EGCG (Epigallocatechin Gallate) / AntiBio Cancer Research Results

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

Epigallocatechin-3-gallate — EGCG is a naturally occurring galloylated flavan-3-ol and the quantitatively dominant catechin in green tea leaves from Camellia sinensis. It is formally classified as a dietary polyphenol, catechin and investigational pleiotropic bioactive compound. EGCG has concentration-, oxidation-, metal- and cellular-context-dependent activity: it can function as an antioxidant and NRF2-associated cytoprotective agent in normal tissues, but may generate reactive oxygen species and induce stress-mediated death in susceptible cancer cells. It is not an approved anticancer drug, and purified high-dose extracts are pharmacologically and toxicologically distinct from brewed green tea.

Primary mechanisms (ranked):

  1. Biphasic redox modulation, including direct radical scavenging and metal chelation at lower exposure, but auto-oxidation, hydrogen-peroxide generation and pro-oxidant stress under permissive cancer-cell culture conditions.
  2. Suppression of proliferative and survival signalling, particularly PI3K–AKT–mTOR, NF-κB, receptor tyrosine kinase, STAT and context-dependent MAPK pathways.
  3. Mitochondrial dysfunction and intrinsic apoptosis through mitochondrial membrane-potential loss, cytochrome-c release and caspase activation.
  4. Cell-cycle arrest through modulation of cyclins, cyclin-dependent kinases, p21, p27 and p53-associated signalling.
  5. Inhibition of invasion, epithelial–mesenchymal transition and extracellular-matrix degradation through reduced FAK, MMP-2, MMP-9, uPA and related motility pathways.
  6. Suppression of HIF-1α–VEGF signalling, angiogenesis and hypoxia adaptation.
  7. Metabolic disruption involving reduced glycolysis, glucose transport and context-dependent mitochondrial energy production.
  8. Epigenetic modulation, including experimental inhibition or altered expression of DNMTs, HDACs and EZH2.
  9. Modulation of proteostasis, autophagy, endoplasmic-reticulum stress and unfolded-protein responses.
  10. NRF2 activation as a secondary adaptive mechanism, generally cytoprotective in normal cells but potentially protective or treatment-resistant in some cancers.
  11. Chemosensitization or radiosensitization in selected experimental models; treatment protection, antagonism or normal-tissue radioprotection can also occur depending on dose, schedule and therapy.

Bioavailability / PK relevance: Oral bioavailability is low and highly variable because EGCG is chemically unstable near neutral or alkaline pH, has limited intestinal permeability, undergoes extensive methylation, glucuronidation and sulfation, and is influenced by food and microbiota. Plasma concentrations after tea consumption are usually submicromolar, while large supplemental doses may transiently produce low-micromolar exposure. Fasting can increase systemic exposure but may also increase hepatic toxicity risk. Nanoencapsulation, lipid carriers and other delivery systems improve exposure experimentally but are not established anticancer treatments.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM EGCG, whereas conventional oral administration generally produces submicromolar to low-micromolar plasma concentrations. Thus, many direct cytotoxic, glycolytic, mitochondrial and kinase effects occur at concentrations substantially exceeding typical achievable systemic exposure. EGCG can also oxidize in culture media and generate extracellular hydrogen peroxide, creating experimental effects that may not translate directly in vivo.

Clinical evidence status: Extensive preclinical evidence; multiple small human biomarker, prevention and early-phase studies; limited randomized evidence for selected premalignant or recurrence-prevention settings; no established therapeutic efficacy against active cancer and no regulatory approval as an anticancer agent. A recent randomized colorectal adenoma study reported reduced recurrence, but this does not establish treatment efficacy for invasive colorectal cancer. Ongoing clinical studies continue to investigate prevention and adjunctive applications.

