Why hepatotoxic: 17α-methylated structure, the same modification that makes oral steroids like Dianabol and Anadrol hepatotoxic.
Classification note. Sold and categorized as a SARM, but structurally a 17α-methylated DHT derivative whose primary mechanism is myostatin inhibition. Its side-effect profile is more similar to oral AAS than to true SARMs; treat it with the caution appropriate to a methylated oral steroid.
Limited human clinical data: dosing extrapolated from animal studies and user reports.
Not FDA-approved for human use. WADA-banned for tested athletes. Sold as a research chemical; clinical safety beyond short-term trials is not established. This page is educational reference only, not a recommendation or endorsement of use.
- Half-life
- 8 h
- Route
- Oral
- Not a true SARM despite being marketed as one; treat with caution appropriate to oral AAS.
- 17α-methylation makes it hepatotoxic. ALT/AST elevations commonly reported.
- Liver strain is the dominant risk; ALT and AST are the markers that track it.
- DHT-derived structure can accelerate male-pattern baldness in susceptible individuals.
Important classification note
YK-11 is not really a SARM. It's sold as one and grouped with SARMs in user communities, but structurally and pharmacologically it's a steroidal compound:
- Structurally: A synthetic derivative of 5α-dihydrotestosterone (DHT) with a 17α-methyl group
- Mechanism: Acts as a weak partial agonist at the androgen receptor, but its primary mechanism is believed to be myostatin inhibition (myostatin is the protein that limits muscle growth — inhibiting it allows more growth)
- Side effects: Behave like an oral anabolic steroid (hepatotoxic, suppressive) rather than a true SARM
The 17α-methyl group is the same modification that makes oral steroids like Dianabol and Anadrol hepatotoxic. Treating YK-11 like a "gentle SARM" is a category error that has put users in liver-injury territory.
This entry is included because users will search for it under SARMs, but the safety profile is much closer to an oral AAS. Treat it accordingly.
Overview
YK-11 was characterized in 2011 by Yuichiro Kanno's research group in Japan (hence "YK"). It was originally studied as a potential treatment for muscle wasting disorders, with early in vitro work suggesting myostatin inhibition as a primary mechanism. Human clinical data is essentially nonexistent — all dosing and safety information comes from animal/in vitro work and user self-reports.
In user communities it has a reputation for significant strength gains and a hardening effect, but with side effects more typical of oral AAS than other SARMs.
Mechanism
Two proposed mechanisms:
- Weak partial agonist at the androgen receptor — contributes some direct anabolic signaling
- Myostatin inhibition — increases follistatin expression in cell culture studies, which would inhibit myostatin and allow greater muscle hypertrophy
The myostatin inhibition mechanism is theoretical in humans — well-characterized in cell models, not validated in human trials.
Pharmacokinetics
- Half-life: unknown in humans; estimated 6-10 hours, with no published human pharmacokinetic study to confirm it
- Tmax (oral): estimated 1-2 hours
- Bioavailability (oral): unknown; assumed moderate to high
- Metabolism: hepatic, first-pass; 17α-methylation slows hepatic breakdown (the source of both its oral activity and its hepatotoxicity)
- Elimination: urinary
YK-11 has never been evaluated in a human clinical trial, so there is no clinical reference for human use of any kind.
Expected effects
- Lean mass gain (modest to moderate) reported
- Significant strength gains reported
- Hardening / density in physique
- Joint discomfort sometimes reported
Side effect profile
Behaves like an oral AAS, not a SARM:
- Hepatotoxicity: This is the defining concern. 17α-methylation makes YK-11 hepatotoxic in the same way as Dianabol, Anadrol, or other oral steroids. Significant ALT/AST elevations are commonly reported. Liver strain from 17α-methylated compounds scales with both the amount and the duration of exposure. Elevated liver enzymes are a marker to discuss with your healthcare provider, and decisions about liver-protective management should be made with a qualified healthcare provider.
- HPTA suppression: Moderate to substantial, with suppressed LH, FSH and total testosterone documented in user bloodwork. Recovery of the axis is a clinical question for a qualified healthcare provider.
- Lipid changes: Notable HDL reductions, LDL elevation — similar pattern to oral AAS.
- Hair loss: As a DHT derivative, YK-11 can accelerate male pattern baldness in susceptible individuals.
- Acne: Possible, given DHT-derived structure.
Bloodwork monitoring
Given YK-11's hepatotoxic profile, reported monitoring protocols align with what is used for oral AAS rather than milder SARMs. Markers to monitor include a baseline panel, a liver-focused check around 3 weeks in, an end-of-cycle panel, and a post-cycle panel at approximately 4 weeks:
- Total + Free Testosterone
- LH, FSH
- Estradiol (sensitive)
- SHBG
- Full lipid panel
- ALT, AST, GGT, total bilirubin (mandatory — liver is the primary concern)
- CBC
Interactions
- Hepatic load is additive. Alongside other 17α-methylated orals, or anything else cleared hard by the liver, the burden on liver markers compounds rather than staying flat.
- Lipid effects add in the same way: HDL reduction and LDL elevation are shared effects of oral 17α-methylated compounds.
- Androgenic effects and HPTA suppression add to those of any other androgen present, including prescribed testosterone.
Pharmacokinetic modeling parameters
ka: 1.5 /day
ke: 2.1 /day
Vd: 60 L
F: 0.70
half_life_hours: 8
Notes and caveats
- The "SARM" classification is misleading. YK-11 is a methylated steroid with myostatin-inhibiting properties. It should be treated with the caution appropriate to oral AAS, not the relative permissiveness applied to true SARMs.
- The 17α-methylation creates a real hepatotoxicity burden; decisions about liver-protective management should be made with a qualified healthcare provider.
- The myostatin inhibition mechanism is well-established in cell culture but has not been validated in human trials — claims about specific muscle growth percentages from "myostatin inhibition" are extrapolation.
- Some users report a flat or muted feel compared to other SARMs (less of a noticeable "kick"), which community harm-reduction discussions note has been associated with dose-escalation and corresponding side effect amplification.