Chlorogenic acid / ROS Cancer Research Results

CGA, Chlorogenic acid: Click to Expand ⟱
Features:
Chlorogenic acid (CGA) is a polyphenol compound found in various plant-based foods, such as green coffee beans, apples, and pears.
Chlorogenic acid (CGA; 5-caffeoylquinic acid) is a dietary polyphenol (coffee/tea/plant ester) whose primary biology in mammals is redox + stress-response modulation: (1) ROS scavenging/antioxidant buffering, (2) Keap1→NRF2 activation with induction of cytoprotective genes, and (3) downstream anti-inflammatory and survival/metabolic signaling changes (e.g., NF-κB, PI3K/Akt/mTOR/AMPK context-dependent). Oral exposure is PK-limited: after coffee doses, median peak plasma concentrations of CGA-related metabolites are ~1–1.5 µM (1088–1526 nM) , while many in-vitro cancer papers use 10–100+ µM, often exceeding realistic systemic exposure; effects can still be relevant in gut/liver (first-pass) but systemic tumor exposures are likely lower. Clinically, CGA has human PK evidence and extensive preclinical oncology; robust RCT-grade anticancer efficacy is not established, and NRF2 activation creates a credible radio/chemo-resistance risk in some contexts
May lower blood pressure, blood sugar, and weight. May improve mood and cognitive function. Chlorogenic acid (CGA), one of the most abundant polyphenols in the human diet, has been reported to inhibit cancer cell growth.
• Inhibiting the growth of cancer cells: CGA has been shown to inhibit the growth of cancer cells in vitro and in vivo, including breast, colon, and prostate cancer cells.
• Inducing apoptosis: CGA has been found to induce apoptosis (cell death) in cancer cells, which can help prevent the spread of cancer.
• Reducing inflammation: CGA has anti-inflammatory properties, which can help reduce the risk of cancer by reducing chronic inflammation.
• Antioxidant activity: CGA has antioxidant properties, which can help protect cells from damage caused by free radicals.
-vast array of sources, present in honeysuckle, potato, cork, eucommia leaves, chrysanthemum, strawberry, mango, blueberries, mulberry leaves, and green coffee

Chlorogenic acid — Chlorogenic acid (CGA) is a dietary hydroxycinnamate polyphenol, classically the caffeoyl ester of quinic acid, with 5-O-caffeoylquinic acid as the major canonical form usually meant by “chlorogenic acid.” It is best classified as a small-molecule natural product/polyphenolic phytochemical rather than an approved anticancer drug. Standard abbreviations include CGA and, in chemistry-focused literature, 5-CQA or 5-O-caffeoylquinic acid. Major natural sources include coffee beans, certain fruits, vegetables, and medicinal plants. In oncology, CGA is best viewed as a context-dependent redox, inflammatory, metabolic, and immune-modulatory scaffold with strong preclinical activity but important translation limits because oral systemic exposure is modest and many cell-culture studies use concentrations above likely plasma-achievable levels.

Primary mechanisms (ranked):

  1. Redox buffering with suppression of excess ROS and oxidative injury.
  2. Keap1/NRF2-axis activation with induction of cytoprotective antioxidant-response programs.
  3. Inflammatory signaling suppression, especially NF-κB-linked cytokine and survival programs.
  4. Antiproliferative and pro-apoptotic signaling in selected tumor models, often involving Akt, MAPK, mitochondrial stress, and caspase shifts.
  5. Metabolic reprogramming effects in some models, including reduced glycolytic signaling and HIF-1α/VEGF-linked adaptation.
  6. Immune-modulatory effects, including reported PD-L1 suppression and improved antitumor T-cell activity in some systems.
  7. Therapy-interaction effects that can diverge by context, with chemosensitizing reports in some models but radio/chemoprotection risk where antioxidant/NRF2 effects dominate.

Bioavailability / PK relevance: Oral CGA is moderately absorbed and extensively metabolized, not absent from circulation. However, systemic exposure is dominated by conjugated and gut-derived metabolites, while exposure to intact parent CGA is relatively limited and variable. For pharmacology, this means dietary CGA can be biologically relevant, but many in-vitro studies still use concentrations above typical circulating parent-compound levels after ordinary oral intake.

