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Compact view
Research pass: medium Compound SKIP-FOR-NOW HIGH

YK-11

Extended Research
High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

◈ Extended Research ◈

Our depth — beyond the mirror

Deeper analysis, verdict reasoning, and per-archetype recommendations from our research team.

▸ Editor's verdict SKIP-FOR-NOW HIGH

ZERO human RCTs (more thinly studied than even RAD-140 which at least has a halted Phase 2 breast cancer program); evidence base is in vitro / cell-line / one rat hippocampus study. 17α-methyl group puts YK-11 in the "structurally hepatotoxic" class alongside oral 17α-alkylated AAS (anadrol, dianabol, winstrol, methyltestosterone) — community reports and the SARM hepatotoxicity literature consistently flag YK-11 as the most liver-aggressive SARM. HPG suppression is reported as severe (more aggressive than RAD-140 in community bloodwork). Class is genuinely contested in the published literature — some pharmacologists call this a steroid, not a SARM. Sourcing reliability is among the worst in the SARM class because YK-11 is harder to synthesize than the non-steroidal SARMs and the JAMA-2017-style label-accuracy data have not been replicated for YK-11 specifically; assume product identity is unverifiable. WADA-banned, FDA-prohibited, untested in humans, structurally hepatotoxic, severely suppressive — the user is a 20yo MMA athlete with peak natural HPG axis and a brain-priority #1 stack; YK-11 attacks every priority. Verdict would not change pre-25 absent unforeseen indication; would not change post-25 either without (a) a published Phase 1 human safety study, (b) verified COA-tested pharmaceutical-grade source, and (c) clear anabolic deficit not addressed by less-aggressive options. None of those conditions are foreseeable.

Research pass: medium
▸ Decision matrix by user profile Per-archetype
  • ★20-30, brain-priority, peak natural HPG axis (this-archetype)
    SKIP-AT-

    Zero human safety data + structural hepatotoxicity + severe HPG suppression + rat hippocampus oxidative-stress signal directly attacking the brain-priority #1 ranking + worst-in-class sourcing reliability + WADA ban (regardless of testing status, contamination cross-positives are real) + zero anabolic deficit at 20 + brain-development window concerns. The body-comp upside doesn't approach the threshold required.

  • 20-30, dedicated competitive lifter, untested division, accepts research-chem risk
    SKIP-FOR-NOW

    Within the SARM class, RAD-140, LGD-4033, and ostarine all have better evidence bases and cleaner safety profiles. YK-11 is the wrong tool even if a SARM is on the table.

  • 30-50, executive maintenance, normal T
    SKIP

    no indication, hepatic + endocrine risk on a cardiovascular-aging curve.

  • 30-50, age-related sarcopenia, low-normal T, advanced lifter, post-25, has tried less aggressive options, COA-verified source
    SKIP-FOR-NOW

    as default; informed-user OPTIONAL-ADD only with comprehensive bloodwork infrastructure (LFTs week 4 and week 8, lipids week 6, full hormone panel +4/+8/+12 post-cycle), pharmaceutical-grade source confirmation, and explicit acknowledgment of zero human safety data. Even at this point most informed lifters would step UP to TRT-base testosterone before stepping SIDEWAYS into YK-11.

  • 50+, sarcopenia
    SKIP

    TRT or pharmaceutical-grade options dominate.

  • Anxiety-prone
    SKIP

    irritability + cycle-end mood crash worsens anxiety baseline.

  • Tested athlete (WADA, USADA, NCAA, professional combat sport)
    SKIP-PERMANENT

    S1.2 banned; multi-week detection window; contamination-driven false-positive pathway exists.

  • High athletic load, untested status (the user's combat-sport profile)
    SKIP-AT-

    same as primary archetype. Combat-sport training load doesn't invert the calculus; BPC-157 + TB-500 + sleep + protein cover recovery without HPG hit and without hepatic load.

  • Sleep-disordered
    SKIP

    sleep disruption common during cycle, recovery harder.

  • Recovery-focused (post-injury, post-illness)
    SKIP

    peptide-based recovery (BPC-157/TB-500) is mechanism-aligned and safer.

  • Strength/anabolic-focused, non-competitive, post-25, accepts research-chem risk
    SKIP-FOR-NOW

    as default; only consider after exhausting cleaner options.