Safety and interactions: Brewed green tea is generally well tolerated, whereas concentrated green-tea extracts and purified EGCG have been associated with dose-dependent aminotransferase elevations and rare clinically significant liver injury. Doses around 800 mg EGCG per day have generated a regulatory safety signal, and a universally safe supplemental dose has not been established. Risk may be higher with fasting administration, pre-existing liver disease or multi-ingredient weight-loss products. EGCG can bind non-heme iron, alter drug transporters or metabolic enzymes, and modify exposure to some medications; oncology use should therefore be reviewed for drug-specific interactions.



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). FDA says <800mg/day (hepatotoxicity)
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

EGCG Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Biphasic redox modulation ↑ ROS or ↓ ROS (dose-dependent) (context-dependent) ↓ ROS; ↑ antioxidant buffering P–R Oxidative stress or antioxidant protection Auto-oxidation and metal-catalysed peroxide formation may drive cancer-cell toxicity; culture-medium oxidation can exaggerate this mechanism.
2 PI3K AKT mTOR survival signalling ↓ PI3K; ↓ AKT; ↓ mTOR ↔ or adaptive modulation R–G Reduced proliferation and survival Frequently reported across models, but direct target engagement at physiologically achievable concentrations remains uncertain.
3 Mitochondrial apoptosis ↓ ΔΨm; ↑ cytochrome c; ↑ caspase-9; ↑ caspase-3; ↑ PARP cleavage ↔ or preserved mitochondrial function R–G Intrinsic apoptotic death Usually downstream of redox stress, calcium disturbance or survival-pathway inhibition.
4 NF-κB inflammatory survival signalling ↓ NF-κB; ↓ COX-2; ↓ inflammatory cytokines ↓ pathological inflammation R–G Reduced inflammatory and anti-apoptotic transcription Potentially relevant to tumour-promoting inflammation and treatment resistance.
5 Cell-cycle regulation ↓ cyclin D1; ↓ cyclin E; ↓ CDK2; ↓ CDK4; ↓ CDK6; ↑ p21; ↑ arrest ↔ or transient arrest G Cytostatic growth inhibition Arrest may occur at G1, S or G2/M depending on tumour type and concentration.
6 Invasion EMT and matrix remodelling ↓ EMT; ↓ FAK; ↓ uPA; ↓ MMP-2; ↓ MMP-9; ↓ migration ↔ G Reduced invasion and metastatic phenotype Predominantly supported by cellular and animal models.
7 HIF-1α VEGF angiogenesis axis ↓ HIF-1α; ↓ VEGF; ↓ angiogenic signalling ↔ or context-dependent vascular protection G Reduced hypoxia adaptation and angiogenesis Responses depend on oxygen tension, cell type and exposure.
8 Glycolysis and energy metabolism ↓ GLUT1; ↓ HK2; ↓ PKM2; ↓ LDHA; ↓ ECAR; ↓ ATP (model-dependent) ↔ or improved metabolic homeostasis R–G Metabolic stress Many metabolic findings use concentrations above typical human plasma exposure.
9 Calcium ER stress and proteostasis ↑ Ca²⁺; ↑ ER stress; ↑ UPR; ↑ GRP78 (context-dependent) ↔ or ↓ pathological ER stress P–G Proteotoxic stress and apoptosis GRP78 and UPR activation may promote death or adaptation depending on intensity and duration.
10 Epigenetic regulation ↓ DNMT activity; ↓ HDAC signalling; ↓ EZH2 (model-dependent) ↔ G Re-expression of suppressed genes Biochemical inhibition and intracellular effects may require different concentrations.
11 NRF2 antioxidant response ↑ NRF2 or ↔ (context-dependent) ↑ NRF2; ↑ HO-1; ↑ GSH; ↑ antioxidant enzymes R–G Secondary adaptive cytoprotection NRF2 can protect normal tissue but may also counteract EGCG-induced oxidative injury or support resistant cancer cells.
12 Cancer stemness signalling ↓ Wnt β-catenin; ↓ Hedgehog GLI; ↓ Notch; ↓ stem-cell markers ↔ G Reduced self-renewal phenotype Evidence remains predominantly preclinical and model-dependent.
13 Chemosensitization ↑ treatment response or ↓ resistance (drug-dependent) ↔ or ↑ tissue protection R–G Adjunctive modulation Reported with several cytotoxic and targeted agents, but EGCG can also alter drug absorption, transport or stability; combinations require individual evaluation.
14 Radiosensitization and radioprotection ↑ radiosensitivity or ↔ (schedule-dependent) ↓ radiation injury in some models R–G Context-dependent radiation modulation Opposing tumour and normal-tissue effects are possible; clinical evidence is insufficient for routine supplementation during radiotherapy.
15 Clinical Translation Constraint Effective experimental exposure often not systemically achievable ↑ hepatic risk with concentrated high-dose extracts G Limited clinical translation Poor oral bioavailability, rapid metabolism, instability, formulation heterogeneity, fasting-related exposure, liver toxicity and limited definitive oncology trials constrain deployment.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer’s disease relevance: EGCG has substantial preclinical neuroprotective evidence but no established clinical efficacy for Alzheimer’s disease. Proposed actions include inhibition or remodelling of amyloid-β aggregation, altered amyloid precursor protein processing, metal chelation, reduced tau-associated injury, suppression of neuroinflammation, mitochondrial protection and activation of NRF2-associated antioxidant defences. Most positive findings derive from biochemical, cellular or animal models, and brain exposure after conventional oral administration is uncertain. EGCG should therefore be classified as preclinical or exploratory for Alzheimer’s disease rather than as a validated disease-modifying therapy.

