BPC-157 Help Lyme Disease Research: Evidence Comparison
Animal tendon repair models (multiple studies, 2010–2020) FAK-paxillin activation, collagen synthesis Potential reduction in joint inflammation post-infection High-quality rodent RCTs No spirochete infection model; outcomes measure acute injury, not chronic im
This comparison does not assign a generated winner or score.
- Animal tendon repair models (multiple studies, 2010–2020)
- FAK-paxillin activation, collagen synthesis
- Potential reduction in joint inflammation post-infection
- High-quality rodent RCTs
- No spirochete infection model; outcomes measure acute injury, not chronic immune dysregulation
- Demonstrates tissue repair in sterile injury. Doesn't model Lyme's persistent inflammation
- Gastric ulcer healing (rat models, published 2015)
- NO modulation, mucosal protection
- Possible reduction in GI symptoms seen in disseminated Lyme
- Moderate. Single-organ focus
- Mechanism unrelated to Borrelia-triggered pathology; no infectious disease component
- Relevant only if Lyme symptoms include GI involvement. Not a primary Lyme target
- Neuroinflammation models (2018 brain injury study)
- VEGF upregulation, blood-brain barrier stabilization
- Could theoretically address neuroborreliosis microvascular damage
- Moderate. Traumatic brain injury model, not infection
- BBB dysfunction in Lyme differs from TBI; no Borrelia antigen exposure in model
- Promising for CNS tissue repair. But zero validation in spirochete-induced CNS inflammation
- Human Lyme disease clinical trials
- None conducted as of 2026
- No data
- N/A
- Complete absence of human evidence specific to Lyme
- Cannot assess efficacy without Phase II/III data. Any claims are speculative