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Commonly combined with LGD-3033 in research protocols.
Ratings are based on published research data and are for informational purposes only.
LGD-3033 is a non-steroidal SARM in the same chemical series as LGD-4033 (Ligandrol), developed as a potential follow-on candidate. It demonstrates high binding affinity to the androgen receptor with full agonist activity in muscle and bone. Preclinical data suggests comparable or superior anabolic potency to LGD-4033 with a shorter half-life. Published human clinical trial data is limited compared to LGD-4033.
Research Post
LGD-4033 (Ligandrol) is widely regarded as the best-characterised SARM in human research, owing to the landmark 2013 Phase I clinical trial conducted by Shalender Basaria and colleagues at Brigham and Women's Hospital. This non-steroidal SARM was developed by Ligand Pharmaceuticals and later licensed to Viking Therapeutics.
LGD-4033 is a full agonist at the androgen receptor in muscle and bone tissue. Its binding affinity for the AR is high (Ki ~1 nM), comparable to testosterone. The compound's selectivity profile arises from its unique molecular structure, which induces a conformational change in the AR that preferentially recruits co-activators in anabolic tissues while acting as a partial agonist or antagonist in androgenic tissues such as the prostate.
Unlike testosterone, LGD-4033 is neither aromatised to oestrogen nor reduced by 5α-reductase to more androgenic metabolites. This means the estrogenic side effects associated with testosterone (e.g., gynecomastia, water retention) are not direct concerns, though testosterone suppression still occurs via hypothalamic-pituitary feedback.
The Basaria et al. (2013) publication in The Lancet remains the cornerstone of LGD-4033 clinical research. This randomised, double-blind, placebo-controlled, dose-escalation trial enrolled 76 healthy men aged 21–50 years across five cohorts (0.1, 0.3, 1.0 mg/day, plus two placebo groups).
Key findings included: dose-dependent increases in lean body mass (+1.21 kg at 1 mg/day at 21 days); dose-dependent decreases in total testosterone and sex hormone-binding globulin (SHBG); no significant changes in prostate-specific antigen (PSA), haematocrit, or liver function tests. Testosterone and SHBG returned to baseline by day 56 following cessation — demonstrating reversible suppression.
This dataset is unique in providing clean, controlled, randomised human data for a SARM at doses relevant to lean mass research. No other SARM has matched this level of published human evidence in the public domain.
LGD-3033 is in the same chemical series as LGD-4033, developed as a potential follow-on candidate. It shares the same structural framework but features a different substitution pattern, resulting in a shorter half-life (approximately 6 hours) and potentially different tissue selectivity profile. Published human clinical data for LGD-3033 is significantly more limited than for LGD-4033, making it a less well-characterised research compound.
In terms of lean mass gains per milligram, LGD-4033 is among the most potent SARMs with published human data. RAD-140 may have a higher anabolic-to-androgenic selectivity ratio in preclinical models, but cross-compound human comparisons in published literature do not exist.
The Basaria 2013 trial documented testosterone and SHBG recovery by day 56 post-cessation across all dose groups. The degree and duration of suppression was dose-dependent, with higher doses producing deeper suppression requiring slightly longer recovery periods.
Viking Therapeutics is investigating VK5211 (LGD-4033) for hip fracture recovery. Phase II trial results demonstrated significant increases in lean body mass in patients recovering from hip fracture. Other potential research applications include muscle-wasting conditions and osteoporosis.