▸ Subjective experience (deep)

Per biohacker community reports at typical 10-15 mg/day oral protocols (no clinical-trial dose reference exists):

  • Week 1-2: Many users report nothing perceptible early; some report mild aggression/drive increase, modest libido shift (up or down), headaches.
  • Week 3-5: Body-comp shift becomes visible — lean mass increase + recomposition described as "stronger feel than ostarine, comparable or harsher than LGD-4033, less euphoric than RAD-140 but more visibly anabolic." Joint comfort reports mixed (some lifters report dryness, others report no change). Fatigue and irritability reported in a meaningful subset.
  • Week 5-8: Strength and lean mass continue to compound; suppression-related symptoms (libido drop, mood lability, lethargy) more common in this window. Hepatotoxicity warning signs (right-upper-quadrant discomfort, dark urine, pruritus, jaundice in severe cases) reported in the case-report literature and forum logs.
  • Cycle end / PCT: Often described as the harshest SARM crash. Libido and morning-erection collapse, mood drop, energy crater, motivation loss. PCT (clomiphene or enclomiphene) recovery routinely reported as taking 8-16 weeks vs. 4-8 for ostarine or LGD-4033. A non-trivial subset of forum users report incomplete recovery requiring prolonged SERM treatment or HCG mono restart.
  • Vs. other SARMs: Users with prior ostarine or LGD-4033 experience consistently rate YK-11 as harsher on suppression, harsher on liver feel, and roughly equivalent or stronger in body-comp output. Users who try YK-11 as a first SARM frequently regret it.

Reality check: Subjective reports are unmonitored, unblinded, and self-selected toward severe presentations on the negative side and successful cycles on the positive side. The structural hepatotoxicity argument plus the limited but consistent forum-bloodwork pattern plus the rat hippocampus oxidative-stress data form a coherent picture: this compound is harsher than the cleaner SARMs and the user community treats it accordingly with TUDCA, NAC, and aggressive PCT planning.

▸ Tolerance + cycling deep dive
  • Tolerance buildup: Not classical pharmacological tolerance — the mechanism is AR transactivation, not receptor-internalizing-style downregulation. The cycling rationale is cumulative endocrine and hepatic damage, not loss of effect.
  • Recommended cycle (community convention): 6-8 weeks on, 12-16+ weeks off (the longer washout vs. ostarine/LGD-4033 reflects the harsher HPG suppression and slower recovery).
  • Reset protocol if needed: Discontinue. Full SERM-based PCT (clomiphene or enclomiphene 4-6 weeks) ± HCG kickstart (250-500 IU 2-3×/week × 1-2 weeks). Bloodwork at +4, +8, +12 weeks post-cycle to confirm HPG recovery before any subsequent use. Liver enzymes at +4 and +8 weeks to confirm normalization.
  • Re-cycling: Should be approached with extreme caution. Cumulative hepatic load and the possibility of incomplete HPG recovery from prior cycles warrant longer washouts and full bloodwork confirmation of baseline restoration before any second cycle.
▸ Stacking deep dive

Synergistic with

  • None recommended. Stacking SARMs (e.g., YK-11 + RAD-140 or YK-11 + LGD-4033) is common in bodybuilding circles but multiplies HPG suppression and hepatic load with no proven additive efficacy. For an athlete who shouldn't be on this in the first place, "synergy" framing is misleading — but for completeness, the only co-administered substances with a defensible role are:
  • TUDCA (250-500 mg/day), NAC (1200-1800 mg/day), milk thistle (200-400 mg/day) — hepatoprotective stack run prophylactically; genuinely useful for hepatic load mitigation though they don't eliminate the risk.
  • Creatine + adequate protein (≥1.6 g/kg) — independent additive lean-mass support, no pharmacological collision.
  • Omega-3 (fish oil) high-dose (≥3 g EPA+DHA/day) — partial offset of HDL crash and lipid derangement; doesn't reverse it.
  • Vitamin D + zinc + magnesium (the user's V's stack already) — supports endogenous T axis during PCT recovery.

