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Best Peptides for NASH Liver: Mechanism Comparison
The table below compares the three peptides with the strongest published evidence for NASH-specific mechanisms. Including their primary pathway of action, documented effects in preclinical models, typical dosing ranges, and the evidence quality supporting thei
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- The table below compares the three peptides with the strongest published evidence for NASH-specific mechanisms. Including their primary pathway of action, documented effects in preclinical models, typical dosing ranges, and the evidence quality supporting their use.
- Thymosin Alpha-1
- HSC deactivation via TLR9 suppression
- 58% reduction in α-SMA, 41% reduction in hepatic steatosis, 67% reduction in fibrosis progression
- 1.6–3.2 mg/kg SC twice weekly (murine); HED ~0.13–0.26 mg/kg
- Preclinical only. Published in peer-reviewed hepatology journals
- Strongest evidence for fibrosis reversal. Addresses the root cause of scar tissue formation
- BPC-157
- Mitochondrial biogenesis via PGC-1α upregulation and AMPK activation
- 73% increase in PGC-1α, 52% reduction in hepatic triglycerides, 38% improvement in mitochondrial respiratory capacity
- 10–20 mcg/kg SC daily (murine); human dosing extrapolation not established
- Preclinical only. Mechanism well-characterized but no human NASH trials
- Most relevant for steatosis reduction and metabolic recovery. Less direct fibrosis effect
- MOTS-c
- Autophagy induction via AMPK activation and mTOR suppression
- 2.4-fold increase in LC3-II/LC3-I, 44% reduction in hepatic lipid content, 29% improvement in NAS score
- 5–15 mg/kg IP or SC 3× weekly (murine); human dosing not established
- Preclinical only. Published in high-impact metabolism journals
- Best evidence for lipid clearance and mitochondrial quality control. Requires long-term administration