EGCG (Epigallocatechin Gallate) Cancer Research Results

EGCG, EGCG (Epigallocatechin Gallate): Click to Expand ⟱

Features:

EGCG (Epigallocatechin Gallate) is found in green tea. 100 times more effective than Vitamin C and 25 times more effective than Vitamin E at protecting cells from damage associated with oxidative stress.
EGCG Epigallocatechin Gallate (Green Tea) -Catechin
Summary:
1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.
2. Poor bioavailability: taking EGCG capsules without food was better.
3. Cancer dosage 4g/day (2g twice per day)? with curcumin may help (another ref says 700–2100 mg/d)
4. EGCG is susceptible to oxidative degradation.
5. “As for the pH level, the acidic environments enhance the stability of EGCG”.
6. “EGCG may enhance nanoparticle uptake by tumor cells”
7. Might be iron chelator (removing iron from cancer cells)
8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.
9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.
10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).
11. EGCG mediated ROS formation can upregulate CTR1 expression via the ERK1/2/NEAT1 pathway, which can increase the intake of chemotherapeutic drugs such as cisplatin in NSCLC cells and act as a chemosensitizer [58]
12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.
13. EGCG is an ENOX2 inhibitor.
14. Nrf2 activator in both cancer and normal cells. This example of lung cancer show both directions in different cell lines, but both toward optimim level.
Biological activity, EGCG has been reported to exhibit a range of effects, including:
    Antioxidant activity: 10-50 μM
   Anti-inflammatory activity: 20-50 μM
   Anticancer activity: 50-100 μM
   Cardiovascular health: 20-50 μM
   Neuroprotective activity: 10-50 μM

Drinking a cup (or two cups) of green tea (in which one might ingest roughly 50–100 mg of EGCG from brewed tea) generally results in peak plasma EGCG concentrations in the range of approximately 0.1 to 0.6 μM.

With higher, supplement-type doses (e.g., oral doses in the 500 mg–800 mg range that are sometimes studied for clinical benefits), peak plasma concentrations in humans can reach the low micromolar range, often reported around ~1–2 μM and in some cases up to 5 μM.

Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.
In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.

-Peak plasma concentration roughly 1 to 2 hours after oral ingestion.
-Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.

Supplemental EGCG
Dose (mg) ≈ Peak Plasma EGCG (µM)
~50 mg ≈ 0.1–0.3 µM
~100 mg ≈ 0.2–0.6 µM
~250 mg ≈ 0.5–1.0 µM
~500 mg ≈ 1–2 µM
~800 mg or higher ≈ 1–5 µM

50mg of EGCG in 1g of matcha tea(1/2 teaspoon)

Studies on green tea extracts have employed doses roughly equivalent to 300–800 mg/day of EGCG. Excessive doses can cause liver toxicity in some cases.

Methods to improve bioavailability
-Lipid-based carriers or nanoemulsions
-Polymer-based nanoparticles or encapsulation
-Co-administration with ascorbic acid (vitamin C)
-Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan) -Using multiple smaller doses rather than one large single dose.
-Taking EGCG on an empty stomach or under fasting conditions, or aligning dosing with optimal pH conditions in the GI tract, may improve its absorption.(acidic environment is generally more favorable for its stability and absorption).
– EGCG is more stable under acidic conditions. In the stomach, where the pH is typically around 1.5 to 3.5, EGCG is less prone to degradation compared to the more neutral or basic environments of the small intestine.
- At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.
– Although the stomach’s acidic pH helps maintain EGCG’s stability, most absorption occurs in the small intestine, where the pH is closer to neutral.
– To counterbalance the inherent instability in the intestine, strategies such as co-administration of pH-modifying agents (like vitamin C) are sometimes used. These agents help to maintain a slightly acidic environment in the gut microenvironment, potentially improving EGCG stability during its transit and absorption.
– The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.

-Note half-life 3–5 hours.
- low BioAv 1%? despite its limited absorption, it is rapidly disseminated throughout the body
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Does NOT Lower AntiOxidant defense in Cancer Cells: NRF2↑, TrxR↓**, SOD, GSH Catalase HO1 GPx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, Notch↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective(possible damage at high dose), CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Label	Primary Interpretation	Notes
1	Reactive oxygen species (ROS)	↑ ROS (dose-, metal-, context-dependent)	↓ ROS / buffered	Conditional Driver	Biphasic redox modulation	EGCG can act as a pro-oxidant in cancer cells (often metal-catalyzed) while functioning as an antioxidant in normal cells
2	Mitochondrial integrity / intrinsic apoptosis	↓ ΔΨm; ↑ caspase activation	↔ preserved	Driver	Execution of intrinsic apoptosis	Mitochondrial stress and apoptosis follow ROS elevation in cancer cells
3	NF-κB signaling	↓ NF-κB activation	↓ inflammatory NF-κB tone	Driver	Suppression of survival and inflammatory transcription	NF-κB inhibition explains chemosensitization and reduced survival signaling
4	PI3K → AKT → mTOR axis	↓ AKT / ↓ mTOR	↔ adaptive suppression	Secondary	Reduced growth and anabolic signaling	AKT/mTOR inhibition contributes to growth suppression and stress responses
5	MAPK stress signaling (JNK / p38)	↑ JNK / ↑ p38	↔ minimal	Secondary	Stress-activated apoptosis signaling	MAPK activation often follows ROS increase and supports apoptotic signaling
6	Cell cycle regulation	↑ G1 or G2/M arrest	↔ largely spared	Phenotypic	Cytostatic growth control	Cell-cycle arrest reflects upstream signaling disruption rather than direct CDK inhibition
7	HIF-1α / VEGF hypoxia–angiogenesis axis	↓ HIF-1α; ↓ VEGF	↔ minimal	Secondary	Anti-angiogenic pressure	EGCG interferes with hypoxia-driven tumor adaptation
8	NRF2 antioxidant response	↑ NRF2 (adaptive, often insufficient)	↑ NRF2 (protective)	Adaptive	Stress compensation	NRF2 reflects response to redox perturbation rather than a kill mechanism

