What is the difference between LGD-3303 and YK-11?

LGD-3303: LGD-3303 is a non-peptide small molecule belonging to the pyrrolo[3,2-f]quinolinone class of selective androgen receptor modulators (SARMs). It has never been approved by the FDA or any regulatory age... YK-11: YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM) — a 19-nor DHT-derived analog with a spiro-dioxolane modification at C-17, structurally distinct from non-steroidal SARMs. I...

What does the research say about LGD-3303 vs YK-11?

LGD-3303: No human data exist for LGD-3303. No completed or registered clinical trials were found on ClinicalTrials.gov, and no PubMed record of a Phase 1 or later human trial exists. In castrated Sprague-Dawley rats, LGD-3303 showed potent anabolic (levator ani muscle) agonist activity but only partial agonist activity on androgenic tissues (ventral prostat… YK-11: No human safety, tolerability, or efficacy trials exist for YK-11. The only published human study administered six-fold deuterated YK-11 to volunteers solely to identify urinary metabolites for anti-doping method development; no intact parent compound was recovered in urine, and 14 metabolites (unconjugated, glucuronidated, sulfated) were character…

LGD-3303 vs YK-11

Q: Can you stack LGD-3303 and YK-11?

LGD-3303 (performance) and YK-11 (performance) are in the same category and may have overlapping mechanisms — researchers should review both profiles carefully before combining. Consult a licensed provider before combining any compounds.

Head-to-head comparison of LGD-3303 and YK-11 — mechanism, side effects, legal status, and pricing.

LGD-3303

LGD-3303 is a non-peptide small molecule belonging to the pyrrolo[3,2-f]quinolinone class of selective androgen receptor modulators (SARMs). It has never been approved by the FDA or any regulatory agency for human use, and no human clinical trials have been conducted or registered. LGD-3303 is prohibited under WADA's S1.2 category (Other Anabolic Agents), which covers all SARMs as a class. All available data are preclinical, derived from in vitro AR binding assays and in vivo studies in castrated rats and horses.

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YK-11

YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM) — a 19-nor DHT-derived analog with a spiro-dioxolane modification at C-17, structurally distinct from non-steroidal SARMs. It is not FDA-approved for any human use and is prohibited in competitive sport; anti-doping laboratories actively screen for YK-11 metabolites. No human safety, tolerability, or efficacy trials exist; the only published human study administered deuterated YK-11 solely to identify urinary metabolites for doping-control method development.

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LGD-3303

YK-11

Category

Performance

Legal Status

Research Only

Mechanism

LGD-3303 is a nonsteroidal androgen receptor (AR) agonist. In castrated rat studies (Vajda et al. 2009, PMID 19017848), it bound and activated the AR to drive potent anabolic activity in levator ani muscle while acting only as a partial agonist in androgenic tissues (preputial gland, ventral prostate), never stimulating ventral prostate above intact-animal levels despite rising plasma concentrations. Tissue-selective activity persisted regardless of oral versus continuous-infusion dosing and despite higher local drug concentrations in prostate than in muscle, indicating the selectivity arises from altered molecular interaction at the AR itself rather than from differences in pharmacokinetic exposure or tissue distribution.

YK-11 acts as a partial androgen receptor (AR) agonist in mouse C2C12 myoblasts, activating AR without inducing the classical N/C-terminal interaction that full agonists like DHT produce. Distinct from DHT, YK-11 induces expression of follistatin, an endogenous myostatin antagonist; this follistatin induction is AR-dependent (blocked by AR antagonist flutamide and by AR knockdown) and is required for YK-11's enhancement of myogenic differentiation. Myostatin inhibition is therefore indirect — via AR-driven follistatin upregulation — rather than direct binding or antagonism of myostatin.

Side Effects

No human safety or adverse-event data exist
Not FDA-approved for any indication
Prohibited under WADA S1.2 (SARMs as a class)

Where Researchers Are Buying

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COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower

LGD-3303

Best $/mg

$0.082/mg

Kimera ChemsC

1 trusted vendor listing

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YK-11

Best $/mg

$0.082/mg

Kimera ChemsC

1 trusted vendor listing

Compare all 1 vendor

Lab Verification

COA corpus from Disclosed Labs — independently tested batches only.

LGD-3303

COAs

99.0%

Avg purity

Labs

Full testing data

YK-11

COAs

99.2%

Avg purity

Labs

Full testing data

LGD-3303 Research Summary

No human data exist for LGD-3303. No completed or registered clinical trials were found on ClinicalTrials.gov, and no PubMed record of a Phase 1 or later human trial exists. In castrated Sprague-Dawley rats, LGD-3303 showed potent anabolic (levator ani muscle) agonist activity but only partial agonist activity on androgenic tissues (ventral prostate, preputial gland); tissue selectivity was maintained across both oral dosing and continuous infusion despite very different plasma exposure-time profiles (Vajda et al. 2009, PMID 19017848). In horses dosed orally at 0.05 mg/kg, eight metabolites (including hydroxylated and carboxylated forms with glucuronic acid conjugates) were tentatively identified in plasma and urine for doping-control purposes, with a monohydroxylated metabolite identified as the most sensitive analytical marker (Nilsson Broberg, Knych, Bondesson et al. 2023, PMID 37224728).

Key references

YK-11 Research Summary

No human safety, tolerability, or efficacy trials exist for YK-11. The only published human study administered six-fold deuterated YK-11 to volunteers solely to identify urinary metabolites for anti-doping method development; no intact parent compound was recovered in urine, and 14 metabolites (unconjugated, glucuronidated, sulfated) were characterized. In vitro (mouse C2C12 myoblasts), YK-11 (1–500 nM) increased myosin heavy chain and myogenic regulatory factor expression more strongly than equimolar DHT and uniquely induced follistatin, a pathway necessary for its pro-differentiation effect. In vivo (mouse model of gram-negative bacterial sepsis), YK-11 reduced circulating pro-inflammatory cytokines and organ-damage markers, decreased sepsis mortality, and was associated with protection against sepsis-induced muscle wasting.

Key references

Can you stack LGD-3303 and YK-11?

LGD-3303 and YK-11 are both in the Performance category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.

Other comparisons

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This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.