YK-11
Myostatin inhibitor (SARM-like)
YK-11 (Myostatin inhibitor (SARM-like)) is a gh & growth research compound. Steroidal compound acting partly as a SARM and partly by increasing follistatin, reducing myostatin's brake on muscle.
YK-11 quick facts
| Reported research dose (Oral) | 5-20mg Oral or 10-20mg Inj |
| Route | Oral |
| Frequency | 1x Daily Oral Or 2x Daily Inj |
| Half-life | Short (~hours; oral) |
| Forms | Oral, Injectable |
| Evidence level | In-vitro + anecdotal |
| Other forms available | Injectable — dosed differently |
Harsh on the system for the payoff. Bloodwork non-negotiable if you run it.
How YK-11 works
Steroidal compound acting partly as a SARM and partly by increasing follistatin, reducing myostatin's brake on muscle.
Proposed benefits
Follistatin increase / myostatin reduction for muscle growth (harsh — bloodwork advised).
Where to get YK-11
See vetted vendors for YK-11 →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for YK-11
Graded by what exists behind each claim.
Human clinical evidence
- No human trials: development stopped at preclinical, so the ceiling on any claim here is a rodent model — and these transfer poorly.
📊 Correlative data
- No human trials, no human series, and it is on WADA's prohibited list — which is a statement about detectability and intent rather than safety.
- Community reports describe strength gains alongside the joint discomfort, lipid changes and suppression associated with androgenic compounds. Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 How the mechanism reads
- Usually described as a SARM; structurally it is a steroidal compound — a gene-edited derivative of DHT — which matters because the 'non-steroidal' framing that makes SARMs sound benign does not apply.
- It acts as a partial androgen receptor agonist and is proposed to inhibit myostatin via follistatin induction, based on cell-culture work in myoblasts. That is the entire evidence base — one cell line — and the androgenic activity predicts hepatic and lipid effects that the myostatin story tends to leave out.
Why an empty tier is not a verdict → · What community dosing logs are worth →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What YK-11 actually does
Start with the name, because the name is the mechanism and this site's own card gets the class wrong. YK11 is (17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester Kanno 2011. Read the middle of that: 19-norpregna-4,20-diene-3-one. It is a steroid — a 19-nor steroid nucleus with an orthoester cap bridging C17 and C20 and a methyl ester on the end of the side chain. The word SARM is used for it everywhere, and the reason SARMs are marketed as safer than steroids is that they are non-steroidal. That argument does not apply to this molecule at all.
What it does at the receptor is stranger than the marketing, and more interesting. In an androgen-response-element luciferase reporter, YK11 behaves as a partial agonist of the androgen receptor. It accelerates AR translocation into the nucleus. And then it does something a normal androgen does not: it does not induce the amino/carboxyl-terminal (N/C) interaction, and it prevents DHT-mediated N/C interaction Kanno 2011.
The N/C interaction is the fold in which the receptor's own N-terminal tail docks onto its ligand-binding domain once an agonist is bound; it stabilizes the hormone-receptor complex and is part of how a full androgen signal is assembled. YK11 activates the receptor without it, which the authors read as the reason for the partial agonism, and which leaves transactivation running off the N-terminal domain as a constitutive activator instead Kanno 2011. Two practical consequences follow. The gene set it turns on is not the gene set DHT turns on — the paper says outright that the effect relative to a full androgen varies depending on the gene context in MDA-MB 453 cells. And because it blocks DHT's N/C interaction, in a body already full of androgen it is partly getting in the way.
Now the myostatin claim, which is the reason anyone buys it, and which the primary paper does not make. In C2C12 mouse myoblasts, YK11 drove myogenic differentiation and induced the myogenic regulatory factors MyoD, Myf5 and myogenin more strongly than DHT did. The mechanistic finding was that YK11, but not DHT, induced follistatin, and that the whole differentiation effect was reversed by an anti-follistatin antibody Kanno 2013. Follistatin is a secreted protein that binds and neutralizes activin A and myostatin. So the honest chain is: YK11 → follistatin protein in a mouse cell line → inferred myostatin sequestration. Myostatin itself has never been measured in anything given YK-11, and calling the compound a myostatin inhibitor skips the only step that would justify the word.
