SARMWADA ProhibitedCompare

YK-11

Also known as: YK11, Myostine

1 · Natty510 · Enhanced

Lower numbers = closer to natural. Higher numbers = more enhanced.

Why this rating?

YK-11 is structurally a steroid despite SARM classification. It is reported to be hepatotoxic (commonly run with TUDCA) and causes significant testosterone suppression requiring full PCT. It acts as both a SARM and myostatin inhibitor through follistatin upregulation. The dual mechanism and steroid structure place it closer to actual steroids than typical SARMs. Human data are almost nonexistent, but the reported side-effect profile mirrors harsh oral steroids. Rated 6: a harsh top-tier SARM kept below testosterone (7) given the near-absence of human efficacy data.

Overview

A synthetic steroidal SARM that also acts as a myostatin inhibitor. Theoretically allows for bypassing genetic muscle limits via follistatin upregulation.

Important Warnings

•Very limited human research
•Structurally a steroid (often described as 17-alpha-methylated, though sources conflict) despite SARM classification
•Reported hepatotoxicity - use liver support and short cycles; stop if liver markers rise or jaundice appears
•Strong HPTA suppression - full SERM PCT is mandatory
•Harsh lipid impact typical of oral androgens
•Myostatin/follistatin "beyond genetics" claim is unproven in humans
•Joint issues common due to rapid strength gains outpacing connective tissue

Purpose & Use Cases

Muscle Growth Beyond Genetics

Myostatin inhibition may allow for exceeding normal genetic muscle potential.

Strength Gains

Significant strength increases through both anabolic and myostatin inhibition pathways.

Benefits

Myostatin inhibition for enhanced growth
Follistatin upregulation
Significant strength increases
Potential to exceed genetic limits
No estrogen conversion

Good to Know

YK-11 is a steroid, not a true SARM, though sources conflict on the details

Despite the "SARM" label, YK-11 has a DHT-related steroidal backbone. Sources genuinely conflict on the specifics: many (including its most common description) call it a 17-alpha-methylated compound, which would explain both its oral activity and its liver toxicity, while others dispute that it is methylated at all. Human data is almost nonexistent either way. What is consistent is the real-world side-effect profile reported by users (liver strain, strong suppression, lipid crash), which mirrors a harsh oral steroid far more than Ostarine or LGD. Given the uncertainty and its steroidal nature, treat it like a harsh oral: liver support, short cycles, and a full PCT.

The myostatin-inhibition claim is mechanistically plausible but not proven in humans

YK-11 upregulates follistatin in cell-culture studies, and follistatin inhibits myostatin (the brake on muscle growth). This is the basis for "grow past your genetic limit" marketing. But there is essentially no human data showing this translates to real-world muscle beyond what its androgenic action provides. Treat the myostatin story as a hypothesis, not a demonstrated effect.

Hepatotoxic and strongly suppressive: full PCT and liver support are non-negotiable

Reported hepatotoxicity (commonly attributed to methylation, though disputed) means YK-11 stresses the liver (TUDCA and short cycles), and it causes significant HPTA suppression requiring a full SERM PCT. This is one of the harsher "SARMs" and should not be treated as a beginner compound.

Almost no human safety data

YK-11 is a research chemical with very limited human evidence, no approved use, and grey-market quality problems. The joint pain many users report is thought to come from strength gains outpacing connective-tissue adaptation, a reason not to chase rapid loading.

Dosage Guidelines

Experience Level	Dosage Range
Beginner	5 – 5 mg/day
Intermediate	10 – 15 mg/day
Advanced	15 – 20 mg/day

Frequency

Daily oral, split doses (AM/PM) due to short half-life

Typical Cycle Length

6 – 8 weeks

Notes

No loading phase: most community protocols start at the intended daily dose from day one, split into two doses (e.g., AM/PM) given the short half-life. Doses above roughly 15-20mg/day are associated with more pronounced liver-enzyme and lipid strain in user reports. Human pharmacokinetic and efficacy data are extremely limited; these ranges reflect community/harm-reduction protocols, not clinical dosing guidance. Start low to assess tolerance.

Half-Life

Community estimate: no formal human pharmacokinetic study of the parent compound has established this precisely.

Side Effects

Joint Pain

common

Severity

3/5

Joint discomfort and pain, possibly due to rapid strength gains outpacing connective tissue adaptation.

Mitigation

Joint support supplements; don't increase weights too rapidly.

Liver Toxicity

common

Severity

4/5

Reported hepatotoxicity, commonly attributed to methylation (disputed); human data are very limited.

Mitigation

TUDCA supplementation; keep cycles short.

Severe Suppression

very common

Severity

4/5

Significant testosterone suppression.

Mitigation

Full PCT required.

General Mitigation Strategies

TUDCA for liver support. Joint support supplements. Full PCT required after cycle. Very limited human data - proceed with caution.

Support Supplements

Ancillary supplements commonly run alongside YK-11 to manage side effects, support the target tissue, or fill nutrient demands it creates.

Liver support (TUDCA)

Key

YK-11 is a steroidal compound often described as 17-alpha-methylated (disputed); methylated orals are hepatotoxic and users report liver strain. TUDCA supports bile flow and hepatocyte health.

Dose: 250-500 mg/day
Timing: With food
When: Support, not a shield: stop the compound if liver markers climb or jaundice/dark urine appears. Keep cycles short.

Lipid support (omega-3 + citrus bergamot)

Key

As an oral steroidal androgen, YK-11 can hit lipids hard (HDL suppression). Omega-3 helps triglycerides; citrus bergamot helps LDL.

Dose: Omega-3 2-4 g/day; citrus bergamot 500-1,000 mg/day
Timing: With meals
When: Monitor a full lipid panel: the methylation makes the lipid hit steeper than non-methylated SARMs.

Post Cycle Therapy (PCT)

⚠️PCT Required

Full PCT with Enclomiphene or Nolvadex required due to significant suppression.

How It Works

YK-11 is structurally a steroid that acts as both a SARM and a myostatin inhibitor. It upregulates follistatin, which inhibits myostatin - the protein that limits muscle growth. This dual mechanism theoretically allows for muscle growth beyond genetic limits.

Hormonal & Androgenic Profile

Aromatizes (→ estrogen)none

Natural test suppressionsevere

Hair loss risk (DHT-prone)moderate

Liver toxicitymoderate

DHT-derivativeNo

Progestogenic (19-nor)No

Anabolic : Androgenic ratio

Not a clean SARM: a steroidal compound (commonly described as 17-alpha-methylated, though this is disputed) that also induces follistatin (myostatin inhibition is the marketing hook).

Estrogen control

Does not aromatize, no AI needed for YK-11 itself.

DHT / 5-AR & finasteride

YK-11 is structurally a steroid with a DHT-related backbone, but it is not a 5-alpha-reductase substrate. Finasteride/dutasteride will not mitigate its androgenic hair loss, which is direct receptor activation.

Cardiovascular impact

Oral steroidal androgen: expect notable HDL suppression and lipid strain, on top of reported hepatotoxicity. Treat cardiovascularly like a harsh oral steroid, not a mild SARM.