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DPreclinical / mechanistic only
No human dataHigh risk

LGD-3303

LGD-3303 is an investigational non-steroidal selective androgen receptor modulator (SARM) originally developed by Ligand Pharmaceuticals and studied only in animals for osteoporosis/muscle-wasting indications. It has never been tested in humans in any published clinical trial: there is no human efficacy, safety, dosing, or pharmacokinetic data. It is sold on the gray market as a muscle- and bone-building "research chemical," but it is not an approved drug anywhere and its purity/identity in consumer products is unverified. Because no human safety data exists, all risk is inferred from the SARM class, where documented harms include drug-induced liver injury (including cholestatic/hepatocellular injury and jaundice), suppression of the body's own testosterone production, cardiovascular events including myocarditis, and tendon damage. Products are frequently mislabeled or contaminated. Anyone using it is effectively self-experimenting with an untested compound; the conservative harm-reduction position is that use should be discouraged and, if it occurs, closely monitored with bloodwork under a clinician's care.

Clinical readoutSARM · sarm
Hepatic strainNone
CardiovascularNone
HPTA suppressionModerate
Half-life
Not established i…
Route
Orally bioavailable
Evidence
D
Active
Unknown in humans
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not established in humans. No published human pharmacokinetic study exists. Preclinical rat data characterized oral and continuous-infusion exposure profiles but a validated human half-life is unknown.
Pharmacology

Mechanism of action

LGD-3303 is a potent, non-steroidal, non-aromatizable ligand that binds the androgen receptor (AR) with high selectivity and little cross-reactivity with related nuclear receptors. In castrated/gonadectomized rat models it acts as a near-full agonist on anabolic tissues (levator ani muscle, cortical and cancellous bone) while behaving as a partial agonist on classically androgenic tissues such as the prostate and preputial gland, never driving ventral prostate weight above intact/eugonadal levels even at high doses. This tissue-selective ("SARM") behavior appears intrinsic to how the compound interacts with the AR rather than a consequence of differential tissue distribution, since local drug concentrations were actually higher in prostate than in muscle. It is not aromatized to estrogen and crosses the blood-brain barrier in rats. All mechanism data are preclinical.
Kinetics

Pharmacokinetics

Half-life

Not established in humans. No published human pharmacokinetic study exists. Preclinical rat data characterized oral and continuous-infusion exposure profiles but a validated human half-life is unknown.

Active duration

Unknown in humans. In an equine oral-administration study a monohydroxylated metabolite was detectable in urine well beyond the parent compound, indicating prolonged detectability, but human duration of biological action has not been defined.

Route

Orally bioavailable (oral gavage in rodent studies; oral administration in equine studies). Human products are typically taken orally.

Metabolism & clearance

Hepatic metabolism via oxidation/hydroxylation with subsequent glucuronide conjugation; multiple hydroxylated and one carboxylated metabolite plus glucuronic-acid conjugates identified in equine in vivo and equine/human liver-microsome in vitro models. Renal (urinary) elimination of conjugated metabolites is documented in animal doping-control work. Human clearance parameters are not published.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Anabolic effects on skeletal muscle demonstrated in rats (increased levator ani muscle mass above eugonadal levels) - not shown in humans
  • Increased bone mineral density and bone mineral content at cortical and cancellous sites in ovariectomized rats, with periosteal anabolic activity; additive to bisphosphonate (alendronate) in preclinical osteoporosis models
  • Partial agonist (reduced) activity on prostate tissue in rats compared with full androgens
  • Effects on sexual behavior in female rats (enhanced male-directed preference and lordosis in sexually experienced animals) - a preclinical finding, not a human indication
  • No demonstrated human efficacy of any kind - all reported effects are from animal studies or inferred from the SARM class
Safety

Adverse effects by system

Cardiovascular

No LGD-3303-specific data. At the SARM class level, human case reports and a systematic review associate SARM use with cardiovascular events including myocarditis; androgenic compounds can also adversely affect lipids. Cardiovascular risk of LGD-3303 in humans is unknown and cannot be assumed safe.

Hepatic

No LGD-3303-specific human data. LGD-3303 is cleared by hepatic oxidative metabolism. The broader SARM class is repeatedly implicated in drug-induced liver injury (hepatocellular and cholestatic patterns, jaundice) in human case reports and reviews; hepatotoxicity for LGD-3303 must be presumed possible until proven otherwise.

Endocrine / HPTA

No LGD-3303-specific human data. As an androgen-receptor agonist, suppression of the hypothalamic-pituitary-testicular axis (lowered endogenous testosterone, LH, FSH) is expected on class grounds; testosterone suppression is documented across SARMs in humans. Degree and reversibility for LGD-3303 are unknown.

