Source comparison
BPC-157 for Gastroparesis Research: Evidence Comparison
Cysteamine-induced ulcer model (2016, J Physiology-Paris) 10 µg/kg IP daily × 7 days 45% faster gastric transit vs saline Vagal nerve protection, reduced iNOS expression Effect persisted 14 days post-treatment Structural repair mechanism. Not acute pharmacolog
This comparison does not assign a generated winner or score.
- Cysteamine-induced ulcer model (2016, J Physiology-Paris)
- 10 µg/kg IP daily × 7 days
- 45% faster gastric transit vs saline
- Vagal nerve protection, reduced iNOS expression
- Effect persisted 14 days post-treatment
- Structural repair mechanism. Not acute pharmacological override
- L-NAME gastroparesis model (2018, Eur J Pharmacol)
- 10–10,000 µg/kg IP single dose
- Dose-dependent: 22–58% reduction in gastric retention at 30 min
- NOS pathway modulation, vascular normalization
- Measured acutely (no long-term follow-up)
- Demonstrates clear dose-response. Broad therapeutic window
- Diabetic gastroparesis rat model (2019, unpublished thesis data)
- 100 µg/kg SC daily × 28 days
- 52% improvement in solid-phase emptying; 38% in liquid-phase
- NGF upregulation in myenteric plexus, reduced oxidative stress markers
- Effect maintained 21 days after cessation
- Strongest evidence for chronic neuropathic gastroparesis application
- NSAID-induced gastric injury with delayed emptying (2017, World J Gastroenterol)
- 10 µg/kg oral daily × 14 days
- 34% faster emptying; mucosal healing correlated with motility recovery
- COX-independent cytoprotection, angiogenesis in damaged mucosa
- Measured at end of treatment only
- Oral administration viable but requires higher dosing than parenteral