Scientific Papers found: Click to Expand⟱

682-

EGCG,

Suppressive Effects of EGCG on Cervical Cancer

Review,

NA,

E7↓, E6↓, PI3K/Akt↓, P53↑, p27↑, P21↑, CDK2↓, mTOR↓, HIF-1↓, IGF-1↓, EGFR↓, ERK↓, VEGF↓,

683-

EGCG,

Targeting the AMP-Activated Protein Kinase for Cancer Prevention and Therapy

Review,

NA,

AMPK↑, TumCP↓, P21↑, mTOR↓, COX2↓,

3593-

EGCG,

Epigallocatechin Gallate (EGCG)

Review,

AD,

AntiTum↑, *Inflam↓, *neuroP↑, *Aβ↓, *BioAv↝, cognitive↑,

4685-

EGCG,

Epigallocathechin gallate, polyphenol present in green tea, inhibits stem-like characteristics and epithelial-mesenchymal transition in nasopharyngeal cancer cell lines

in-vitro,

NPC,

TW01

in-vitro,

NPC,

TW06

CSCs↓, EMT↓, TumCMig↓, TumCI↓, OCT4↓, Snail↓, Vim↓, E-cadherin↓, HSP70/HSPA5↓, HSP90↓, AntiTum↓,

4684-

EGCG,

EGCG inhibits CSC-like properties through targeting miR-485/CD44 axis in A549-cisplatin resistant cells

in-vivo,

NSCLC,

A549

miR-485↑, CSCs↓, CD44↓,

4683-

EGCG,

Epigallocatechin-3-gallate inhibits self-renewal ability of lung cancer stem-like cells through inhibition of CLOCK

in-vitro,

Lung,

A549

in-vitro,

Lung,

H1299

in-vivo,

Lung,

A549

CSCs nude mouse xenograft model

CSCs↓, CD133↓, CLOCK↓, Wnt↓, β-catenin/ZEB1↓, CD44↓, SOX2↓, Nanog↓, OCT4↓,

4682-

EGCG,

Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate

Review,

Var,

CSCs↓, EMT↓, ChemoSen↑, CD133↓, CD44↓, ALDH1A1↓, Nanog↓, OCT4↓, TumCP↓, Apoptosis↑, p‑GSK‐3β↓, GSK‐3β↑, β-catenin/ZEB1↓, cMyc↓, XIAP↓, Bcl-2↓, survivin↓, Vim↓, Slug↓, Snail↓,

4681-

EGCG,

Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling

in-vitro,

Ovarian,

ES-2

TumCP↓, Apoptosis↑, Nanog↓, SOX2↓, Fibronectin↓, CD133↓,

4680-

EGCG,

The Potential of Epigallocatechin Gallate in Targeting Cancer Stem Cells: A Comprehensive Review

Review,

Var,

CSCs↓, EMT↓, TumMeta↓, RadioS↑, ChemoSen↑, BioAv↓,

4291-

EGCG,

Structure-based discovery of small molecules that disaggregate Alzheimer’s disease tissue derived tau fibrils in vitro

in-vitro,

AD,

*tau↓, *BBB∅,

4290-

EGCG,

EGCG impedes human Tau aggregation and interacts with Tau

in-vitro,

AD,

 64.2 μM.

