YK-11

Overview

YK-11 (also written YK11; sometimes sold as "Myostine") is a synthetic steroid. Despite being marketed — and even WADA-listed — as a "SARM," it is NOT a peptide and, on strict pharmacology, NOT a classic nonsteroidal SARM. Structurally it is derived from 19-norprogesterone and is described as a gene-modified DHT-type steroid: a norpregnadiene steroid with a 17-modification and a methoxy-diene ester. Its molecular formula C25H34O6 contains only carbon, hydrogen and oxygen — no nitrogen — which is the tell-tale of a steroidal scaffold rather than the aryl-propionamide or diaryl scaffold of true nonsteroidal SARMs.

Its muscle-building rationale is unusual: YK-11 acts as a partial agonist of the androgen receptor (AR), but its distinctive effect is to induce follistatin in muscle cells — an effect DHT does not produce — which indirectly suppresses myostatin (GDF-8) signalling. This is why it is loosely called a "myostatin inhibitor," but it does not bind or inhibit myostatin directly (Kanno et al. 2013). It appears on this peptide reference because it is discussed, sold, and stacked alongside peptides in the fitness and "research chemical" community — not because it is one.

Chemistry and structure

YK-11 is a steroid, not an amino-acid chain — its formula contains no nitrogen.

Mechanism of action

• Partial agonism of the androgen receptor (AR). YK-11 binds and partially activates the AR, inducing AR-dependent myogenic differentiation of C2C12 mouse myoblasts comparable to DHT. [In vitro]
• Induction of follistatin — the key mediator. Unlike DHT, YK-11 induces follistatin (Fst) expression in muscle cells. YK-11-driven myogenic differentiation is reversed by an anti-follistatin antibody, which establishes follistatin as the critical mediator of its anabolic signal. [In vitro]
• Indirect follistatin→myostatin axis (not direct myostatin inhibition). The muscle-growth signal is indirect: induced follistatin sequesters/suppresses myostatin (GDF-8) signalling. YK-11 does not bind or inhibit myostatin directly, so the popular "myostatin inhibitor" label is mechanistically loose — the pathway is inferred from the follistatin data, not from direct myostatin-binding assays. [In vitro] / [Hypothesis]
• Upregulation of myogenic regulatory factors. In C2C12 cells YK-11 upregulated MyoD, Myf5 and myogenin more strongly than DHT. [In vitro]
• Steroidal scaffold. YK-11 is structurally a steroid — (17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester — a 19-norprogesterone / gene-modified-DHT-derived steroid, not an aryl-propionamide or diaryl nonsteroidal SARM scaffold. Its formula C25H34O6 has no nitrogen. [In vitro]

Research and evidence

The honest phase framing: preclinical only. All efficacy data are in cultured mouse myoblasts; there are no human efficacy trials, and the only human data are detection/metabolism studies from anti-doping science.

Human evidence in context. There is no human efficacy evidence for YK-11. The AR partial agonism and follistatin-mediated differentiation were shown only in cultured C2C12 mouse myoblasts. The only human data are anti-doping work: a metabolism/elimination study (Piper et al. 2018) and a confirmed detection in an athlete's doping-control sample (Sobolevsky et al. 2024) — evidence of real-world black-market use, not of benefit or safety. Human efficacy for muscle growth is unproven.

Status and regulation

• Regulatory approval: None. YK-11 is not approved by the FDA, the EMA, or any other regulator for any indication, and is not a recognized medicine anywhere. It is a research reagent with no clinical development program and no pharmaceutical sponsor.
• Origin: First characterized in academic work by Yuichiro Kanno and colleagues at Toho University, Japan (2011–2013). There is no pharmaceutical developer or clinical sponsor.
• Anti-doping: Prohibited by the World Anti-Doping Agency (WADA) at all times (in- and out-of-competition), listed under S1.2 (Anabolic Agents) — grouped with "other anabolic agents / SARMs" by regulatory effect, even though it is steroidal by strict pharmacology. WADA is a sport-eligibility axis and is separate from any question of legality.
• Market reality: Outside academic research it is sold only as an unregulated "research chemical" of unknown identity, purity, and potency.

Safety

Documented and expected safety signals (tagged by evidence type):

• Steroidal hepatotoxicity / DILI [Animal / Hypothesis for YK-11 specifically]. Inferred from the steroid structure plus SARM-class DILI reports; there is no YK-11-specific controlled human liver data, so the magnitude and incidence are not quantified.
• HPTA / testosterone suppression [Hypothesis — class/mechanistic inference]. As an androgenic (AR partial agonist) steroid, gonadal-axis suppression is plausible, but there are no controlled human endocrine data for YK-11 specifically.
• FDA class warnings [Human]. The FDA has stated that SARM-marketed products can cause serious liver injury (including acute liver failure), increase heart-attack and stroke risk, and are unapproved drugs — not dietary supplements — with reports of life-threatening, hospitalization-requiring reactions.
• No established safe dose or protocol [Human — absence of data]. There is no human safety, toxicology, reproductive, cardiovascular, lipid, renal, long-term or carcinogenicity data. Adverse effects are characterized only from case reports and structure-based inference. No dosing, "cycle," or post-cycle guidance is given here.

Legal status

How it compares

YK-11 is habitually grouped with SARMs, but the honest framing separates mechanism from marketing:

• Testolone (RAD-140), ligandrol (LGD-4033), ostarine, andarine — these are true nonsteroidal SARMs (nitrogen-containing small molecules) that bind the AR directly. YK-11 differs: it is a steroid whose anabolic signal runs mainly through follistatin induction, and it shares their WADA S1.2 status and lack of approval but not their scaffold.
• Cardarine (GW-501516) and stenabolic (SR9009) — often sold alongside SARMs but are NOT SARMs at all (a PPARδ agonist and a Rev-ErbA agonist, respectively).
• MK-677 (ibutamoren) — frequently grouped with SARMs but is a GH secretagogue / ghrelin agonist, not a SARM.

The decisive point: YK-11 is a preclinical-only steroid, not approved for anything, with no human efficacy data — not a benchmarked, evidence-backed physique therapy. See the Muscle, growth & hormones overview.

Common misconceptions

• "YK-11 is a SARM." Only by marketing and WADA-listing convention. Mechanistically it is a steroid (formula C25H34O6, no nitrogen) that works largely through follistatin induction, not a nonsteroidal AR-modulator scaffold.
• "YK-11 is a peptide." No. It is a synthetic steroid, not an amino-acid chain. It is covered here only because it is discussed and stacked with peptides.
• "It directly inhibits myostatin." No. It induces follistatin, which indirectly suppresses myostatin. YK-11 does not bind or inhibit myostatin directly.
• "Being a 'SARM' means it's liver-safe." No. YK-11 is steroidal and plausibly carries the liver-injury profile of oral anabolic-androgenic steroids. "SARM" does not mean "safe."
• "The muscle benefits are proven in humans." No. All efficacy data are in vitro (C2C12 mouse myoblasts). Human data are limited to doping-detection studies.
• "Buying it as a 'research chemical' means it's clean and correctly dosed." No. Independent testing (JAMA 2017) found most products sold as SARMs were mislabeled, contained a different drug, or contained nothing.

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This entry is educational and summarizes published research and public regulatory information as of the "updated" date above. It is not medical advice, not legal advice, a recommendation, or a guide to obtaining or using any substance.