Understand the source comparison
Best Peptides for Endometriosis: Mechanism Comparison
BPC-157 VEGF modulation, angiogenesis regulation, tissue repair Lesion neovascularisation, adhesion formation Preclinical only. In vitro and animal models Strongest theoretical basis for anti-adhesion effects; no human trials in endometriosis KPV NF-κB inhibit
No winner is assigned.
This page preserves a source comparison for education. It does not add a rating, recommendation or clinical judgment.
- BPC-157
- VEGF modulation, angiogenesis regulation, tissue repair
- Lesion neovascularisation, adhesion formation
- Preclinical only. In vitro and animal models
- Strongest theoretical basis for anti-adhesion effects; no human trials in endometriosis
- KPV
- NF-κB inhibition, melanocortin receptor agonism
- Peritoneal inflammation, macrophage activation
- In vitro studies in colitis models; none in endometriosis
- Mechanistically sound for localised inflammation; clinical validation absent
- Thymosin Beta-4
- TGF-β suppression, macrophage polarisation, actin regulation
- Fibrosis, adhesion formation, immune dysregulation
- Phase 2 trials in wound healing; none in gynecological conditions
- Best evidence for fibrosis reduction; dosing and safety unclear for endometriosis
- Thymalin
- Thymic peptide immune regulation, mast cell stabilisation
- Immune dysregulation, neurogenic inflammation
- Studied in autoimmune contexts; no gynecological research
- Potential mast cell benefit but entirely speculative for endometriosis
- MK-677
- GH secretagogue, IGF-1 elevation
- Tissue repair post-surgery (theoretical); risk of lesion proliferation
- None. IGF-1 shown to worsen aromatase expression in vitro
- Contraindicated. Growth factors may worsen disease
- Cerebrolysin
- Neurotrophic peptides (BDNF, NGF precursors)
- Neuroangiogenesis (mechanism unclear. May worsen or mitigate)
- Neurodegenerative disease trials only
- Insufficient data; BDNF elevation could worsen nerve infiltration