Avoid stacking with

  • Other SARMs (LGD-4033, RAD-140, ostarine, S-23, andarine): Compounding HPG suppression and hepatic load; no proven additive efficacy.
  • 17α-alkylated oral AAS (anadrol, dianabol, winstrol, oxandrolone, methyltestosterone): Structural hepatotoxicity stacking — this is the worst of the worst combinations. YK-11's 17α-methyl group plus another 17α-alkylated compound multiplies the cholestatic-hepatitis risk pattern.
  • Other 17α-alkylated SARMs / prohormones: Same logic.
  • Hepatotoxic medications/supplements: Acetaminophen ≥3 g/day chronic, isoniazid, methotrexate, high-dose niacin, kava, high-dose curcumin extracts, DMAA. Additive liver risk.
  • Heavy alcohol: Liver-load compounding (the user is zero-alcohol — non-issue, but flagged generically).
  • Concurrent VEGF inhibitors: Mechanism-irrelevant; flagged for completeness.
  • Other research-chem compounds with unknown contamination profiles: Multiplies counterfeit risk.

Neutral / safe co-administration

  • Most non-hormonal nootropics in the user's V stack: modafinil, citicoline, alpha-GPC, theanine, rhodiola, beta-alanine. No documented interactions.
  • DHA, magnesium, fish oil, vitamin C — no interaction.
  • Caveat: This is "neutral co-administration" for those substances. It does NOT make YK-11 itself safe.
▸ Drug interactions deep dive
  • CYP3A4 substrate (assumed, by structural analogy): No human PK data. By structural analogy to other 17α-methylated steroids, hepatic CYP3A4 metabolism is presumed; inducers (rifampin, carbamazepine, St. John's Wort) may reduce exposure; inhibitors (azole antifungals, macrolides, grapefruit) may elevate it. Clinically uncharacterized.
  • Hepatobiliary drugs: Anything cleared by the liver gains additive hepatic load; statins potentially additive on LFTs.
  • SERMs used in PCT (clomiphene, tamoxifen): CYP2D6 substrates — relevant for CYP2D6 PMs.
  • Hormonal contraceptives (relevant for female users): SARMs disrupt menstrual cycle and contraceptive efficacy unpredictable; not relevant-to-archetype.
  • Anti-doping: WADA S1.2 (Other Anabolic Agents — SARMs) — full ban, in- and out-of-competition. Detection window via glucuronidated metabolites >48h, with longer-term metabolites identified in Piper 2018 work likely extending detection to multi-week range.
▸ Pharmacogenomics
  • AR CAG repeat length: Shorter CAG repeats (<22) correlate with higher AR transactivation efficiency; may modulate YK-11 response magnitude — completely unstudied for YK-11 specifically.
  • CYP3A4 polymorphisms: Plausibly affect YK-11 clearance (no data).
  • UGT polymorphisms: May affect glucuronidation rate of YK-11 metabolites — relevant for both detection-window prediction and possibly toxicity (no data).
  • CYP2D6 PMs: Relevant for clomiphene-based PCT efficacy, not YK-11 itself.
  • Practical: No genotype currently used to dose YK-11 clinically; no clinical use exists.
▸ Sourcing deep dive
Path Vendor Cost Reliability Notes
US Rx None N/A N/A Not FDA-approved. No legal pharmaceutical source anywhere.
FDA-prohibited "supplement" channel Various pre-warning brands N/A very low FDA bodybuilding-products consumer warning names YK-11 as a banned ingredient. Sale in supplements is FDA-actionable.
Research-chem vendor Chemyo, Sports Technology Labs, Behemoth Labz, Loti Labs, etc. $40-90 / 30 mL @ 5-10 mg/mL low (worst-in-SARM-class) "For research purposes only" labeling. YK-11 is harder to synthesize than non-steroidal SARMs, raising counterfeit/substitution risk. Independent testing of "YK-11" liquids has identified RAD-140, methylstenbolone, or no active compound at varying rates. COA verification with third-party HPLC + MS is necessary but not sufficient — assume product identity is unverifiable in any single lot.
International / Indian / Chinese pharmacy Various $30-80 / cycle low API quality varies; counterfeit risk; legality murky outside source country.

FDA status (current): Prohibited in dietary supplements. YK-11 is named in FDA bodybuilding-products consumer advisories. Not DEA-scheduled. Research-chem "for research use only" sale exists in legal gray zone but is FDA-actionable when sold for human consumption.

Sourcing reliability is materially worse than for ostarine, LGD-4033, or RAD-140. The compound is structurally complex and harder to synthesize; independent forum testing patterns suggest substitution and adulteration are more common than for the better-established SARMs. The Cohen 2017 JAMA SARM-product label-accuracy study (52% accurate label, 39% no SARM, 9% wrong SARM, 25% banned substances) did not include YK-11-specific testing — assume the actual rate of mislabeling for YK-11 is at least as bad and likely worse.