Reproductive

No LGD-3303-specific human data. Expected class effects of AR agonists include reduced spermatogenesis and testicular size via HPTA suppression, and (with androgens generally) potential prostate effects; LGD-3303 was a partial prostate agonist in rats. Human reproductive effects are uncharacterized and use is contraindicated in pregnancy.

Neuropsychiatric

No LGD-3303-specific human data. Androgenic agents can affect mood, libido and behavior; LGD-3303 crosses the blood-brain barrier in rats and altered sexual behavior was seen in female rats. Human neuropsychiatric effects are uncharacterized.

Renal

No LGD-3303-specific human data. Conjugated metabolites undergo renal elimination in animals. A SARM systematic review notes reports of kidney enlargement with SARM use; direct renal toxicity of LGD-3303 in humans is unknown.

Hematologic

No LGD-3303-specific human data. Androgens can raise hematocrit/erythropoiesis (polycythemia risk); whether LGD-3303 does so in humans is unknown.

Dermatologic

No LGD-3303-specific human data. Androgenic dermatologic effects (acne, oily skin, hair changes) are theoretically possible for AR agonists, though LGD-3303 showed reduced classic androgenic activity in rats. Human skin/hair effects are unknown.

Recovery

HPTA suppression & recovery

Suppression: Unknown/uncharacterized for LGD-3303 in humans; suppression of endogenous testosterone is expected on pharmacologic grounds and is documented across the SARM class

No human data describe the magnitude or time-course of HPTA suppression or recovery after LGD-3303. As an AR agonist it would be expected to lower endogenous testosterone, LH and FSH. Recovery cannot be predicted or promised. Anyone concerned about suppressed testosterone, infertility, or post-use recovery should consult a qualified endocrinologist for individualized evaluation and management; do not attempt self-directed hormonal 'recovery' protocols. Per StackItSmart policy, only single-agent SERM approaches are ever discussed and only under a physician's direction - no multi-drug recovery protocols are provided here.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function panel (ALT, AST, ALP, total/direct bilirubin, GGT)Total and free testosterone, LH, FSH (to detect HPTA suppression)Lipid panel (total, LDL, HDL, triglycerides)Complete blood count including hematocrit/hemoglobin (polycythemia)Renal function (creatinine, eGFR)If cardiac symptoms: troponin, ECG, and cardiology evaluation for possible myocarditis

Cadence: Baseline before any use, then periodically during use (e.g., roughly every 4-8 weeks) and after stopping, with immediate testing if warning signs appear. Any use should be under a clinician who orders and interprets these labs; because the compound is human-untested, close monitoring is essential.

Warning signs — seek care
  • Jaundice (yellowing of skin/eyes), dark urine, pale stools
  • Right-upper-quadrant abdominal pain, nausea, vomiting, unusual fatigue or malaise (possible liver injury)
  • Chest pain, shortness of breath, palpitations, exercise intolerance (possible myocarditis/cardiac event) - seek emergency care
  • Marked drop in libido, testicular shrinkage, mood disturbance (HPTA suppression)
  • New tendon pain or sudden tendon rupture
  • Any severe or unexplained new symptom - stop the compound and seek medical care
Do not use if

Contraindications

  • Pregnancy and breastfeeding (androgenic agents risk fetal virilization; absolutely avoid)
  • Anyone trying to conceive or preserve fertility (expected spermatogenesis suppression)
  • Pre-existing or active liver disease, or elevated baseline liver enzymes
  • Known or suspected prostate or breast cancer, or other androgen-sensitive malignancy
  • Pre-existing cardiovascular disease, cardiomyopathy, or significant dyslipidemia
  • Polycythemia or elevated hematocrit
  • Adolescents/individuals who are still growing
  • Concurrent use of other hepatotoxic agents, anabolic steroids, or other SARMs
  • General: an unapproved, human-untested investigational compound - not appropriate for use outside a supervised research setting
Combinations

Interaction profile

  • ModerateWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Recognize this is an unapproved, human-untested compound: there is no dose known to be safe, and no efficacy proven in people. The lowest-risk choice is not to use it.
  • Do not assume 'selective' means safe - class evidence shows real liver, heart, hormonal and tendon harms in humans.
  • Get baseline bloodwork (liver panel, testosterone/LH/FSH, lipids, CBC/hematocrit, renal function) before any use and monitor periodically with a clinician; do not use if baseline liver enzymes are elevated or liver/heart/prostate disease is present.
  • Stop immediately and seek medical care for jaundice, dark urine, right-upper-quadrant pain, nausea/vomiting, or unusual fatigue (possible liver injury), or for chest pain, breathlessness or palpitations (possible myocarditis - treat as an emergency).
  • Avoid combining with alcohol, other hepatotoxic drugs, anabolic steroids, or other SARMs, which compounds liver and cardiovascular risk.
  • Gray-market products are commonly mislabeled or contaminated with other active substances; the actual contents and dose are unverifiable.
  • Never use during pregnancy, breastfeeding, or while trying to conceive.
  • For any concern about suppressed testosterone, fertility, or recovery after use, consult a qualified endocrinologist rather than attempting self-directed hormonal protocols; only physician-supervised, single-agent approaches are appropriate.
Evidence