The number that does not exist. Neither primary paper publishes a binding affinity for YK11 at the androgen receptor — no Ki, no IC50, no displacement curve against DHT. Every potency statement about this compound in circulation is derived from a reporter-gene readout in transfected cells, which measures transcriptional output rather than occupancy. For a compound sold on the claim that it is stronger than a steroid, the absence of a single affinity constant is the most informative fact about its literature.
Cell, rodent, human — and where it stops
Step one, a reporter plasmid. ARE-luciferase in transfected cells, plus gene-expression work in MDA-MB 453 — a human breast carcinoma line chosen because it is androgen-responsive Kanno 2011. Not muscle. This is where partial agonism, nuclear translocation and the absent N/C interaction were established.
Step two, a mouse muscle cell line. C2C12 myoblasts, with YK11 in the culture medium; MyoD, Myf5 and myogenin induction greater than with DHT, follistatin induced, effect abolished by anti-follistatin antibody Kanno 2013. This is the entire anabolic evidence base for the compound. It is a immortalized mouse myoblast line differentiating in a dish, at a concentration the authors chose, with no circulation, no liver, no androgen background and no load.
Step three, a living animal — once, and not for muscle. The only published in vivo work with YK11 is a mouse study of bacterial sepsis, framing the compound as a preventative health supplement Lee 2021. That is the whole animal record. There is no rodent hypertrophy study, no dose-ranging study, no toxicology study, and no measurement of muscle mass in an animal given YK-11 by any route.
Step four, humans: there is no step four. No phase 1, no maximum tolerated dose, no pharmacokinetics, no safety database, no efficacy endpoint. The compound's entire human record is adverse: a review of published SARM adverse-event reports found 20 reports since 2020, most of them drug-induced liver injury, presenting as cholestatic or hepatocellular injury and jaundice, with the authors noting that data on dosage and purity of the supplements involved are limited Leciejewska 2023; a separate case report and literature review reaches the same place Mohamed 2023.
The obstacles, named one at a time. (1) Follistatin regulation in a mouse myoblast line is not follistatin regulation in adult human muscle, and the experiment that would bridge it — serum follistatin before and after in a person — has never been run even though the assay is a routine ELISA. (2) The receptor result cuts against the user: preventing DHT's N/C interaction Kanno 2011 means that in a man with normal or elevated androgens, YK11 is competing with a full agonist while delivering a partial signal. (3) Because it is a 19-nor steroid, the safety class it belongs to is the one with the best-documented hepatic and lipid liabilities, not the non-steroidal SARM class it is sold inside. (4) Nothing in the record connects any concentration used in C2C12 to any dose in a person, because no pharmacokinetic study of YK-11 exists in any species.
YK-11 pharmacokinetics — how much of it actually gets in
The honest headline: there is no published pharmacokinetic study of YK-11 in any species. No half-life, no oral bioavailability, no Cmax, no metabolite map, no excretion route. The card's “short, roughly hours, oral” is an inference, not a measurement, and everything below is the arithmetic that bounds it rather than data that settles it.
What the structure predicts about the oral route, and it is specific. The molecule carries two hydrolytically labile groups. The first is a methyl ester on the C21 carboxylic acid Kanno 2011; esters of this kind are substrates for carboxylesterases, which are abundant in the intestinal wall, in plasma and in liver, so first-pass hydrolysis to the free acid is the expected fate and the free acid is a different molecule with no published pharmacology at all. The second is the 1-methoxyethylidene bis(oxy) bridge at C17/C20 — a cyclic orthoester. Orthoesters are the textbook acid-labile protecting group: they hydrolyze rapidly below about pH 4. Gastric fluid sits at roughly pH 1.5 to 3.5. An oral capsule therefore presents this molecule to the exact chemistry it is least stable to, and no one has published the gastric-stability experiment that would say how much survives.
