LGD-4033 vs Pitavastatin
Moderate Research vs FDA Approved
avoid Mechanism-based · 64% Both LGD-4033 and Pitavastatin carry hepatotoxic risk. Combining hepatotoxic compounds significantly increases liver damage potential. If unavoidable, include liver support (TUDCA/NAC) and monitor ALT/AST frequently.
Molecular Data
LGD-4033 Pitavastatin
Weight 338.25 Da 421.46 Da
Half-life ~24-36 hours ~12 hours
Type Nonsteroidal selective androgen receptor modulator (C14H12F6N2O) Synthetic statin (C25H24FNO4)
Key Benefits
LGD-4033
01 Strongest SARM for lean muscle mass accrual, with clinical trial data supporting dose-dependent increases in lean body mass
02 Tissue-selective action with minimal stimulation of the prostate and other androgen-sensitive tissues
03 Clinical evidence of improved physical function (leg press strength, stair-climbing speed) in hip fracture patients
04 No aromatization to estrogen (no estrogen-related water retention or gynecomastia at the receptor level)
05 No conversion to DHT (reduced risk of androgenic hair loss and prostate stimulation compared to testosterone)
06 Convenient once-daily oral dosing due to 24-36 hour half-life
07 Phase 2 clinical data available, providing a stronger evidence base than most other SARMs
Pitavastatin
01 Minimal CYP450 metabolism — does not interact with CYP3A4, making it ideal for users taking multiple compounds
02 Lowest risk of new-onset diabetes among all statins, supported by the LIVES study and J-PREDICT trial data
03 LDL reductions of 38-45% at standard doses (2-4 mg/day)
04 More robust HDL-raising effect (5-15%) compared to other statins in the class
05 12-hour half-life supports convenient once-daily dosing
06 Favorable safety profile with low incidence of muscle-related side effects
07 Compatible with CYP3A4 inhibitors and inducers that would alter levels of other statins
08 Effective at counteracting AAS-induced lipid disturbances without adding to drug interaction burden
Side Effects
LGD-4033
Testosterone suppression (dose-dependent; more suppressive than Ostarine at equivalent doses, occurs in most users by week 4-6)
Water retention (non-estrogenic mechanism, typically mild to moderate, contributes to scale weight increase)
HDL cholesterol reduction (dose-dependent lipid impact observed in clinical trials)
Headaches (most common in the first 1-2 weeks, usually transient)
Fatigue or lethargy (related to testosterone suppression, typically becomes noticeable mid-cycle)
Reduced libido (related to HPG axis suppression, severity varies by dose and individual)
Pitavastatin
Myalgia and muscle discomfort (approximately 3-5% of users) — generally mild and less frequent than with lipophilic statins
Headache
Minimal liver enzyme elevation — typically transient and clinically insignificant
Back pain
Constipation or diarrhea
Contraindications
Pre-existing liver disease or elevated liver enzymes at baseline
Hormone-sensitive cancers (prostate cancer or other androgen-driven malignancies)
Pregnancy or potential pregnancy (teratogenic risk from androgen receptor agonism)
Breastfeeding
Age under 25 (incomplete endocrine system maturation and higher risk of HPG axis disruption)
Concurrent use of hepatotoxic medications without medical supervision
Known cardiovascular disease (insufficient long-term safety data for this population)
History of significant lipid abnormalities (LGD-4033 suppresses HDL)
Active liver disease or unexplained persistent elevations in hepatic transaminases
Known hypersensitivity to pitavastatin or any excipients
Pregnancy and breastfeeding (Category X — statins are teratogenic)
Concomitant use with cyclosporine (significantly increases pitavastatin levels via OATP1B1 inhibition)
Concomitant use with lopinavir/ritonavir or atazanavir/ritonavir combinations
Research Evidence
LGD-4033 Pitavastatin
Status Moderate Research FDA Approved
References 5 studies 5 studies
Latest 2018 2023
FDA Approved No Yes
This comparison is for educational and research purposes only. Consult a healthcare professional before use.