EGCG in Alzheimer’s Disease

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Amyloid beta aggregation ↓ fibril formation; ↑ non-toxic aggregate remodelling Reduced amyloid-associated toxicity Strong biochemical and preclinical rationale; effective brain exposure in humans remains uncertain.
2 Amyloid precursor protein processing ↑ non-amyloidogenic processing; ↓ amyloidogenic burden (model-dependent) Reduced amyloid generation Primarily demonstrated in cellular and animal systems.
3 Neuroinflammation ↓ NF-κB; ↓ NLRP3; ↓ inflammatory cytokines; ↓ microglial activation Reduced inflammatory neurotoxicity Inflammatory effects are context-, model- and dose-dependent.
4 Oxidative stress and NRF2 ↓ ROS; ↑ NRF2; ↑ HO-1; ↑ endogenous antioxidant defence Neuronal cytoprotection Antioxidant signalling is more relevant at achievable exposure than many direct cytotoxic cancer mechanisms.
5 Mitochondrial function ↑ membrane stability; ↑ ATP preservation; ↓ mitochondrial ROS Improved neuronal bioenergetics Supported mainly by experimental injury and transgenic models.
6 Tau pathology ↓ tau phosphorylation or aggregation (model-dependent) Reduced cytoskeletal and synaptic injury Less developed evidence base than amyloid-related mechanisms.
7 Metal homeostasis ↓ redox-active iron and copper interactions Reduced metal-promoted aggregation and oxidative injury Chelation may contribute mechanistically but could also impair dietary non-heme iron absorption.
8 Clinical Translation Constraint ↓ oral and brain exposure; ↑ formulation variability Uncertain human efficacy No convincing evidence currently establishes EGCG as an Alzheimer’s disease-modifying treatment.


AntiBio, Antibiotic/Antimicrobial activity: Click to Expand ⟱
Source:
Type:

Antibiotic / antimicrobial activity: The ability of a substance to suppress or kill microorganisms, especially bacteria, by disrupting microbial survival, growth, biofilm formation, cell-wall integrity, membrane function, protein synthesis, nucleic-acid synthesis, quorum sensing, or virulence.