▸ Biomarkers to track (deep)
  • Baseline (before starting): Total testosterone (LC-MS/MS), free T, SHBG, LH, FSH, sensitive E2, prolactin, full lipid panel (HDL especially), CMP w/ LFTs (ALT, AST, GGT, alk phos, total bilirubin), CBC w/ hematocrit, fasting glucose, creatinine, blood pressure. For the user: this is the June 2026 panel regardless — no YK-11-specific addition needed because he won't be on it.
  • During use (if hypothetically used): ALT/AST/GGT/bilirubin at week 4 and week 8 (highest hepatotoxicity risk window). Lipid panel at week 6 (HDL trajectory). Total T + LH + FSH + sensitive E2 at week 6-8 to assess suppression. CBC w/ hematocrit at week 6. Blood pressure weekly. Symptom diary throughout (RUQ pain, jaundice, dark urine, pruritus, libido, mood, energy).
  • Post-cycle: Total T, LH, FSH, E2 at +2, +4, +6, +8 weeks post to confirm axis recovery. LFTs at +4 and +8 weeks to confirm normalization. Lipid panel at +6 weeks to confirm HDL recovery. Confirm full HPG and hepatic recovery before any subsequent cycle.
▸ Controversies / open debates Live debate

1. SARM vs. synthetic steroid classification

The claim: "YK-11 is a SARM."
Reality: Structurally YK-11 is a 17α-methylated 19-nor-pregnane — a steroid, not a non-steroidal SARM scaffold. Functionally it is an AR partial agonist (Kanno 2011), which fits the regulatory/WADA definition of a SARM. Both framings are defensible, and they imply different safety stories. The "SARM" framing borrows the "tissue-selective, milder than AAS" connotation without the structural basis for that selectivity. The "17α-methyl steroid" framing puts YK-11 in the same hepatotoxicity class as anadrol and dianabol — which the structural argument and the community bloodwork pattern both support. The honest summary: YK-11 is a partial-agonist 17α-methylated steroid that is also-correctly-but-misleadingly called a SARM.

2. The "myostatin inhibitor SARM" framing

The claim: "YK-11 is a SARM AND a myostatin inhibitor — dual-action."
Reality: The myostatin-inhibition story rests on a single 2013 paper (Kanno, PMID 23995658) showing follistatin upregulation in C2C12 mouse myoblasts. This finding has not been replicated in human myoblasts, has not been replicated in any in vivo animal model, and has not been demonstrated to translate to clinically meaningful muscle hypertrophy. It is mechanistically interesting but evidentiarily thin. The bodybuilding community's "SARM + myostatin inhibitor" framing treats the cell-line finding as if it were a Phase 2 result. It isn't.

3. "Most aggressive SARM" community lore

The claim: "YK-11 is the strongest SARM for body comp; the harshest on suppression and liver."
Reality: Likely true on suppression and liver, structurally and per forum bloodwork. Likely unverified on body-comp efficacy because there is no head-to-head human data with any other SARM. The community ranking is built on subjective experience plus the structural-hepatotoxicity argument, not on RCT evidence.

4. Hepatotoxicity — case reports vs. true incidence

The structural argument (17α-methyl group) is robust: this scaffold is hepatotoxic across the AAS class. But YK-11-specific case reports are few (<10 identifiable as YK-11-specific in the published literature), partly because the user base is smaller than for ostarine/LGD-4033 and partly because polysubstance use and product-identity uncertainty muddy attribution. The honest claim: incidence is unknown but predicted by structural class to be at least as bad as anadrol or dianabol; the case-report literature is too thin to estimate quantitatively.

5. Sourcing reliability

YK-11 is harder to synthesize than non-steroidal SARMs and counterfeiting/substitution patterns are worse than for the better-established SARMs. The Cohen 2017 JAMA SARM label-accuracy study (52% accurate label) did not include YK-11; assume the actual rate is at least as bad. A "YK-11" cycle may not be a YK-11 cycle. This is independent of whether YK-11 itself is dangerous; it means the dangers experienced may not even be the dangers expected.

6. Hippocampal oxidative-stress finding (Dahleh 2023)

The claim: "YK-11 may impair hippocampal mitochondrial function."
Reality: Single rat in vivo study (5 weeks oral, 0.35 g/kg, male Wistar). Concurrent exercise was neuroprotective alone but did not reverse YK-11's hippocampal damage. For a brain-priority user this is the most concerning piece of YK-11 data and the only in vivo published study. Translation to humans unverified but mechanistically plausible. Replication needed; in the absence of replication, treat as a real signal not a one-off.

