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SARM

YK-11

Steroidal selective androgen receptor modulator with myostatin-inhibiting properties. Half-life approximately 6 hours. Short half-life necessitates split dosing for stable plasma levels.

Emerging Evidence
~6 h
Half-Life
95%
Bioavailability
5–15 mg/day
Typical Dose
Oral
Routes

Overview

YK-11 is a selective androgen receptor modulator (SARM) — a class of compounds that selectively bind to androgen receptors in muscle and bone tissue. Steroidal selective androgen receptor modulator with myostatin-inhibiting properties.

With a half-life of ~6 hours, YK-11 requires daily administration in most observed protocols. Taken orally, it has a bioavailability of approximately 95% via its primary route.

Half-life approximately 6 hours. Short half-life necessitates split dosing for stable plasma levels. Very limited human pharmacokinetic data. One-compartment model.

Mechanism of Action

YK-11's pharmacological activity involves the following key pathways:

Selective Receptor Binding

YK-11 is designed to selectively bind to androgen receptors in muscle and bone tissue, with reduced activity in other androgen-sensitive tissues.

Tissue Selectivity

The selectivity of YK-11 is achieved through differential coactivator recruitment — the compound activates different downstream pathways depending on the tissue type.

Pharmacokinetics

Parameter Value
Half-Life ~6 hours
Bioavailability ~95%
Time to Peak ~1.5 hours
Duration of Activity ~12 hours
Routes Oral

Dosing Protocols

The following protocols represent commonly observed dosing patterns. These are observational summaries, not recommendations.

Standard Protocol
Dose 5 mg/day
Route Oral
Frequency Once daily
Duration 8-12 weeks
Higher-Dose Protocol
Dose 15 mg/day
Route Oral
Frequency Once daily
Duration 8-12 weeks

Frequently Asked Questions

What is YK-11 and how does it work?
YK-11 is a synthetic steroidal compound that functions as both a partial androgen receptor agonist and a myostatin inhibitor. Unlike typical non-steroidal SARMs, YK-11 is derived from dihydrotestosterone (DHT) and carries a unique dual mechanism: it partially activates androgen receptors while simultaneously stimulating follistatin expression, which suppresses myostatin – a protein that limits muscle growth.
Does YK-11 actually inhibit myostatin?
In vitro studies have demonstrated that YK-11 induces muscle cells to produce significantly more follistatin, a protein that directly antagonizes myostatin. Myostatin acts as a natural brake on muscle growth, so its inhibition via increased follistatin is the primary mechanism behind YK-11's reported anabolic effects. This myostatin-inhibiting property distinguishes YK-11 from all other SARMs, which rely solely on androgen receptor activation.
What is the half-life of YK-11?
YK-11 has an estimated half-life of approximately 6–12 hours, though no formal human pharmacokinetic studies have been published. The relatively short half-life means split dosing – typically twice daily – is commonly observed to maintain more consistent plasma levels throughout the day. The compound's steroidal structure and 17α-alkylation influence its oral absorption and hepatic metabolism.
Is YK-11 a SARM or a steroid?
YK-11 occupies a unique position between traditional SARMs and anabolic steroids. It is structurally a steroidal compound derived from DHT, but it acts as a gene-selective partial agonist of the androgen receptor rather than a full agonist like conventional steroids. This partial agonism combined with its myostatin-inhibiting mechanism means YK-11 does not fit neatly into either category.
What are the side effects of YK-11?
The most commonly reported effects of YK-11 include testosterone suppression (mild to moderate), potential liver enzyme elevations related to its 17α-alkylated structure, and joint discomfort. Hair thinning has also been reported, consistent with its DHT-derived structure. Long-term safety data is notably absent, as YK-11 has never progressed beyond in vitro cell studies to animal or human clinical trials.
How long does YK-11 take to show results?
Strength increases and improved muscle fullness are commonly reported within 2–3 weeks of consistent dosing. The myostatin-inhibiting effects via follistatin induction are believed to contribute to progressive gains over the full cycle duration. Visible body composition changes are most frequently reported in the 4–6 week range, which aligns with the timeframe needed for follistatin-mediated muscle growth signaling to translate into measurable tissue changes.

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