EGCG (Epigallocatechin Gallate)
EGCG inhibits PI3K/mTOR for proliferation ↓, DNMT for epigenetic reactivation, MMPs/VEGF for anti-invasion/angiogenesis, + apoptosis ↑ via Bax/NF-κB. Strong clinical support in lung/CRC/breast/prostate/pancreatic; safe at 200–1200 mg/day but monitor LFTs/CYP.
Forms: Oral capsules/extracts (supplement, 200–800 mg EGCG)
Key Takeaway
Green tea extract that may turn tumor-suppressing genes back on and block blood supply to tumors, while slowing cancer growth and triggering cell death, with evidence from human trials.
Evidence at a glance
Moderate-strong clinical (RCTs, meta-analyses) + robust preclinical; especially preventive/adjunct in CRC/lung/prostate.
How it may work
EGCG, the primary catechin in green tea, inhibits PI3K/Akt/mTOR signaling, reducing cell proliferation and survival. It acts as a DNMT inhibitor, demethylating tumor suppressor genes (e.g., p16, MGMT) to restore their expression. EGCG suppresses MMP-2 and MMP-9, limiting tumor invasion and metastasis, and downregulates VEGF to inhibit angiogenesis. It also induces apoptosis by upregulating Bax, activating caspases, and modulating NF-κB pathways. Clinical studies show enhanced chemotherapy efficacy.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
- PI3K/Akt/mTOR↓Reduces proliferation/survival signaling
- DNMT↓Demethylates tumor suppressors (p16, MGMT)
- MMP-2/-9↓Limits invasion/metastasis
- VEGF↓Inhibits angiogenesis
- Apoptosis↑Bax ↑, caspases activation, NF-κB modulation
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- Doxorubicin / Chemotherapy: Efficacy enhancement via apoptosis.
- Curcumin: PI3K/apoptosis in breast.
- Resveratrol: DNMT/angiogenesis in CRC.
- Quercetin: MMP inhibition in prostate.
Overlapping mechanisms
- PI3K ↓ / MMP ↓ / VEGF ↓: Avoid excess stacking with other PI3K/MMP/anti-angiogenic agents; risk GI/CYP overload without added benefit.
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.
- CYP450 substrates (e.g., tamoxifen, bortezomib)MonitorModerateTheoreticalEGCG inhibits CYP3A4/1A2; may alter drug levels.
- Bortezomib / Other proteasome inhibitorsMonitorModerateTheoreticalPotential antagonism in some cancers; synergy in others.
- Chemotherapy (e.g., doxorubicin)ConsiderBeneficialTheoreticalEnhances efficacy via apoptosis/angiogenesis inhibition.
- Curcumin / Resveratrol / QuercetinConsiderBeneficialTheoreticalSynergistic PI3K/DNMT/MMP/apoptosis in breast/CRC/prostate.
Timing
- With meals: Improves absorption, reduces GI upset.
- Divided doses: BID-TID for steady levels; avoid bedtime if caffeinated.
References
- Anti-Cancer Effects of Green Tea Polyphenols Against Prostate Cancer
- Green Tea and Lung Cancer: A Systematic Review
- Green tea and green tea extract in oncological treatment: A systematic review
- Green Tea (Chinese Tea)
- Focus on the Use of Green Tea in Cancer Setting: Between Lights and Shadows
Research
No published studies for EGCG (Epigallocatechin Gallate) yet
New studies appear here once they’ve been reviewed. Browse all studies.
Dose: as studied, not a recommendation
Ranges seen in adjunct / practice use: 200–1200 mg (po) Typical: 200–800 mg/day divided (e.g., 400 mg BID). Trials: 400 mg TID (1200 mg/day) in breast; 800 mg/day in prostate; up to 1 g/m² TID (~2000 mg/day) tolerated short-term. Safe bolus: ≤338 mg/day., From green tea extract supplements standardized to EGCG. Divided doses with meals. Higher doses (e.g., 1200+ mg) in trials but monitor LFTs. Bioavailability low; consider piperine or nano-forms for enhancement. Not Rx; quality varies—third-party tested..
Trials studying EGCG (Epigallocatechin Gallate)
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Appears in these protocol claims
EGCG (Epigallocatechin Gallate) is named in these protocols discussed online. Listed for transparency: being part of a protocol is not evidence that it works, and OncoForge does not endorse them.
- Jane McLelland / Metabolic Blocking Claims : Multi-pathway metabolic strategy based around starving cancer fuel routes and blocking escape pathways.