Natural Products that might have antimicrobial properties

Natural supplement or product Principal constituents Potential antimicrobial activity Evidence assessment Reference
Garlic
Allium sativum		 Allicin, ajoene and diallyl sulfides Antibacterial and antifungal activity, with some antiviral and antiparasitic effects reported in laboratory studies. Extensive laboratory evidence, but insufficient clinical evidence to use garlic as a treatment for established infections. Tesfaye A. Revealing the therapeutic uses of garlic and its potential for drug discovery. Scientific review.
Berberine Berberine isoquinoline alkaloid May damage bacterial membranes, inhibit efflux pumps, interfere with nucleic-acid and protein synthesis, and inhibit biofilm formation. Strong preclinical evidence and limited indication-specific clinical evidence. Poor oral bioavailability and drug interactions limit its use as a general antimicrobial. Berberine as a therapeutic alkaloid against ESKAPE and multidrug-resistant bacteria: a comprehensive review.
Cranberry extract
Vaccinium macrocarpon		 A-type proanthocyanidins Primarily reduces adhesion of uropathogenic bacteria, particularly Escherichia coli, to urinary epithelial cells. May reduce recurrent urinary tract infections in selected populations. It is preventive rather than a reliable treatment for an active UTI. National Center for Complementary and Integrative Health: Cranberry—Usefulness and Safety.
Probiotics
Lactobacillus, Bifidobacterium and Saccharomyces boulardii 		Live microorganisms; effects are strain-specific Competitive exclusion of pathogens, production of bacteriocins, inhibition of pathogen adhesion and restoration of microbiome function. Some human evidence for antibiotic-associated diarrhea and selected gastrointestinal or vaginal indications. Results cannot be generalized from one strain to another. NIH Office of Dietary Supplements: Probiotics—Health Professional Fact Sheet.
Medical-grade honey / Manuka honey Methylglyoxal, hydrogen peroxide, defensin-1, organic acids and high osmolarity Broad topical antibacterial and antibiofilm activity; also supports autolytic debridement and wound healing. Clinically relevant primarily as a standardized, medical-grade topical wound product. Ordinary food honey is not equivalent. Jull AB et al. Honey as a topical treatment for wounds. Cochrane systematic review.
Oregano oil
Origanum vulgare		 Carvacrol and thymol Antibacterial, antifungal and antibiofilm activity, largely through disruption of microbial membranes. Strong laboratory activity, but inadequate human evidence for oral treatment of infections. Concentrated oil can cause irritation. Chemical composition, biological activity and potential uses of oregano and oregano essential oil: a review.
Thyme
Thymus vulgaris		 Thymol and carvacrol Antibacterial, antifungal and antibiofilm activity through membrane damage and altered microbial permeability. Better established as a constituent of topical antiseptic and oral-care formulations than as an oral treatment for systemic infection. PubMed literature: thyme, thymol and antimicrobial activity.
Tea tree oil
Melaleuca alternifolia		 Terpinen-4-ol and related monoterpenes Topical antibacterial and antifungal activity with some antiviral laboratory activity. Some clinical evidence for topical acne and fungal skin conditions. Tea tree oil is toxic when swallowed and may cause contact dermatitis. Carson CF et al. Melaleuca alternifolia oil: a review of antimicrobial and other medicinal properties.
Echinacea
Echinacea species		 Alkamides, caffeic-acid derivatives, polysaccharides and glycoproteins Primarily immunomodulatory; relatively weak and inconsistent direct antimicrobial activity. Evidence for preventing or shortening respiratory infections is inconsistent and preparation-dependent. National Center for Complementary and Integrative Health: Echinacea—Usefulness and Safety.
Elderberry
Sambucus nigra		 Anthocyanins, flavonols and phenolic acids Antiviral effects have been reported in cell-culture and preclinical studies, including interference with viral entry or replication. Small human trials have examined respiratory symptoms, but evidence remains insufficient to establish treatment of influenza or other viral infections. National Center for Complementary and Integrative Health: Elderberry.
Curcumin / turmeric
Curcuma longa		 Curcumin and related curcuminoids Antibacterial, antifungal, antiviral and antibiofilm activity through multiple membrane, enzyme and signalling effects. Predominantly laboratory evidence. Poor aqueous solubility and low systemic bioavailability are major clinical limitations. Moghadamtousi SZ et al. A review on antibacterial, antiviral and antifungal activity of curcumin.
Ginger
Zingiber officinale		 Gingerols, shogaols and zingerone Antibacterial and antifungal activity, including possible inhibition of microbial adhesion and biofilm formation. Primarily laboratory evidence; there is little direct clinical evidence that ginger supplements treat infections. PubMed literature: ginger, gingerols and antimicrobial activity.
Clove
