Endometriosis
No direct peptide trials; GLP-1 emerging, GnRH agonists standard. Repair peptides are extrapolation.
Decision support, not prescription. You decide.
Monitor — GLP-1 constipation risk in bowel-endo
GLP-1 constipation is problematic in bowel-endometriosis/resection patients.
Candidate agents
4 agents · tap to expand▶TirzepatideLeadEmerging⚠ cautionA dual GIP/GLP-1 receptor agonist proposed as a multi-axis adjuvant for treatment-refractory endometriosis. Take it as a mechanistic hypothesis only — there is no endometriosis-specific trial, animal efficacy study, or any experimental data yet.expand
Monitor — GLP-1 constipation risk in bowel-endo
A dual GIP/GLP-1 receptor agonist proposed as a multi-axis adjuvant for treatment-refractory endometriosis. Take it as a mechanistic hypothesis only — there is no endometriosis-specific trial, animal efficacy study, or any experimental data yet.
▸Full clinical story
The rationale ties tirzepatide to four proposed endometriosis axes — Warburg-type metabolic reprogramming, peritoneal immune dysfunction, NF-kB/NLRP3/TGF-beta1 inflammatory-fibrotic remodeling, and nociceptive sensitization — converging on AMPK signaling and GLP-1 receptor activity in peritoneal macrophages and spinal microglia. A speculative 'peritoneal incretin deficiency' (low peritoneal GLP-1, high incretin-degrading proteases) is offered as the entry point for incretin-based modulation.
Weakest possible tier of support: a single 2026 hypothesis/review paper that explicitly labels itself hypothesis-generating and states that direct experimental or clinical validation in endometriosis-specific models is currently absent, with the 'peritoneal incretin deficiency' concept resting on one non-replicated case-control study. There is no endometriosis RCT, no human endometriosis outcome data, and no endometriosis animal or in-vitro efficacy study — the class's anti-inflammatory/metabolic effects are extrapolated from adjacent disease models. Grade set to none: the only endometriosis-specific literature is a mechanistic framework, not experimental data of any kind.
Anecdotal community signal only: patients with coexisting obesity, PCOS, or metabolic syndrome on tirzepatide/semaglutide for weight loss sometimes report incidental improvement in pelvic pain or menstrual symptoms, and a few clinicians discuss GLP-1 agents as an off-label metabolic adjuvant. This is uncontrolled, confounded by weight loss and menstrual changes, and must not be read as evidence of an endometriosis-specific effect.
No endometriosis-specific dosing exists. Context only: FDA-approved metabolic dosing is subcutaneous once weekly, titrated from 2.5 mg up to 15 mg. Any use here would be off-label and unstudied for this indication.
Endometriosis-relevant flags: many patients are of reproductive age, and GLP-1/GIP agents are not established as safe in pregnancy — reliable contraception and washout before conception planning matter, which conflicts with fertility goals common in this population. GI effects and delayed gastric emptying can compound the nausea and bloating already frequent in endometriosis, and weight loss itself alters menstrual/hormonal dynamics, confounding any perceived benefit.
An intriguing, biologically-reasoned hypothesis with zero endometriosis-specific evidence. Reasonable to keep on the radar for patients who already have a metabolic indication for a GLP-1/GIP agent, but not something to start for endometriosis pain on current data.
- Positive9 corroboratinganecdotal
Microdosed for inflammation/pain post-excision; ovulation pain gone, mood/energy up
Side effects: constipation (bowel-endo)
access barrierr/endometriosis
No peer data yet. Aggregates appear once ≥3 clinicians log an outcome.
▶BPC-157NoneA synthetic gastric peptide marketed for tissue repair, with no connection to endometriosis beyond general anti-inflammatory extrapolation. Take any endometriosis claim as unsupported.expand
A synthetic gastric peptide marketed for tissue repair, with no connection to endometriosis beyond general anti-inflammatory extrapolation. Take any endometriosis claim as unsupported.
▸Full clinical story
Proposed actions are generic: angiogenic/cytoprotective and anti-inflammatory signaling (VEGF, nitric oxide, growth-factor pathways) shown in tendon, gut, and wound models. None of this has been studied in endometriotic lesions, and its pro-angiogenic profile is a theoretical concern rather than a benefit in a disease driven partly by angiogenesis.
None for this condition. A PubMed search for BPC-157 and endometriosis returns zero results — no RCT, no human data, no animal model, no in-vitro endometriosis study. All rationale is extrapolation from unrelated tissue-repair literature (much of it low-quality and industry/self-experiment adjacent).
Anecdotal community signal only: BPC-157 is popular in peptide/biohacking communities (typical self-reported use for gut and musculoskeletal healing), and some endometriosis patients try it hoping for a general anti-inflammatory or post-surgical recovery effect. Reports are scattered, uncontrolled, and not endometriosis-specific; treat purely as hearsay.
No endometriosis dosing exists. Community context only (not a protocol): commonly self-administered around 200-500 mcg subcutaneously once or twice daily; product quality is unregulated.
Condition-specific concern: theoretical pro-angiogenic activity is unattractive in an angiogenesis-dependent disease. BPC-157 is not an approved drug, sourcing is unregulated, and long-term human safety data are lacking — relevant for reproductive-age patients who may be trying to conceive.
No endometriosis evidence of any kind. Nothing to recommend here; any use is experimental self-treatment on generic reasoning.
