BPC-157 for Diabetic Neuropathy Research: Study Type Comparison
Preclinical (2019) Streptozotocin-induced diabetic rats Nerve conduction velocity (NCV) 10 mcg/kg/day subcutaneous 8 weeks 34% improvement in NCV vs untreated controls; GAP-43 upregulation confirmed Strongest evidence for structural nerve repair. Not symptom m
This comparison does not assign a generated winner or score.
- Preclinical (2019)
- Streptozotocin-induced diabetic rats
- Nerve conduction velocity (NCV)
- 10 mcg/kg/day subcutaneous
- 8 weeks
- 34% improvement in NCV vs untreated controls; GAP-43 upregulation confirmed
- Strongest evidence for structural nerve repair. Not symptom masking
- Preclinical (2020)
- Alloxan-induced diabetic mice
- Thermal sensitivity threshold, oxidative stress markers
- 5–15 mcg/kg/day subcutaneous
- 6 weeks
- 47% increase in GAP-43, 38% reduction in MDA (oxidative stress marker)
- Dual mechanism: promotes repair while reducing ongoing damage
- In Vitro (2021)
- Schwann cell cultures exposed to high glucose
- Schwann cell proliferation, myelin protein expression
- 0.1–10 μg/mL culture medium
- 72 hours
- Dose-dependent increase in myelin basic protein (MBP) expression; VEGF upregulation
- Mechanism confirmation. Directly affects myelinating cells, not just systemic inflammation
- Preclinical (2018)
- Diabetic rats with autonomic neuropathy
- Gastric emptying rate (autonomic nerve function)
- 4 weeks
- Normalized gastric motility to 87% of healthy baseline vs 52% in controls
- Evidence extends beyond sensory nerves. Autonomic nerve microvascular supply restored