YK-11.

Quick Overview.

YK-11 is one of the most misunderstood compounds in the fitness industry. It is widely sold and marketed as a SARM (Selective Androgen Receptor Modulator), but chemically, it is a synthetic steroid derived from DHT (Dihydrotestosterone).[1]

What makes YK-11 unique is that it acts as a hybrid. It binds to the androgen receptor to build muscle (like a steroid), but it also forces your muscle cells to produce more Follistatin. Follistatin is a protein that blocks Myostatin (the hormone that tells your muscles to stop growing). By doing both simultaneously, YK-11 allows users to push past their natural genetic limits for muscle growth.[2]

• Primary Use Case: Rapid, dry muscle growth and extreme strength gains.
• Mechanism: A partial agonist of the androgen receptor that uniquely induces the expression of Follistatin in muscle cells, thereby inhibiting Myostatin.[2][3]
• Who it is for: Advanced users who understand the risks of oral steroids and are prepared to run a full Post Cycle Therapy (PCT).
• Who it is NOT for: Beginners, women, anyone under 25, or anyone who thinks this is a "safe, side-effect-free SARM."

The Protocol & Usage Guide.

confidence_tier: community

There is absolutely zero human clinical data on this drug; you are entirely a guinea pig when taking it.[4]

Standard Dosing

Note: Because the half-life is estimated to be short (6-12 hours), the dose is split to maintain stable blood levels.

Cycle Length & Discontinuation Protocol

• Cycle Length: 6 to 8 weeks maximum.
• Discontinuation (PCT): Immediately upon stopping, begin a 4-week Post Cycle Therapy (e.g., Enclomiphene at 12.5mg/day or Nolvadex) to restart your natural testosterone production. YK-11 is highly suppressive.

Nutritional Support & Recommended Supplements.

confidence_tier: well-established

Safety, Interactions & Side Effect Management.

confidence_tier: well-established

YK-11 is a synthetic steroid. It carries all the risks associated with oral anabolic steroids.

Side Effect Profile

Contraindications

• Absolute: Women (high risk of virilization/masculinization).
• Absolute: Individuals under 25 (do not mess with your endocrine system while it is still developing).
• Absolute: Individuals with pre-existing liver or kidney issues.

Drug Interactions

• Other Oral SARMs/Steroids: SEVERE. Stacking YK-11 with RAD-140 or oral steroids will cause massive liver toxicity and completely shut down your natural testosterone.
• Alcohol: High. Do not drink alcohol while taking a liver-toxic oral androgen.

Common Stacks & Combinations.

confidence_tier: community

Body Composition & Training Guide.

confidence_tier: community

• The "Dry" Gains: Users report that YK-11 does not cause water retention. The muscle gained is very dry, hard, and vascular, similar to the steroid Winstrol.
• Strength Focus: YK-11 produces rapid strength gains. However, because of the joint dryness, you must warm up extensively and avoid ego-lifting to prevent tendon tears.
• Tracking Progress: Track strength increases weekly. Monitor your mood and energy levels (signs of testosterone suppression).

Storage, Handling & Accessibility.

confidence_tier: well-established

• Storage: Store liquid suspensions or capsules at room temperature in a cool, dry place away from direct sunlight.
• WADA Status: Banned in competitive sports under section S1 (Anabolic Agents).
• Cost & Accessibility: Widely available from research chemical vendors, usually ~$60 - $90 for a 30ml bottle (10mg/mL).

Bloodwork Monitoring Guide.

confidence_tier: well-established

Mandatory Bloodwork:

• Pre-Cycle: Total/Free Testosterone, LH, FSH, AST/ALT (Liver), Lipid Panel (Cholesterol).
• Post-Cycle: You must check your Testosterone and Liver enzymes to ensure you need a PCT and that your liver is recovering.

