Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of ACP-105 and LGD-3303 — mechanism, side effects, legal status, and pricing.
ACP-105 is a non-peptide nonsteroidal selective androgen receptor modulator (SARM) of the azabicyclooctane chemotype, structurally related to AC-262536 and RAD140. It acts as a partial agonist at the androgen receptor with tissue-selective anabolic effects demonstrated in preclinical models. ACP-105 is not an approved drug in any jurisdiction and has never entered human clinical trials. SARMs as a class are prohibited at all times under WADA Prohibited List S1.2 'Other Anabolic Agents'; ACP-105 falls under this class-wide ban and has been the subject of equine anti-doping metabolite-detection research.
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.
ACP-105
LGD-3303
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
ACP-105
LGD-3303
COA corpus from Disclosed Labs — independently tested batches only.
ACP-105
2
COAs
99.3%
Avg purity
1
Labs
LGD-3303
2
COAs
99.0%
Avg purity
2
Labs
No human data exist for ACP-105. In castrated male rats, 2-week oral dosing improved anabolic parameters consistent with tissue-selective partial AR agonism, suppressed the LH surge, and produced levator ani muscle anabolic effects. In female mice (whole-body irradiated and sham-irradiated), ACP-105 preserved rotorod sensorimotor performance impaired by radiation and enhanced cued fear conditioning while reducing MAP-2 immunoreactivity in sensorimotor cortex. In male gonadectomized 3xTg-AD Alzheimer's-model mice, ACP-105 alone reduced anxiety-like behavior; combined with the ER-beta agonist AC-186, it improved cognition (Morris water maze), increased amyloid-beta-degrading enzymes (neprilysin, IDE), and decreased brain amyloid-beta versus vehicle. Equine in vitro liver microsome studies identified twelve Phase I metabolites for doping-control detection purposes.
Key references
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).
ACP-105 and LGD-3303 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.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing
Key references