LGD-4033 — ligandrol, and under its one pharmaceutical name VK5211 — is the compound people reach for when they have decided steroids are too much and creatine is not enough. It is genuinely the best-studied selective androgen receptor modulator a consumer can actually buy: there are two randomised, placebo-controlled human trials with real numbers in them. That is the reason this page exists, and it is also the reason it will probably disappoint you. The data is real, it is small, and most of what it says is not what the sales copy says.
What LGD-4033 actually is
LGD-4033 is a small non-steroidal molecule that binds the androgen receptor directly, with very high affinity — a Ki of about 1 nanomolar — and, unlike testosterone, does so without a steroid backbone.[1] That structural difference is the entire premise of the drug class. Testosterone and its esters are substrates for aromatase and 5α-reductase, so they are converted in the body into oestradiol and dihydrotestosterone, which is where much of the prostate and breast tissue signalling comes from. A non-steroidal ligand is not a substrate for either enzyme, so in principle it can switch the receptor on in muscle and bone while leaving prostate signalling comparatively alone. In preclinical work LGD-4033 showed exactly that: anabolic activity in muscle, both anti-resorptive and anabolic activity in bone, and marked selectivity for muscle over prostate.[1]
Two things follow from that description, and both get lost in the marketing. First, tissue selectivity is relative, not absolute. The receptor being activated is the same receptor, and the hypothalamic–pituitary–gonadal axis reads that activation as androgen and turns your own production down — which is precisely what the human trial found. Second, LGD-4033 is not a peptide. It is an orally active small molecule, which is why it is swallowed rather than injected and why it has a 24–36 hour elimination half-life.[1] If you arrived here from the peptide aisle, the distinction matters more than the marketing suggests — we lay it out in peptides vs SARMs.
The phase 1 trial, in full — because it is most of the evidence
Basaria and colleagues, publishing in The Journals of Gerontology in 2013, ran a randomised, double-blind, placebo-controlled ascending-dose study at Boston University. Seventy-six healthy men aged 21–50 were randomised to placebo or to 0.1, 0.3 or 1.0 mg of LGD-4033 once daily for 21 days, followed by five weeks of observation. Blood counts, chemistries, lipids, PSA, ECG, hormones, DXA body composition and one-repetition-maximum strength were all measured.[1] This is a well-built small trial: concealed randomisation, blinding, an independent Data and Safety Monitoring Board, and 100% compliance among the men in the efficacy analysis.
The anabolic result. Lean body mass increased dose-dependently (p for trend = .04), and at the 1.0 mg dose the increase averaged 1.21 kg over 21 days (p = .047 versus placebo). Against a mean baseline lean mass of 63.9 kg in that group, that is a gain of about 1.9%. It is a genuine, statistically significant androgenic signal in three weeks, and the authors are right to call it notable for so short a study.
What did not move. Appendicular skeletal muscle mass — the muscle in your arms and legs, the part that does the work — did not separate from placebo (p for trend = .078). Leg press strength rose by 68.3 N at the top dose, and that change was not significantly different from placebo. Stair-climbing speed and power showed a trend and no more. And the mechanistic test the investigators built into the study — fractional synthetic rate of mixed-muscle protein, measured with a labelled-phenylalanine infusion and vastus lateralis biopsies — found no difference at all between the 0.3 mg group and placebo (0.033 vs 0.031, p = .99).[1] Three weeks is short, and the trial was powered for safety rather than efficacy; the honest reading is that the DXA number moved and nothing you could feel did.