Which makes the injectable listing on this card mechanistically interesting rather than merely alternative. Injection bypasses both gastric acid and the intestinal carboxylesterase barrier. If the orthoester really is acid-labile, then oral and injected YK-11 are not two routes for one drug — they are two different exposures, quite possibly to two different molecules. Nobody has compared them, and there is no assay in circulation that would let a user tell.
What the class comparator supplies. 19-nor steroids are cleared hepatically, by cytochrome P450 oxidation and glucuronide conjugation, and the only human data on how a body handles YK-11 is the injury record: cholestatic or hepatocellular patterns with jaundice, across 20 published SARM adverse-event reports since 2020 Leciejewska 2023. A cholestatic pattern is a statement about biliary handling, which is a clearance route. That is the closest thing to human pharmacokinetics this compound has, and it comes from people who were harmed.
What would have to be true, and how you would know it was not
Five predictions with a marker, a direction and a window. Two of them cut against the compound, and the fourth is the one nobody draws.
1. Total Testosterone and LH & FSH should fall, and fast. An androgen receptor agonist in the hypothalamus and pituitary suppresses gonadotropin output; YK11 is an AR agonist that reaches the nucleus Kanno 2011. Draw Total Testosterone, Free Testosterone and LH & FSH at baseline and at 4 weeks. Prediction: LH and FSH fall first, testosterone follows. If nothing moves at all over four weeks, the most likely explanation is not tolerance — it is that the capsule does not contain what the label says, which is a documented problem in this market Leciejewska 2023.
2. The prediction that cuts against it: your estradiol will fall, and it will not be the drug being an anti-estrogen. Draw Estradiol, Sensitive (LC/MS-MS) beside the testosterone. A 19-nor steroid with an orthoester cap has no published aromatase substrate profile, so the expected fall in estradiol is simply the consequence of losing endogenous testosterone — less substrate, less estrogen. Anyone reading dry joints, flat libido and low mood as “the compound working” is reading the signature of induced hypogonadism, and the two are only separable with both numbers on the same draw.
3. Liver, on a schedule, because this is where the human record actually is. A CMP (which carries ALT, AST, bilirubin and albumin) plus GGT at baseline, week 3 and week 6. The published human presentations are cholestatic or hepatocellular injury with jaundice Leciejewska 2023 Mohamed 2023, and a cholestatic pattern shows in GGT and bilirubin before it shows anywhere a person would notice. A rise in bilirubin with a normal-ish ALT is the pattern to stop on.
4. The mechanistic biomarker nobody draws: serum follistatin. The entire anabolic claim rests on YK11 inducing follistatin in C2C12 cells Kanno 2013. Follistatin is secreted, circulates, and is measured by a commercially available ELISA. Baseline and 3 weeks. Prediction: if the mouse-cell mechanism transfers, serum follistatin rises measurably; if it does not move, the marketing claim has failed its own test and whatever the user is feeling is coming from androgen receptor agonism, which is a different and much older drug story.
5. Lipids, which the class does not spare. A Lipid Panel and ApoB at baseline and 6 weeks. Oral 17-modified and 19-nor androgens suppress HDL sharply through hepatic lipase induction. This is reasoned from the class rather than measured on this molecule — no lipid data on YK-11 exist in any species — and it is stated here as an extrapolation, which is exactly what makes it worth measuring.
What nobody has tested yet
Nobody has measured follistatin or myostatin in a human, or any animal, given YK-11. That sentence should end the marketing argument on its own. The compound is sold as a myostatin inhibitor on the strength of a follistatin measurement in a mouse myoblast line Kanno 2013. Twenty people with a baseline and a three-week serum follistatin would produce more information about whether this mechanism exists in people than the entire literature currently contains.
Nobody has run a pharmacokinetic study in any species. One oral dose, one injected dose, serial plasma sampling, LC-MS/MS for parent and for the free acid. That is a single-day experiment which would settle the half-life, the bioavailability and whether the orthoester survives the stomach — three numbers that every person taking this compound is currently guessing.
Nobody has tested the acid stability of the orthoester. Incubate YK-11 in simulated gastric fluid at pH 1.2 for two hours and run the mass spectrum. It is an undergraduate experiment. If the orthoester hydrolyzes, the entire oral market is selling a degradation product, and that is a claim that can be checked before lunch.