Citations (10)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    LGD-3303 is a potent non-steroidal AR ligand with little cross-reactivity to related nuclear receptors; near-full agonist on muscle and bone but partial agonist on prostate, never raising ventral prostate above ~50% of eugonadal levels; increases muscle, BMD and BMC in rats and is additive with alendronate.

    PreclinicalCombination treatment with a selective androgen receptor modulator (SARM) and a bisphosphonate has additive effects in osteopenic female rats.PMID 18847323 ↗

  2. 02

    LGD-3303 has potent activity on levator ani muscle but is only a partial agonist on prostate and preputial gland, never stimulating ventral prostate above intact levels; tissue-selectivity is intrinsic to AR interaction and independent of pharmacokinetics; characterized in castrated rats orally and by infusion.

    PreclinicalPharmacokinetics and pharmacodynamics of LGD-3303, an orally available nonsteroidal-selective androgen receptor modulator.DOI 10.1124/jpet.108.146811 ↗

  3. 03

    LGD-3303 is a non-steroidal, non-aromatizable, highly selective AR ligand that crosses the blood-brain barrier and alters sexual behavior in female rats; effect blocked by the AR antagonist flutamide.

    PreclinicalA selective androgen receptor modulator enhances male-directed sexual preference, proceptive behavior, and lordosis behavior in sexually experienced, but not sexually naive, female rats.PMID 20392832 ↗

  4. 04

    LGD-3303 undergoes hepatic hydroxylation and carboxylation with glucuronide conjugation and renal (urinary) elimination of metabolites; orally administered and studied for doping control (equine in vivo).

    PreclinicalEquine in vivo metabolite profiling of the selective androgen receptor modulator LGD-3303 for doping control.DOI 10.1016/j.jpba.2023.115468 ↗

  5. 05

    LGD-3303 is metabolized by liver microsomes (phase I hydroxylated metabolites); SARMs including LGD-3303 are widely available online and abused in sport.

    PreclinicalIdentification of equine in vitro metabolites of seven non-steroidal selective androgen receptor modulators for doping control purposes.DOI 10.1002/dta.3189 ↗

  6. 06

    LGD-3303 (LGD3303) is among SARMs metabolized by human liver microsomes and detectable in human urine; part of a class of unapproved compounds monitored in anti-doping analysis.

    PreclinicalSimultaneous detection of different chemical classes of selective androgen receptor modulators in urine by liquid chromatography-mass spectrometry-based techniques.DOI 10.1016/j.jpba.2020.113849 ↗

  7. 07

    SARMs as a class are associated in humans with hepatotoxicity, cardiotoxicity including myocarditis, tendon damage, testosterone suppression, and prostate/kidney enlargement; users take doses far above those clinically studied and products are frequently contaminated; no SARM is FDA-approved.

    ReviewAthlete Selective Androgen Receptor Modulators Abuse: A Systematic Review.DOI 10.1177/03635465241252435 ↗

  8. 08

    SARM use in humans is associated with drug-induced liver injury presenting as cholestatic or hepatocellular injury and jaundice; product quality/purity is poorly controlled, and none are approved by FDA/EMA.

    ReviewSelective androgen receptor modulator use and related adverse events including drug-induced liver injury: Analysis of suspected cases.PMID 38059982 ↗

  9. 09

    Case of SARM (Stenabolic)-related hepatocellular drug-induced liver injury; class shares structural/pharmacologic similarity to anabolic steroids raising hepatotoxicity concern via idiosyncratic immune-mediated mechanism; use should be discouraged.

    Case reportWhen Gains Go Wrong: A Case of Selective Androgen Receptor Modulator-Related Liver Injury.DOI 10.7759/cureus.87376 ↗

  10. 10

    Case of SARM (RAD-140)-induced liver injury with jaundice and elevated enzymes resolving after discontinuation, illustrating class hepatotoxicity and reversibility on stopping.

    Case reportSelective Androgen Receptor Modulators Leading to Liver Injury: A Case Report.DOI 10.7759/cureus.67958 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice