Research Radartracking 4 published studies · 1 human · 2 clinical trials · 2 cancer pages · updated Jun 2026Open the Research Map →

PEA (Palmitoylethanolamide)

Endogenous amide: PPAR-α ↑, neuro-inflammation/pain ↓; moderate CIPN adjunct in lung/breast/colorectal/ovarian.

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Human-reviewed · How we review →

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👥⭐⭐⭐ Moderate — Human neuropathy studies and mechanistic rationale support use; oncology-specific RCTs for CIPN are emerging.PEAMicronized PEAum-PEA

Forms: Ultra-micronized capsules (300-600 mg) · Co-micronized with luteolin (PEA-Lut)

Educational only, not medical advice. OncoForge makes no claim that PEA (Palmitoylethanolamide) treats, prevents, or cures any condition, beyond what the linked studies show. Evidence levels vary; effects may not translate to people, and some compounds can cause harm. Always coordinate with your oncology team.

Key Takeaway

Endogenous fatty-acid amide that activates PPAR-α to calm mast cells/microglia and reduce neuropathic pain; promising adjunct for chemotherapy-induced peripheral neuropathy (CIPN) with supportive human data.

Evidence at a glance

Tier 3 · early humanLungBreastColorectalOvarian

Neuropathy RCTs (diabetic > CIPN); VAS SMD -0.5 in meta; phase II CIPN signals; mechanistic glial data strong; ongoing trials in oxaliplatin/paclitaxel neuropathy.

How it may work

PEA binds/activates PPAR-α and engages the ‘ALIA’ mechanism (Autacoid Local Injury Antagonism) to inhibit mast-cell degranulation and microglial activation. Downstream, it lowers pro-inflammatory cytokines and neuronal hyperexcitability, easing allodynia/hyperalgesia. Studies show benefit in diabetic neuropathy and emerging signals in CIPN; ultra-micronized forms may improve bioavailability.

Targets & pathways

Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.

  • PPAR-αActivation for anti-inflammatory transcription
  • Neuro-InflammationMast cell/microglia degranulation inhibition
  • Neuropathic PainAllodynia/hyperalgesia relief via ALIA
  • CytokinesIL-6/TNF-α reduction
  • Neuronal ExcitabilityHyperexcitability dampening
PPARNeuro-InflammationNeuropathic Pain

Often studied / combined with

Combinations reported in the literature, not a protocol or a recommendation.

Overlapping mechanisms

Safety & interactions

Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.

Risk categories
Gi UpsetSomnolenceHeadache
Potential interactions
  • sedativesMonitorLowTheoreticalAdditive calming effects.
  • neuropathic analgesicsSynergizeLowTheoreticalEnhances duloxetine/gabapentin in CIPN.
  • DuloxetineSynergizeLowTheoreticalImproved pain scores in combo trials.

Timing

References

Research

No published studies for PEA (Palmitoylethanolamide) yet

New studies appear here once they’ve been reviewed. Browse all studies.

Dose: as studied, not a recommendation

These are doses as studied or reported, never a recommendation. The right amount of PEA (Palmitoylethanolamide) depends on you, your other medicines, and your situation; decide it with your oncology team and pharmacist, not from a web page.

Ranges seen in adjunct / practice use: 600–1200 mg/day (po) divided BID; with or without food, CIPN adjunct 600-1200 mg/day um-PEA; start 300 mg BID; micronized for better absorption; 4-8 week trial..

Trials studying PEA (Palmitoylethanolamide)

Loading current trials from ClinicalTrials.gov… Search ClinicalTrials.gov →

Inclusion here is not an endorsement. OncoForge makes no claim beyond what the linked studies show. Discuss anything on this page with your oncology team before acting on it.

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