What is the half-life of YK-11?

YK-11 has a half-life of 6-10 hours (estimated, limited pharmacokinetic data), which is why it's typically administered Once daily (oral or injectable, split AM/PM by some researchers) for optimal therapeutic effect.

How do I reconstitute YK-11?

Add bacteriostatic water to the peptide vial slowly down the side. Typical reconstitution uses 2-3ml of water for a 5mg vial. Gently swirl, do not shake.

Muscle Growth

Preclinical

YK-11

Also known as: YK11, YK-11 Myostatin Inhibitor

Overview

Key Facts

Primary Goal: A steroidal compound structurally derived from dihydrotestosterone (DHT) that exhibits a dual mechanism: partial agonism at the androgen receptor (SARM-like activity) combined with myostatin inhibition through increased follistatin expression

A steroidal compound structurally derived from dihydrotestosterone (DHT) that exhibits a dual mechanism: partial agonism at the androgen receptor (SARM-like activity) combined with myostatin inhibition through increased follistatin expression. While often classified with SARMs, its steroidal backbone and unique follistatin-inducing properties place it in a distinct pharmacological category. It is technically a gene-selective androgen receptor modulator with anti-myostatin activity. Half-Life 6-10 hours (estimated, limited pharmacokinetic data) Typical Dose 5–15 mg Frequency Once daily (oral or injectable, split AM/PM by some researchers) Cycle Length 6-8 weeks (with mail-cycle therapy consideration)

Dosing Information

Half-Life

6-10 hours (estimated, limited pharmacokinetic data)

Typical Dose

5–15 mg

Frequency

Once daily (oral or injectable, split AM/PM by some researchers)

Cycle Length

6-8 weeks (with post-cycle therapy consideration)

Administration Routes:

intramuscularoral

Storage & Reconstitution

Unreconstituted (Powder)

Temperature15–25°C (59–77°F)

DurationUp to 3 months

Reconstituted (Mixed)

Temperature15–25°C (59–77°F)

Duration2-4 weeks

Research Summary

Preclinical

YK-11 was first described by Kanno et al. (2011) in a study on C2C12 myoblast cells, demonstrating that it induced myogenic differentiation and increased follistatin expression more effectively than DHT. Subsequent in vitro studies confirmed its dual AR-agonist and myostatin-inhibiting activity. No in vivo animal or human clinical trials have been published. Its classification remains debated — it shares features with both SARMs and anabolic steroids. Extreme caution is warranted due to the complete absence of clinical safety data.