▶MetforminPreclinicalAn AMPK-activating insulin sensitizer with consistent implant-regression signals in animal endometriosis models but no human endometriosis trial. Take it as a mechanistically attractive, preclinical-only candidate.expand
An AMPK-activating insulin sensitizer with consistent implant-regression signals in animal endometriosis models but no human endometriosis trial. Take it as a mechanistically attractive, preclinical-only candidate.
▸Full clinical story
Metformin activates AMPK, inhibiting mTOR and modulating autophagy, while acting as an anti-inflammatory, anti-angiogenic, and anti-proliferative agent in endometriotic tissue. In animal models it raises superoxide dismutase and TIMP-2 and lowers VEGF and MMP-9, and it may alter stroma-epithelium Wnt/beta-catenin crosstalk and improve endometriosis-associated endothelial dysfunction (downregulating ET-1, upregulating eNOS).
Preclinical only. Multiple rodent studies show statistically significant regression of surgically induced endometriotic implants: metformin reduced implant size, weight, and histologic score and lowered VEGF/MMP-9 while raising SOD/TIMP-2, with effect comparable to letrozole in a head-to-head rat model. A mouse study confirms anti-endothelial-dysfunction effects, and a 2022 review summarizes the mechanistic case. No human endometriosis RCT exists — grade correctly remains preclinical.
Anecdotal community signal only: metformin is already widely used off-label in reproductive medicine (PCOS, insulin resistance), so some endometriosis patients — especially those with metabolic overlap — take it and report reduced pain or inflammation. These reports are confounded by coexisting PCOS/weight effects and are not endometriosis-specific evidence.
No endometriosis-specific protocol. Context only: standard adult metabolic dosing is 500-2000 mg/day orally in divided doses, titrated to tolerance; animal endometriosis work used 25-200 mg/kg/day, which does not translate directly to human dosing.
Condition-specific flags: frequently co-prescribed with GnRH agonists or hormonal therapy (additive rather than tested combinations), and used in reproductive-age patients — metformin is generally considered compatible with conception planning but should be reviewed against fertility goals. Watch GI intolerance (overlaps with endometriosis bowel symptoms), rare lactic acidosis with renal impairment, and possible B12 depletion on long-term use.
A cheap, well-characterized drug with reproducible animal regression data and a coherent mechanism, but still unproven for endometriosis in humans. Reasonable to consider in patients with a metabolic co-indication; not yet a standalone endometriosis therapy.
- Metformin regresses endometriotic implants in rats by improving implant levels of superoxide dismutase, vascular endothelial growth factor, tissue inhibitor of metalloproteinase-2, and matrix metalloproteinase-9. ↗
- The effects of metformin and letrozole on endometriosis and comparison of the two treatment agents in a rat model. ↗
- Metformin as a Potential Treatment Option for Endometriosis. ↗
- Metformin Prevents Endothelial Dysfunction in Endometriosis through Downregulation of ET-1 and Upregulation of eNOS. ↗
Not recommended for this condition
Shown to close the loop — the evidence points the wrong way here.
▶VIPPreclinicalVasoactive intestinal peptide is a pain-associated biomarker that is elevated in endometriosis tissue — this is a known-negative for supplementation, not a therapeutic. Administering VIP would be expected to worsen, not help.expand
Vasoactive intestinal peptide is a pain-associated biomarker that is elevated in endometriosis tissue — this is a known-negative for supplementation, not a therapeutic. Administering VIP would be expected to worsen, not help.
▸Full clinical story
VIP is a pro-inflammatory, pro-angiogenic neuropeptide expressed in the sensory and autonomic nerve fibers that innervate endometriotic lesions. In endometriosis its transcript and protein are upregulated in endometrium and lesions, tracking with microvessel density and IL-6 — so exogenous VIP would plausibly add to angiogenesis, inflammation, and nociceptive signaling in the pelvic microenvironment.
Human observational/biomarker studies (immunohistochemistry, Western blot, RT-qPCR, ELISA on patient tissue, serum, and peritoneal fluid): VIP is significantly higher in endometriosis patients and highest in those with chronic pelvic pain, and VIP-positive nerve fibers are found in lesion-associated innervation. This is solid human evidence of an association, but it establishes VIP as a correlate of disease/pain, not as a treatment — hence the preclinical/biomarker grade and the avoid framing.
Anecdotal community signal only: VIP (e.g. intranasal 'Aviptadil'-type peptides) circulates in longevity, CIRS/mold, and chronic-inflammation biohacking circles for unrelated indications. There is no meaningful endometriosis-specific community use, and given the biology, clinicians should actively steer patients away from it for this condition.
No endometriosis dosing exists and none should be inferred; the biology points to net harm. Any dosing figures come from unrelated experimental respiratory/vasodilator contexts and are not applicable here.
Direction is effectively adverse for endometriosis: because endogenous VIP is already elevated and pain-linked, supplementing VIP is mechanistically counterproductive and could aggravate angiogenesis, inflammation, and pelvic pain. VIP is also a systemic vasodilator with hypotension risk, unrelated to any endometriosis benefit.
Useful as a disease/pain biomarker and a mechanistic target for antagonism — never as a peptide to give. Flag as avoid for endometriosis.
Matching protocol templates
Browse all →Body recomposition, injury recovery, fat trimming
Skin tightening, collagen repair, wound healing
Gut healing, barrier repair, anti-inflammatory
The platform surfaces evidence, community signal and peer outcomes with enforced cautions. It never decides treatment — the licensed clinician orders labs, writes notes, and prescribes.