Comparison to Similar Compounds.

confidence_tier: well-established

Deep Dive (For Advanced Researchers).

confidence_tier: well-established

Mechanism of Action

YK-11 ((17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester) was first described in 2011 by Japanese researcher Yuichiro Kanno.[5]

Despite being marketed as a SARM, YK-11 has the exact four-ring steroidal backbone of a DHT (dihydrotestosterone) derivative. It is structurally very similar to the anabolic steroid Norethindrone.[1]

Because it has never been studied in humans or animals, its exact half-life and metabolic pathways are unknown. Based on its steroidal structure and user reports of dosing frequency, the half-life is estimated at 6-12 hours.

Cellular Pathways

1. Partial Agonism: YK-11 binds to the Androgen Receptor (AR). However, in vitro studies show it is only a partial agonist. It does not induce the full N/C interaction (the folding of the receptor) that full agonists like DHT do.[5]
2. The Follistatin Secretion: This is where YK-11 is unique. When YK-11 binds to the AR in C2C12 myoblasts (muscle cells), it induces the expression of Follistatin (FST) to a much greater degree than DHT.[2]
3. The Myostatin Blockade: The locally produced Follistatin then binds to and neutralizes Myostatin, removing the negative regulator of muscle growth. Therefore, YK-11 exerts anabolic effects through two distinct pathways: direct AR stimulation and indirect Myostatin inhibition.[3]

Clinical Trial Summary

• ZERO In Vivo Data: There are absolutely no published animal (mouse/rat) or human clinical trials on YK-11. All data regarding its mechanism of action comes from in vitro (petri dish) cellular assays performed by Kanno et al. between 2011 and 2013.[4]
• The Unknowns: Because it has never been tested in a living organism by scientists, its true toxicity, optimal dosage, and long-term effects are entirely based on anecdotal reports from the biohacking community.

Synergy & Antagonism Analysis

• Receptor Competition: Because YK-11 is a partial agonist, if you stack it with a full agonist (like Testosterone or RAD-140), YK-11 will actually compete for the receptor and potentially weaken the direct androgenic effect of the stronger drug, while still providing the Follistatin boost.[6]

Frequently Asked Questions (FAQ).

confidence_tier: community

Q: Is YK-11 a SARM or a Steroid? A: Chemically, it is a synthetic steroid (a DHT derivative). It is marketed as a SARM because it was discovered during the SARM boom and is sold by SARM companies, but its molecular structure is steroidal.

Q: Do I really need a PCT for this? A: YES. YK-11 is highly suppressive. If you do not run a PCT (like Enclomiphene or Nolvadex), your testosterone levels will remain crashed for months, you will lose all the muscle you gained, and you will feel terrible.

Q: Will it cause hair loss? A: Because it is a DHT derivative, it can accelerate hair loss in men who are genetically predisposed to male pattern baldness. Finasteride will not prevent this, as YK-11 does not need the 5-alpha reductase enzyme to convert to DHT; it is already structurally similar to DHT.

International Regulatory Status.

confidence_tier: well-established

Decision Tree.

confidence_tier: community

[Goal: Rapid, Dry Muscle Growth?]
  |
  +-- Are you under 25 or female?
        |
        +-- (Yes) -> STOP: Do not use YK-11.
        |
        +-- (No) -> Do you have a PCT (Enclomiphene/Nolvadex) and Liver Support ready?
              |
              +-- (No) -> STOP: Do not start the cycle until you have them.
              |
              +-- (Yes) -> Take 5mg twice daily for 6-8 weeks.
                           Begin PCT immediately after the last dose.

Schema.org Data.

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  "@context": "https://schema.org",
  "@type": "MedicalEntity",
  "name": "YK-11",
  "alternateName": ["(17α,20E)-17,20-[(1-methoxyethylidene)bis(oxy)]-3-oxo-19-norpregna-4,20-diene-21-carboxylic acid methyl ester"],
  "description": "A synthetic steroidal compound marketed as a SARM that acts as a partial androgen receptor agonist and uniquely induces Follistatin expression to inhibit Myostatin.",
  "legalStatus": {
    "@type": "DrugLegalStatus",
    "description": "Unapproved by FDA; available as a research chemical. Prohibited in-competition by WADA."
  }
}

What we cited.