Nobody has asked what happens when a partial agonist that blocks the N/C interaction meets a full androgen. Kanno 2011 showed YK11 prevents DHT-mediated N/C interaction in vitro. The obvious extension — YK11 plus a full androgen in the same cells, measuring whether the combination gives more transcriptional output or less — has not been published, and it is the single most relevant experiment for a population that runs this alongside testosterone.
YK-11 — its own safety story, not its class's
There is no safety database for this compound. Not a reassuring one — none. No human has been dosed under observation in a published study, so there is no adverse-event table, no laboratory-abnormality rate, no discontinuation rate and no denominator. Every safety claim made about YK-11 in either direction is an extrapolation from two cell papers and one mouse sepsis model.
What does exist is an injury record, and it is specific. A 2023 review of published SARM-associated adverse events identified 20 reports since 2020, most of them drug-induced liver injury, with the dominant presentations being cholestatic or hepatocellular injury and jaundice; the authors note that limited data are related to the dosages and purity of the products involved, and that no SARM has been approved by the FDA or the European Medicines Agency Leciejewska 2023. A separate case report and review documents the same pattern Mohamed 2023. Those reports span the SARM category rather than YK-11 alone, which is itself the point: the products are usually taken in combination and the purity is usually unknown, so attribution to one molecule is rarely possible.
The structural risk argument, stated plainly. This is a 19-nor steroid Kanno 2011. The risk profile that belongs to it is the steroid profile — suppression of the gonadal axis, hepatic handling, HDL suppression, and the mood and libido changes that follow crushed endogenous hormones — and not the milder profile implied by the non-steroidal SARM label it is sold under. A reader who would not run an oral 19-nor steroid without bloodwork has already decided how to treat this one.
The two practical risks that are not biological. First, identity: this is a research chemical sold without pharmacopeial standards, and the adverse-event literature explicitly flags unknown purity Leciejewska 2023. Second, detection: YK-11 is a prohibited substance in tested sport and analytical methods for it are published, so any tested athlete using it will be caught. Neither of those is a safety statement, and both change the decision.
Sources read for this page
- Kanno Y, Hikosaka R, Zhang SY, Inoue Y, Nakahama T, Kato K, Yamaguchi A, Tominaga N, Kohra S, Arizono K, Inouye Y. (17alpha,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester (YK11) is a partial agonist of the androgen receptor.. Biol Pharm Bull 2011 · PMID 21372378
- Kanno Y, Ota R, Someya K, Kusakabe T, Kato K, Inouye Y. Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression.. Biol Pharm Bull 2013 · PMID 23995658
- Lee SJ, Gharbi A, Shin JE, Jung ID, Park YM. Myostatin inhibitor YK11 as a preventative health supplement for bacterial sepsis.. Biochem Biophys Res Commun 2021 · PMID 33588136
- Mohamed WT, Jahagirdar V, Fatima I, Ahmed MK, Jaber F, Wang K, Hassan A, Ewing E, Clarkston W, Likhitsup A. Selective Androgen Receptor Modulators (SARMs)-Induced Liver Injury: A Case Report and Review of Literature.. Cureus 2023 · PMID 36945289
- Leciejewska N, Jedrejko K, Gomez-Renaud VM, Manriquez-Nunez J, Muszynska B, Pokrywka A. Selective androgen receptor modulator use and related adverse events including drug-induced liver injury: Analysis of suspected cases.. Eur J Clin Pharmacol 2023 · PMID 38059982
YK-11 — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These inhibit myostatin or activin signaling — the brake on muscle growth. Removing a brake the body installed deliberately is the whole premise, and the predicted problems follow from that.
- Myostatin and activin are not muscle-only signals. The same TGF-β family regulates tendon and connective tissue, and the concern that follows is muscle gaining force capacity faster than tendon adapts — predicting tendon and joint injury rather than muscle injury.
- Activin signaling also has roles in reproduction and inflammation, so systemic inhibition has predicted consequences well beyond the muscle the user is aiming at.
