Source comparison
BPC-157 Lyme Disease Research Mechanism: Comparison Table
This table compares BPC-157's documented mechanisms in preclinical models against the pathophysiological targets relevant in Lyme disease and post-treatment Lyme disease syndrome. Nitric Oxide Modulation Downregulates iNOS in sepsis; upregulates eNOS in ischem
This comparison does not assign a generated winner or score.
- This table compares BPC-157's documented mechanisms in preclinical models against the pathophysiological targets relevant in Lyme disease and post-treatment Lyme disease syndrome.
- Nitric Oxide Modulation
- Downregulates iNOS in sepsis; upregulates eNOS in ischemia
- Lyme triggers iNOS overexpression and chronic NO elevation
- Persistent inflammation and vascular dysfunction in PTLDS may involve NO dysregulation
- Animal models only. No human Lyme trials
- VEGF Upregulation
- Increases VEGF expression and VEGFR-2 signalling in tendon and vascular injury models
- Lyme causes endothelial damage and microvascular inflammation
- Chronic joint effusions and synovial thickening may benefit from angiogenic support
- Mechanistic overlap. No direct Lyme testing
- NF-κB Pathway Inhibition
- Reduces NF-κB activation in IBD and sepsis models
- Borrelia infection activates NF-κB, driving cytokine release (TNF-α, IL-6)
- Residual immune activation in PTLDS may involve persistent NF-κB signalling
- Indirect evidence from inflammatory models
- Blood-Brain Barrier Stabilisation
- Protects tight junction proteins (occludin, claudin-5) and reduces MMP-9 in TBI models
- Neuroborreliosis disrupts BBB integrity
- Cognitive symptoms and neuroinflammation in PTLDS overlap with TBI sequelae
- No neuroborreliosis studies published
- Tissue Repair and Collagen Remodelling
- Accelerates tendon healing and improves collagen organisation via FAK-paxillin signalling
- Lyme arthritis causes cartilage and synovial damage
- Persistent joint symptoms after antibiotic treatment may reflect incomplete repair
- Connective tissue models. Not infection-driven damage
- Antimicrobial Activity
- None. BPC-157 is not bactericidal or bacteriostatic
- Borrelia burgdorferi eradication requires antibiotics
- BPC-157 cannot replace doxycycline or ceftriaxone
- Established. Peptide has no direct antimicrobial effect