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

Indole-3-Carbinol / DIM

I3C/DIM favors 2-OH estrogen (CYP1A1 ↑), curbs NF-κB/AhR for apoptosis/cell arrest, ↓ ER-α/AR in hormone cancers. Human biomarkers strong in breast/prostate/cervical; 200–400 mg PO safe—monitor hormones/CYP; adjunct for ER+ settings.

← All agents

Human-reviewed · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed

👥⭐⭐⭐ Moderate — Supported by preclinical studies and early human trials; more RCTs needed for confirmation.I3CDIMDiindolylmethaneIndole-3-carbinol

Forms: Oral capsules (supplement, 200–400 mg)

Educational only, not medical advice. OncoForge makes no claim that Indole-3-Carbinol / DIM 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

Cruciferous compound pair that shifts estrogen metabolism toward 2-OH pathways, induces CYP1A1, and can trigger apoptosis; useful adjunct in hormone-sensitive settings with emerging human data.

Evidence at a glance

Tier 3 · early humanBreastProstateCervical

Moderate clinical (biomarker/early trials) + robust preclinical; RCTs for efficacy pending.

How it may work

Indole-3-carbinol (I3C) and its metabolite diindolylmethane (DIM) shift estrogen metabolism toward the protective 2-hydroxyestrone (2-OH) pathway by inducing CYP1A1 and other phase I enzymes, reducing estrogen-driven carcinogenesis. They inhibit NF-κB and AhR signaling, inducing apoptosis and cell cycle arrest in cancer cells. I3C/DIM also suppress hormone-sensitive tumor growth by downregulating ER-α and modulating androgen receptors. Preclinical and human studies show efficacy in breast, prostate, and cervical cancers.

Targets & pathways

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

  • Estrogen MetabolismShifts to 2-OH pathway; reduces 16α-OH
  • CYP1A1Induces phase I enzymes via AhR
  • ApoptosisVia NF-κB/AhR inhibition; cell cycle arrest
  • ER-αSuppresses hormone-sensitive growth
  • Androgen ReceptorModulates in prostate contexts
Estrogen ModCYP1A1Apoptosis

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
Hormone AlterationGi Upset MildHepatotoxicity Risk LowPregnancy Caution
Potential interactions
  • Endocrine therapies (e.g., tamoxifen)MonitorModerateTheoreticalAdditive estrogen modulation; hormone assays.
  • CYP1A2 substrates (e.g., caffeine)MonitorLowTheoreticalInduction alters metabolism.

Timing

References

Research

No published studies for Indole-3-Carbinol / DIM 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 Indole-3-Carbinol / DIM 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: 200–400 mg (po) I3C: 200–400 mg/day; DIM: 100–300 mg/day divided. Trials: 400 mg/day I3C for estrogen modulation. Preclinical HED from rat (50–200 mg/kg) ~8–32 mg/kg (~560–2240 mg for 70 kg); human uses lower for safety., From cruciferous extracts or pure. Divided BID with meals. Monitor hormones/LFTs. Not Rx; DIM more stable than I3C in acid..

Trials studying Indole-3-Carbinol / DIM

No actively-recruiting trials matched right now. Recruiting is not the same as proven. 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.

← All agents · Research Radar