Syzygium aromaticum		 Eugenol and eugenyl acetate Antibacterial, antifungal and local antiseptic activity, principally through membrane and protein disruption. Relevant mainly to topical, food-preservation and dental applications. Evidence for systemic infection treatment is insufficient. PubMed literature: clove, eugenol and antimicrobial activity.
Cinnamon
Cinnamomum species		 Cinnamaldehyde, eugenol and cinnamic acid derivatives Antibacterial, antifungal and antibiofilm activity; may alter microbial membranes and quorum-sensing pathways. Predominantly laboratory evidence. Cassia cinnamon can contribute substantial coumarin exposure when consumed in concentrated amounts. PubMed literature: cinnamon, cinnamaldehyde and antimicrobial activity.
Neem
Azadirachta indica		 Nimbidin, nimbin, nimbolide, azadirachtin and other limonoids Antibacterial, antifungal, antiparasitic and antibiofilm effects have been reported. Some topical and dental research exists, but systemic clinical evidence is inadequate. Oral neem preparations have important safety concerns. PubMed literature: Azadirachta indica and antimicrobial activity.
Black seed
Nigella sativa		 Thymoquinone, thymohydroquinone and related volatile compounds Antibacterial, antifungal, antiparasitic and possible antiviral activity. Considerable laboratory research but limited, heterogeneous clinical evidence for infectious diseases. PubMed literature: Nigella sativa, thymoquinone and antimicrobial activity.
Green tea extract
Camellia sinensis		 Epigallocatechin gallate (EGCG) and other catechins Antibacterial, antiviral and antibiofilm activity; may damage membranes, inhibit microbial enzymes and enhance some antibiotics. Some localized oral-health evidence, but limited evidence for treating systemic infections. Concentrated extracts may cause liver injury in susceptible individuals. PubMed literature: EGCG, green tea and antimicrobial activity.
Licorice root
Glycyrrhiza species		 Glycyrrhizin, glycyrrhetinic acid, liquiritigenin and other flavonoids Antiviral, antibacterial and antifungal effects have been reported in laboratory and preclinical studies. Limited clinical antimicrobial evidence. Glycyrrhizin can cause hypertension, hypokalemia, fluid retention and clinically important drug interactions. National Center for Complementary and Integrative Health: Licorice Root.
Andrographis
Andrographis paniculata		 Andrographolide and related diterpenoid lactones Immunomodulatory, anti-inflammatory and possible antiviral or antibacterial activity. Some evidence for modest symptom reduction in uncomplicated respiratory infections, but this does not establish direct pathogen eradication. PubMed literature: Andrographis and respiratory infections.
Pelargonium sidoides Proanthocyanidins, phenolic acids and oxygenated coumarin derivatives Possible antiviral, antibacterial anti-adhesive and immunomodulatory activity. Some human evidence for modest symptom improvement in acute bronchitis and selected respiratory infections. It is not a substitute for antibiotics when bacterial treatment is indicated. Timmer A et al. Pelargonium sidoides extract for acute respiratory tract infections. Cochrane systematic review.
Monolaurin
Glycerol monolaurate		 Monolaurin, a monoester derived from lauric acid May disrupt lipid membranes and interfere with signalling or virulence in certain bacteria and enveloped viruses. Predominantly laboratory and animal evidence. There is insufficient clinical evidence to recommend oral monolaurin for infections. PubMed literature: glycerol monolaurate and antimicrobial activity.
Caprylic acid Octanoic acid, an eight-carbon medium-chain fatty acid Antifungal and membrane-disrupting activity, particularly against Candida species, has been reported in vitro. Insufficient human evidence for treating candidiasis or systemic fungal infection. Marketing claims commonly exceed the evidence. PubMed literature: caprylic acid and Candida.
Olive leaf extract
Olea europaea		 Oleuropein, hydroxytyrosol and elenolic-acid derivatives Antibacterial, antiviral and antifungal activity has been observed in laboratory studies. Preliminary evidence only; clinical trials have not established it as a treatment for infectious disease. PubMed literature: olive leaf, oleuropein and antimicrobial activity.
Goldenseal
Hydrastis canadensis		 Hydrastine, canadine and berberine Extracts and individual alkaloids show antibacterial activity in laboratory studies. There is no good clinical evidence that goldenseal treats human infections. Product composition, absorption and drug interactions are important limitations. National Center for Complementary and Integrative Health: Goldenseal.
Sweet wormwood / artemisinin
Artemisia annua 		Artemisinin and related sesquiterpene lactones Artemisinin derivatives are potent antimalarial agents. Additional antibacterial, antiviral and antiparasitic effects are being studied. Artemisinin-based combination therapies are established medicines, not ordinary supplements. Herbal preparations should not replace standardized malaria treatment because dose variability can promote treatment failure and resistance. World Health Organization: Guidelines for malaria.