The pharmacokinetics. LGD-4033 had a prolonged elimination half-life of 24–36 hours and linear kinetics, with serum concentrations on day 21 nearly threefold higher than on day 1 — it accumulates. Mean 24-hour exposure on day 21 rose in step with dose: 19, 85 and 238 ng·24 h/mL at 0.1, 0.3 and 1.0 mg.[1]
The trade, at each dose
| Daily dose, 21 days | Lean body mass | Testosterone axis | HDL cholesterol |
|---|---|---|---|
| Placebo | Reference | No meaningful change | −1.7 mg/dL (baseline 52.5) |
| 0.1 mg | Dose trend only (p for trend = .04) | Total testosterone and SHBG fall dose-dependently | −1.0 mg/dL (baseline 56.1) |
| 0.3 mg | Dose trend only | Total testosterone and SHBG suppressed | −10.4 mg/dL (baseline 50.3) — about −21% |
| 1.0 mg | +1.21 kg vs placebo (p = .047) | Total testosterone and SHBG suppressed; free testosterone and FSH suppressed only at this dose | −19.4 mg/dL (baseline 49.2) — about −39% |
Read the table across rather than down. The dose that produced the only statistically significant lean-mass gain is also the dose that suppressed free testosterone and FSH and cut HDL cholesterol by roughly two-fifths. There is no row where you get the anabolic effect without the endocrine one, because they are the same receptor event seen from two directions.
VK5211: the one real clinical trial, and what it stopped short of
Ligand Pharmaceuticals licensed LGD-4033 to Viking Therapeutics, which renamed it VK5211 and took it into the only registered clinical trial the molecule has ever had: NCT02578095, a phase 2, randomised, quadruple-masked, placebo-controlled study in 108 ambulatory patients aged 65 or older, enrolled three to seven weeks after an acute hip fracture and treated for 12 weeks with 0.5, 1.0 or 2.0 mg daily or placebo. It ran from October 2015 to December 2017.[2]
The posted results are unambiguous on their own terms. The primary endpoint — placebo-corrected percentage change in total-body-less-head lean mass on DXA at week 12 — rose 4.75% at 0.5 mg (95% CI 1.70–7.80; p = .0032), 7.15% at 1.0 mg (3.76–10.54; p < .0001) and 9.08% at 2.0 mg (5.55–12.60; p < .0001). Serious adverse events were distributed 4/28, 2/29, 3/26 and 5/25 across placebo and the three dose arms, with no deaths.[2]
Now the part that matters more. That lean-mass number is the only outcome measure posted on the registry. There is no reported endpoint for gait speed, for the short physical performance battery, for time to independent ambulation, for falls, for fracture healing, or for returning home. Nobody showed that these patients walked better, stood up more easily, or recovered faster — only that a DXA scanner counted more lean tissue, in a population that is catabolic and losing muscle by default after a hip fracture, which is part of why the placebo-corrected percentages look large. The study completed in December 2017 and no phase 3 has been registered since. A search of ClinicalTrials.gov under LGD-4033, ligandrol and VK5211 returns this trial and nothing else.[2]
Nor is that gap peculiar to this molecule. A 2025 systematic review pooled every randomised controlled trial of any SARM reporting physical performance: nine studies, 970 patients, six different compounds, and a mean follow-up of 80 days with a maximum of 180.[3] The reviewers concluded SARMs improve body composition and physical performance with mostly mild-to-moderate adverse events — a fair summary of a literature in which no trial of any SARM, in any indication, has yet run longer than six months. If you want to know what daily androgen-receptor agonism does to a body over years, the honest answer is that the trials to tell you have not been run. What we do have is the testosterone therapy evidence base, which is far larger and far longer — and which is not the same drug.
The liver signal
The FDA’s standing consumer warning on bodybuilding products containing SARMs lists liver injuries that required hospitalisation among reported life-threatening reactions, alongside increased risk of heart attack or stroke, psychosis and hallucinations, sleep disturbance, sexual dysfunction, acute liver failure, infertility, pregnancy miscarriage and testicular shrinkage.[12] The agency tells clinicians to watch for liver injury, kidney injury, stroke, pulmonary embolism and deep vein thrombosis in patients using these products, and tells consumers to seek care for nausea, weakness or fatigue, fever, abdominal or chest pain, shortness of breath, jaundice, or brown urine.[12]
Not approved, banned in sport, and often not what the label says
Regulatory status. LGD-4033 is not approved for any indication in any jurisdiction. The FDA is explicit that products marketed as SARMs are not dietary supplements: “these products are unapproved drugs that FDA has not reviewed for safety and effectiveness,” and they are illegally marketed. The agency specifically notes that such products are sometimes labelled “for research purposes” or “not for human consumption” while being sold direct to consumers with dosing instructions, and that it has issued warning letters and pursued criminal actions against distributors.[12] USADA adds that the FDA has clarified LGD-4033 is not a legitimate dietary ingredient.[13]
Anti-doping. LGD-4033 is named by name on the WADA Prohibited List under S1.2, Other Anabolic Agents, in the section of substances prohibited at all times, in and out of competition.[10][13] This is not a theoretical risk: LGD-4033 produced 62 adverse analytical findings in 2019 alone, and anti-doping laboratories have validated detection down to a limit of 8 pg/mL, picking the drug and its metabolites out of urine after deliberate micro-doses of as little as 1 µg.[11] Its long half-life and long-term hydroxylated metabolites mean the detection window is measured in weeks, not days. Tested athletes should treat this as a career-ending compound; so should anyone in a workplace that screens for anabolic agents.
