SARM, this one included, and found reports of liver injury alongside visual impairment, cerebrovascular events, abnormal hormone.
Study models remain visible so laboratory and animal findings are not mistaken for established human outcomes.
2 protocol rows on this page come from human trials, trial registrations, regulator labels or reviews of human data. Approval status and populations are stated per row.
2 protocol rows describe animal, cell or toxicology work. Amounts from these rows do not translate to people.
1 row record what blogs, vendor write-ups or forums describe for YK-11. None has been verified against primary literature.
Sequence, synonyms and registry identifiers as recorded in PubChem, the National Library of Medicine's open chemistry database. Formula, mass and CAS number are summarized at the top of the page.
YK11, (17alpha,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester, UNII Z9748J6B0R, DTXSID301107018, DA-59221, EX-A727
KCQHQCDHFVGNMK-PQUNLUOYSA-N
methyl (2E)-2-[(8R,9S,10R,13S,14S,17S)-2'-methoxy-2',13-dimethyl-3-oxospiro[1,2,6,7,8,9,10,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthrene-17,5'-1,3-dioxolane]-4'-ylidene]acetate
6 curated references, each with its journal, year and study model, plus 1 community resource reported but not linked.