Evidence interpretation

  • Clinical evidence: Effects have been studied in human participants, but usually for a specific preparation, route, dose and indication.
  • Preclinical evidence: Activity has mainly been demonstrated in cell culture, microbial cultures or animal models.
  • Anti-adhesive or probiotic activity: The product may reduce colonization or pathogen attachment without directly killing the microorganism.
  • Topical evidence: Results from topical use cannot be assumed to apply to an orally administered supplement.


Scientific Papers found: Click to Expand⟱
6778- EGCG,    The antimicrobial possibilities of green tea
- Review, Nor, NA
*AntiBio↑, *Bacteria↓,
6783- EGCG,    Absorption, metabolism, bioactivity, and biotransformation of epigallocatechin gallate
- Review, Nor, NA
*antiOx↑, *Inflam↓, *AntiCan↑, *Bacteria↓, *AntiBio↑, *BioAv↓, *GutMicro↑,
6784- EGCG,    Dietary (−)-Epigallocatechin Gallate (EGCG): State-of-the-Art Advances in Bioactivities, Bioavailability Enhancement Strategies, and Applications in Nutrition and Health
- Review, Nor, NA
*antiOx↑, *Inflam↓, *AntiCan↑, *cardioP↑, *neuroP↑, *GutMicro↑, *AntiBio↑, *ROS↓, *TNF-α↓, *IL6↓, TumCP↓, *LDL↓, *NO↓, *Obesity↓, *p‑tau↓, *Aβ↓, *NRF2↑, *SOD↑, *Catalase↑, *GPx↑, *NLRP3↓, *mTOR↓, TumCCA↑, NRF2↓, Apoptosis↑, SIRT1↓, miR-25-5p↓, PARP↑, Casp3↑, Casp9↑, ER Stress↑, TumAuto↑, EMT↓, TumCI↓, TumCMig↓, TGF-β↓, Smad1↓, STAT3↓, VEGF↓, angioG↓, Imm↑, EGFR↓, *GutMicro↑, *Bacteria↓, *AntiViral↑, *BioAv↓, *BioAv↑, *eff↑, *BioAv↑, eff↑, ChemoSen↑, *toxicity↝,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

NRF2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp9↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

miR-25-5p↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

Smad1↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 3,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDL↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

mTOR↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   Inflam↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 3,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   cardioP↑, 1,   neuroP↑, 1,   Obesity↓, 1,   toxicity↝, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 3,  
Total Targets: 28

Scientific Paper Hit Count for: AntiBio, Antibiotic/Antimicrobial activity
3 EGCG (Epigallocatechin Gallate)
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#:1483  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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