The supply chain. This is the part that undermines everything above, because none of the trial data applies to a product that does not contain the trial drug. Researchers bought 44 products marketed and sold online as SARMs and analysed them under chain of custody with WADA-approved methods: only 52% contained any SARM at all. Another 39% contained a different unapproved drug — ibutamoren, GW501516, SR9009. In 9% no active compound was detected. A quarter contained substances not listed on the label, and in only 41% did the amount of active compound match what the label claimed.[8] A five-year European market-surveillance programme across 13 countries reached the same place from a different angle: of 324 seized samples, ligandrol was the second most frequently identified molecule after ibutamoren; 24% were presented as dietary supplements, meaning the buyer did not know they were taking an unapproved pharmaceutical; and most samples contained active doses, some overdosed.[9] Supplement contamination is also a documented route to a positive doping test rather than a convenient excuse for one.[11][13]
The honest bottom line
LGD-4033 has better human data than any other SARM a consumer can buy, and the data is good enough to say something definite. It works, in the narrow sense that a DXA scanner registers more lean tissue: 1.21 kg over 21 days at 1.0 mg in healthy men, and a placebo-corrected 4.75–9.08% over 12 weeks in elderly hip-fracture patients.[1][2] That is a real androgenic effect and it should be stated plainly.
Everything else is a subtraction. Nobody has demonstrated that the added lean mass makes you stronger — strength, stair-climbing power and muscle protein synthesis all failed to separate from placebo in the trial that measured them.[1] Nobody has demonstrated a clinical benefit in the one patient population it was tested in; the trial reported a body-composition number and no functional outcome, and no phase 3 followed.[2] Hormonal suppression is not a risk you might avoid at the right dose; it is the same receptor event as the muscle gain, it happened at every dose tested, and the largest dose ever formally studied was one-tenth of what a documented user was taking.[1][7]The longest randomised exposure to any SARM on record is six months, so nobody — including the people selling it — knows what a year of this does.[3] Multiple published cases of cholestatic liver injury are attached to it.[4][5][6] It is prohibited in sport at all times and detectable for weeks.[10][11] And roughly half the products sold as SARMs do not contain the drug on the label.[8][9]
A drug that adds a kilogram of lean mass without adding strength, shuts down your own hormone production while it does so, has never been shown to help a patient with anything, and arrives in a bottle with a coin-flip chance of containing what it claims, is not a shortcut. It is a small pharmacological effect wrapped in a large amount of unmeasured risk. If low testosterone is the actual problem you are trying to solve, that is a diagnosable condition with a real evidence base and a prescriber attached to it — start with what testosterone therapy does and does not do instead.
This article is research information, not medical advice, and it is deliberately not a dosing or cycle guide. LGD-4033 is an unapproved investigational drug, not a dietary supplement and not a legal ingredient in one; the FDA has warned that products sold as SARMs are illegally marketed unapproved drugs associated with hospitalisation for liver injury and with heart attack, stroke, psychosis, infertility and testicular shrinkage. It is prohibited at all times under WADA class S1.2 and is detectable in urine for weeks. If you have taken it and develop jaundice, dark urine, abdominal pain, unusual fatigue or chest pain, seek medical care and tell the clinician exactly what you took. Anyone considering it should speak to a licensed clinician first — particularly if you have liver disease, cardiovascular risk factors, or are being screened by a sports or employment testing programme.