What has actually been reported
- Trials of myostatin-pathway drugs have repeatedly shown the dissociation that matters: muscle mass increases without a proportional increase in strength or function. That result recurs across programs and is the main reason several were discontinued.
- Bimagrumab produced muscle gain and fat loss in trials alongside diarrhea and muscle spasms.
- YK-11 has no human trial data at all. It is frequently described as a myostatin inhibitor on the strength of a single cell-culture study.
How to reduce the risk
Same mechanism as the prediction.
- If tendon lags muscle, the answer is loading tendon deliberately — slow heavy resistance work — and not adding load as fast as the new muscle allows.
- Treat rapid strength gain as a reason to be more conservative with progression, not less.
What it does to your bloodwork
A fact about the assay.
- Liver function, especially for the oral compounds in this group. Creatine kinase if you are getting unusual soreness or spasm.
Don't run this if
- You have a history of tendon injury, or you are progressing loading aggressively already.
The honest unknown
- Almost everything. No compound in this group has established long-term human safety, and the consistent trial finding is that mass gained this way has not translated into function.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
YK-11 — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What YK-11 moves on your bloodwork
Expected direction, not a measured one.
- IGF-1 (Insulin-like Growth Factor 1) — ↑ expected to rise
This is the point. IGF-1 rising is the compound doing its job — it is the stable downstream readout of a GH pulse.
What to do: Test it before you start and again at 6–8 weeks. It is the only number that tells you whether the product was real and the dose was enough. - Growth Hormone, Serum — ✕ unreliable here
A random GH level is close to meaningless here. GH is secreted in pulses during deep sleep and sits undetectable between them, so a daytime draw catches a trough almost every time — including when the compound is working perfectly.
What to do: Do not use GH to judge a secretagogue. Read IGF-1 instead. - Fasting Insulin — ↑ expected to rise
GH is a counter-regulatory hormone: it opposes insulin. Fasting insulin and glucose drifting up is the predicted trade-off, not a surprise.
What to do: Check fasting insulin and HbA1c at baseline and again at 8–12 weeks. This is the marker that decides whether you keep running it. - HbA1c (Hemoglobin A1c) — ↑ expected to rise
Same mechanism, longer window — a slow drift rather than a jump.
What to do: Pair it with fasting insulin; either alone can mislead. - Free T4 (Thyroxine) — ↓ expected to fall
GH accelerates the peripheral conversion of T4 to T3, so free T4 can fall while free T3 holds or rises. Read alone it looks like new hypothyroidism, and it usually isn't.
What to do: Run a full thyroid panel rather than TSH alone before concluding anything.
Everything above follows from one fact: these raise GH and therefore IGF-1. Nothing here needs a trial of the specific molecule.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — YK-11 in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside YK-11
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Comprehensive Metabolic Panel (CMP) | Liver. Methylated structure — treat it like an oral steroid, not a peptide |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | SARMs crush HDL, often dramatically |
| Total Testosterone | Suppresses your own production |
| LH & FSH | Confirms the suppression is real |
The Enhanced Athlete — On-Cycle Monitoring panel covers these in one order — 11 markers, $228.15 with the discount applied.
Check results you already have → · All 103 markers A–Z
YK-11 — frequently asked questions
What is YK-11?
YK-11 (Myostatin inhibitor (SARM-like)) is a gh & growth research compound. Steroidal compound acting partly as a SARM and partly by increasing follistatin, reducing myostatin's brake on muscle.
Is the full YK-11 protocol on this page?
The reported research dose is on this page, along with how YK-11 works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of YK-11?
YK-11 has an approximate half-life of Short (~hours; oral), which is part of what determines how often it's dosed.
What forms does YK-11 come in?
YK-11 is available as: Oral, Injectable.
What's the evidence behind YK-11?
Current evidence level: In-vitro + anecdotal. YK-11 is offered for research purposes only and is not an approved medicine.
YK-11 inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What YK-11 is used for
YK-11 appears under 1 goal in the goal router.
Related GH & Growth compounds
Where this goes next
YK-11 is the myostatin arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.