7. Bone effect (Yang 2024) vs. muscle effect (Kanno 2013)

The 2024 BMSC/bone-defect paper is the first in vivo study showing an anabolic effect from YK-11 — and it's in bone, not muscle. The muscle effect, despite being the entire bodybuilding pitch, has never been confirmed in vivo in any species. The compound may be more reliably anabolic in bone than in muscle, which would invert the bodybuilding use case. Evidence is too thin to draw conclusions but the asymmetry is notable.

▸ Verdict change log
  • 2026-05-10 — Initial verdict: SKIP-AT-20 HIGH. Zero human RCTs (thinnest evidence base in the SARM family); 17α-methyl structural hepatotoxicity class; severe HPG suppression in community bloodwork; rat hippocampus oxidative-stress / mitochondrial dysfunction signal directly attacking the brain-priority #1 ranking; classification (SARM vs. synthetic steroid) genuinely contested in the published literature; sourcing reliability worst-in-class. The combination is a clear SKIP regardless of body-comp upside. Cross-linked to rad-140, ostarine, lgd-4033 as less-bad SARM-class options (still not recommended at 20).
▸ Open questions / gaps Open
  • Any human Phase 1 safety study: Does not exist. Closest is Piper 2018 deuterium-labeled metabolism work for doping-control method development.
  • Replication of follistatin upregulation in human myoblasts: Not done.
  • In vivo confirmation of muscle hypertrophy in any animal model: Not done.
  • True population incidence of cholestatic hepatotoxicity: Unknown; case-report-based estimates only.
  • Long-term (>1 year) HPG-axis effects of cycled use in young men: Unstudied.
  • Hippocampal effects in humans: Unknown; Dahleh 2023 rat data is the only in vivo signal.
  • Pharmacogenomic responder phenotyping: Plausible candidates (CYP3A4, AR CAG, UGT), no data.
  • Head-to-head comparison vs. other SARMs: Doesn't exist.
  • Independent product-identity testing program: Not published; community-level tracking only.

References

Kanno Y et al. 2013 — Selective androgen receptor modulator, YK11, regulates myogenic differentiation of C2C12 myoblasts by follistatin expression (Biol Pharm Bull, PMID 23995658)

pubmed.ncbi.nlm.nih.gov · 2013

follistatin upregulation / myostatin antagonism mechanism in mouse myoblasts

View Study

Yatsu T et al. 2018 — Selective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1 Cells (Biol Pharm Bull, PMID 29491216)

pubmed.ncbi.nlm.nih.gov · 2018

bone effects in osteoblast cell line

View Study

Piper T et al. 2018 — Studies on the in vivo metabolism of the SARM YK11: Identification and characterization of metabolites potentially useful for doping controls (Drug Test Anal, PMID 30379415)

pubmed.ncbi.nlm.nih.gov · 2018

deuterium-labeled metabolism, 14 urinary metabolites, doping-control methodology

View Study

Kanno Y et al. 2022 — Differential DNA-binding and cofactor recruitment are possible determinants of the synthetic steroid YK11-dependent gene expression by androgen receptor in breast cancer MDA-MB 453 cells (Exp Cell Res, PMID 36030969)

pubmed.ncbi.nlm.nih.gov · 2022

differential AR-coregulator recruitment

View Study

Dahleh MMM et al. 2023 — YK11 induces oxidative stress and mitochondrial dysfunction in hippocampus: The interplay between a selective androgen receptor modulator (SARM) and exercise (J Steroid Biochem Mol Biol, PMID 37468001)

pubmed.ncbi.nlm.nih.gov · 2023

rat hippocampus oxidative stress, mitochondrial dysfunction, exercise interaction

View Study

WADA Prohibited List — S1.2 Other Anabolic Agents (SARMs)

wada-ama.org

current banned-list status

View Source

FDA — Certain Bodybuilding Products Put Consumers at Risk (Consumer Update)

fda.gov

YK-11 named as a banned ingredient

View Source

LiverTox — Selective Androgen Receptor Modulators (NIH/NIDDK)

ncbi.nlm.nih.gov

SARM class hepatotoxicity reference

View Source

How was your experience with this compound?

Anonymous · one vote per session · results below at 5+ votes.

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