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LGD-3303

Also known as: LGD3303, 9-chloro-2-ethyl-1-methyl-3-(2,2,2-trifluoroethyl)-3H-pyrrolo[3,2-f]quinolin-7(6H)-one

5
1 · Natty510 · Enhanced

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

Why this rating?

LGD-3303 is a nonsteroidal selective androgen receptor modulator (SARM) with good oral bioavailability, investigated preclinically for osteoporosis. Wikipedia describes it as achieving "functional selectivity with effective dissociation of anabolic and androgenic effects", a partial agonist for androgenic effects but a FULL agonist for anabolic effects. Crucially, the efficacy data are from animal studies only; there is no human clinical trial data. Rated 5 as a presumptively suppressive research SARM whose effects in humans are essentially unknown, the rating reflects the drug class, not proven human results.

Overview

A nonsteroidal selective androgen receptor modulator (SARM) with good oral bioavailability, originally investigated as a possible treatment for osteoporosis. Wikipedia notes it functions as a selective androgen-receptor agonist with functional selectivity, a partial agonist for androgenic effects but a full agonist for anabolic effects. It is a distinct compound from LGD-4033 (Ligandrol): a different molecule (PubChem CID 25195253) whose evidence base is preclinical, whereas LGD-4033 has actual human trial data.

Important Warnings

  • Evidence is preclinical (animal) only, no human clinical trials, pharmacokinetics, or safety data
  • Not approved for human use; sold as a grey-market research chemical and frequently mislabelled
  • Assume it is suppressive like other SARMs, bloodwork and PCT apply
  • Distinct compound from LGD-4033 despite the similar name

Purpose & Use Cases

Bone / Anti-Osteoporosis (Preclinical)

Its primary studied application: improving bone in osteopenic rats, including additive benefit with a bisphosphonate. This is animal data, not a human indication.

Lean Mass (Presumed)

As a full anabolic agonist it is marketed for muscle building, but muscle outcomes come from preclinical pharmacology, not human trials.

Benefits

  • Good oral bioavailability
  • Functional selectivity: full agonist for anabolic effects, only partial agonist for androgenic effects (preclinical)
  • Demonstrated bone benefit in osteopenic rats, additive with a bisphosphonate
  • Does not aromatize (nonsteroidal SARM), no estrogenic water retention from the compound itself

Good to Know

Different molecule from LGD-4033: and far less proven

Despite the similar "LGD" name, LGD-3303 (PubChem CID 25195253) is a distinct compound from LGD-4033/Ligandrol. LGD-4033 has real human trial data; LGD-3303's evidence is preclinical (rats), built around bone/osteoporosis and its full-anabolic / partial-androgenic selectivity.

Its headline evidence is bone, in animals

The main published work is anti-osteoporosis: LGD-3303 improved bone in osteopenic female rats and was additive with a bisphosphonate (Vajda et al., 2009). Muscle/anabolic activity comes from preclinical pharmacology, not human results.

A preclinical research chemical, treated as a SARM

It was encountered as a novel designer drug by at least 2020. It is not approved for human use, has no human safety data, and should be assumed suppressive like other SARMs, bloodwork and PCT apply.

Dosage Guidelines

Experience LevelDosage Range
Beginner510 mg/day
Intermediate1015 mg/day
Advanced1520 mg/day
Frequency
Community protocols are split on this: several grey-market guides split the daily total into 2-3 doses, citing an unconfirmed ~6-8h half-life extrapolated from animal PK; others recommend a single daily dose. No human PK study exists to settle it.
Typical Cycle Length
812 weeks
Notes

There is NO established human dose. LGD-3303 has only been studied in animals (Vajda et al. 2009). These beginner/intermediate/advanced figures are grey-market vendor/community label ranges with no clinical validation, not doses derived from human trials. Human pharmacokinetics (including a true half-life) are unknown, and products are frequently mislabelled. Treat any dosing as unregulated self-experimentation.

Half-Life

No human pharmacokinetics exist: only animal PK (Vajda et al. 2009). Some grey-market guides extrapolate an unconfirmed ~6-8 hour half-life from that animal data.

Side Effects

Testosterone Suppression (Expected)

very common
Severity
3/5

As an androgen-receptor agonist it is expected to suppress the HPTA like other SARMs, though no human suppression data exists specifically for LGD-3303.

Mitigation

Treat as a hormonal cycle: bloodwork and a SERM PCT.

Lipid Changes (Expected)

common
Severity
2.5/5

Oral SARMs typically lower HDL; presumed here by class, not measured in humans.

Mitigation

Lipid panel before/during; omega-3 and citrus bergamot; cardio.

Unknown Human Safety

common
Severity
3/5

No human safety, toxicology or long-term data exist; it is a preclinical research chemical sold on the grey market.

Mitigation

Recognise the data gap; third-party testing where possible.

General Mitigation Strategies

Because LGD-3303 has no human data, borrow the standard suppressive-SARM precautions: bloodwork before/during/after, a SERM PCT, lipid monitoring, and short cycles. The biggest issue is the near-total absence of human evidence. Do not treat preclinical selectivity as proof of a clean human profile.

Post Cycle Therapy (PCT)

⚠️PCT Required

No human data, but treat as a suppressive SARM. SERM PCT with enclomiphene (12.5-25 mg/day) or tamoxifen (20/20/10/10) for ~4 weeks, guided by bloodwork.

How It Works

LGD-3303 binds the androgen receptor and, per Wikipedia, shows "functional selectivity with effective dissociation of anabolic and androgenic effects," behaving as a partial agonist for androgenic activity but a full agonist for anabolic activity. In osteopenic female rats it improved bone and was shown to have additive effects when combined with a bisphosphonate (Vajda et al., 2009). Its pharmacokinetics/pharmacodynamics were characterised in animals (Vajda et al., 2009), which established its oral availability and anabolic activity, but no human pharmacology has been published.

Hormonal & Androgenic Profile

Aromatizes (→ estrogen)none
Natural test suppressionmoderate
Hair loss risk (DHT-prone)moderate
Liver toxicitylow
DHT-derivativeNo
Progestogenic (19-nor)No
Anabolic : Androgenic ratio

Not a numeric ratio, but Wikipedia describes functional selectivity: a FULL agonist for anabolic effects and only a PARTIAL agonist for androgenic effects (preclinical).

Estrogen control

Nonsteroidal SARM: does not aromatize, so no AI is needed for LGD-3303 itself.

DHT / 5-AR & finasteride

Not a 5α-reductase substrate: finasteride/dutasteride do nothing for any SARM-related shedding, which is direct androgen-receptor activation at the follicle.

Cardiovascular impact

Expected to lower HDL like other oral SARMs; no aromatization means no estrogenic water retention. No human lipid data specific to LGD-3303.

Fundamentals

WADA Status

Prohibited by WADA
Category: S1. Anabolic Agents
In-Competition: ProhibitedOut-of-Competition: Prohibited

SARMs are prohibited at all times under S1.2 (Other Anabolic Agents). LGD-3303 is a selective androgen receptor modulator and is captured by the class prohibition even where not individually named.

References

Last updated: July 18, 2026