*tau↓, *Dose↝, *neuroP↑, *antiOx↑,

4152-

EGCG,

Green tea catechins potentiate the neuritogenic action of brain-derived neurotrophic factor: role of 67-kDa laminin receptor and hydrogen peroxide

in-vitro,

AD,

*BDNF↑,

3594-

EGCG,

Epigallocatechin-3-gallate inhibits secretion of TNF-alpha, IL-6 and IL-8 through the attenuation of ERK and NF-kappaB in HMC-1 cells

in-vitro,

AD,

HMC1

PMA+A23187-induced (treated as normal cells)

*TNF-α↓, *IL6↓, *IL8↓, *Ca+2↓,

3592-

EGCG,

(-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease

in-vivo,

AD,

mouse

*neuroP↑, *memory↑, *p‑tau↓,

4664-

GEN,

CUR,

RES,

EGCG,

SFN

Targeting cancer stem cells by nutraceuticals for cancer therapy

Review,

Var,

CSCs↓, other↝, eff↑, CD44↓, p‑STAT3↓,

166-

GEN,

EGCG,

RES,

CUR,

Common botanical compounds inhibit the hedgehog signaling pathway in prostate cancer

in-vivo,

Pca,

HH↓, Gli1↓,

1292-

GSE,

EGCG,

Antiproliferative and Apoptotic Effects Triggered by Grape Seed Extract (GSE) versus Epigallocatechin and Procyanidins on Colon Cancer Cell Lines

in-vitro,

Colon,

Caco-2

100ug/L

in-vitro,

CRC,

HCT8

TumCG↓, Apoptosis↑,

1534-

LT,

Api,

EGCG,

RES,

Plant polyphenol induced cell death in human cancer cells involves mobilization of intracellular copper ions and reactive oxygen species generation: a mechanism for cancer chemopreventive action

in-vitro,

Nor,

MCF10

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MDA-MB-468

in-vitro,

PC,

Bxpc-3

TumCP↓, Apoptosis↑, eff↓, *toxicity↑, Dose?, eff↓, eff↓,

81-

QC,

EGCG,

Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea

in-vivo,

Pca,

 0.2%, 0.4%

COMT↓, MRP1↓, Ki-67↓, Bax:Bcl2↑, AR↓, Akt↓, p‑ERK↓, COMT↓, eff↑, chemoPv↑, BioAv↑,

77-

QC,

EGCG,

The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition

in-vitro,

Pca,

CD44+

 20 uM

 CD44+ and CD133+ CSCs can be isolated from PC-3 and LNCaP

in-vitro,

NA,

CD133+

in-vitro,

NA,

PC3

in-vitro,

NA,

LNCaP

Casp3↑, Casp7↑, Bcl-2↓, survivin↓, XIAP↓, EMT↓, Vim↓, Slug↓, Snail↓, β-catenin/ZEB1↓, LEF1↓, TCF↓, eff↑, CSCs↓, TumCG↓, tumCV↓,

74-

QC,

EGCG,

Prospective randomized trial evaluating blood and prostate tissue concentrations of green tea polyphenols and quercetin in men with prostate cancer

Human,

Pca,

 Orally, 400 mg/twice daily

BioAv↑, BioAv↑, toxicity↓,

60-

QC,

EGCG,

isoFl,

The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition

in-vitro,

Pca,

pCSCs

 20 uM

Casp3↑, Casp7↑, Bcl-2↓, survivin↓, XIAP↓, EMT↓, Slug↓, Snail↓, β-catenin/ZEB1↓, LEF1↓, CSCs↓, Apoptosis↑, TumCMig↓, TumCI↓, CD44↓, CD133↓,

4670-

RES,

CUR,

EGCG,

TQ,

Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrol

Review,

Nor,

*antiOx↑, *Inflam↓, *AntiAge↑, *SIRT1↑, *SIRT3↑, *FOXO↑, *ROS↓,

4874-

Uro,

EGCG,

A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's Disease

in-vivo,

AD,

humanized homozygous amyloid beta knockin (hAbKI) mice of late-onset Alzheimer’s disease

*motorD↑, *memory↑, *MitoP↑, *Aβ↓, *mitResp↑, *Nrf1↑, *PINK1↑, *PARK2↑, *ATG5↑, *Bcl-2↑, *H2O2↓, *ROS↓, *lipid-P↓, *mt-ATP↑,

Showing Research Papers: 151 to 174 of 174
Prev Page 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 174

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 2, H2O2↓, 1, lipid-P↓, 1, Nrf1↑, 1, PARK2↑, 1, ROS↓, 2, SIRT3↑, 1,

Mitochondria & Bioenergetics ⓘ

mt-ATP↑, 1, mitResp↑, 1, PINK1↑, 1,

Core Metabolism/Glycolysis ⓘ

SIRT1↑, 1,

Cell Death ⓘ

Bcl-2↑, 1,

Autophagy & Lysosomes ⓘ

ATG5↑, 1, MitoP↑, 1,

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,

Migration ⓘ

Ca+2↓, 1,

Barriers & Transport ⓘ

BBB∅, 1,

Immune & Inflammatory Signaling ⓘ

IL6↓, 1, IL8↓, 1, Inflam↓, 2, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1, tau↓, 2, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↝, 1, Dose↝, 1,

Clinical Biomarkers ⓘ

IL6↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, memory↑, 2, motorD↑, 1, neuroP↑, 3, toxicity↑, 1,
Total Targets: 33

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:73  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

EGCG (Epigallocatechin Gallate) Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Autophagy & Lysosomes ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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