In-vitro vs systemic exposure relevance: This is a major translation constraint. Many oncology papers use roughly 10–200 µM or higher, while realistic oral systemic parent-CGA exposure is usually much lower; therefore many direct cytotoxic, anti-stemness, or signaling claims are likely more relevant to gut/liver first-pass settings, local delivery concepts, metabolite biology, or formulated/injectable products than to ordinary dietary exposure.

Clinical evidence status: Extensive preclinical evidence; limited small-human oncology evidence. Early-phase clinical development exists for injectable CGA in recurrent high-grade glioma/advanced lung cancer programs, but robust randomized evidence for standard anticancer use is not established. Current evidence supports CGA mainly as a preclinical or adjunctive candidate, not a validated standalone cancer therapy.

Plant Source 	       CGA(mg/kg in dw)
Instant coffee  	2650–11,600
Mate tea 	        4800–24,900
Sunflower seeds 	630–970
Sweet potato leaves 	9600
English potato 1 	3.3–9
Okra 1 	                3.9–21.6
Eggplant 	        4980–8050
Carrot 	                300–18,800
Tomato 	                200–400

Chlorogenic Acid Mechanistic Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS redox modulation ↔ mixed (context-dependent) ↓ ROS P–R Bidirectional redox modulation CGA is centrally redox-active, but not in a one-direction way. In cancer cells it can either raise or lower ROS depending on model, dose, and treatment context; overall literature supports redox buffering/antioxidant behavior as the dominant general profile, while some tumor models show ROS elevation linked to cytotoxicity.
2 NRF2 antioxidant response ↑ NRF2 (context-dependent) ↑ NRF2 R–G Cytoprotective gene induction Important dual-use axis. In normal tissue this is often protective; in stressed tumors it can reinforce survival and treatment resistance.
3 NF-κB inflammatory survival signaling ↓ NF-κB ↓ NF-κB R–G Anti-inflammatory and anti-survival modulation Frequently linked to reduced proliferation, invasion, cytokine tone, and improved immune context in preclinical models.
4 Mitochondrial apoptosis program ↑ Bax caspases; ↓ Bcl-2 (model-dependent; often higher concentration) ↓ stress-induced apoptosis R–G Programmed cell-death tuning Common anticancer readout in vitro and xenografts, but often concentration-sensitive and not necessarily representative of dietary exposure.
5 PI3K Akt mTOR growth signaling ↓ PI3K Akt mTOR (model-dependent) ↔ R–G Antiproliferative signaling restraint Supported in several tumor systems, but usually not the single dominant axis and often intertwined with upstream redox or receptor effects.
6 Glycolysis and HIF-1α adaptation ↓ glycolysis; ↓ HIF-1α (model-dependent) ↔ R–G Metabolic stress and anti-angiogenic pressure Includes reports of reduced HK2, PKM2, LDHA, GLUT1, and VEGF-linked signaling in selected models; likely secondary rather than universal.
7 EMT invasion and metastasis circuitry ↓ EMT; ↓ MMP2 MMP9; ↑ epithelial markers ↔ G Reduced motility and invasive phenotype Seen in breast, cholangiocarcinoma, tongue, and other models; translationally interesting but still preclinical.
8 Immune checkpoint and antitumor immunity ↓ PD-L1 (model-dependent) ↔ to ↑ immune support G Potential immunotherapy support One of the more interesting recent directions. May improve T-cell–mediated antitumor activity in selected systems, but remains early-stage.
9 Radiosensitization or chemoprotection balance ↔ to ↑ resistance (ROS NRF2 dominant contexts) ↑ protection P–R Therapy interaction risk Not a classic radiosensitizer. In at least some HCC models CGA reduced radiotherapy efficacy through ROS scavenging and NRF2 activation.
10 Chemosensitization ↑ chemosensitivity (model-dependent) ↔ G Adjunct enhancement of selected anticancer drugs Best described as a context-dependent secondary mechanism or therapeutic interaction. Preclinical evidence supports enhancement of some agents such as 5-FU in selected models, but this is not the core defining mechanism of CGA.
11 Ca²⁺ signaling ↔ ↔ — Usually secondary Not a strongly established primary axis for CGA in cancer. Include only for model-specific mechanistic discussions.
12 Ferroptosis relevance ↔ to ↓ ferroptotic drive (context-dependent) ↔ to ↓ ferroptotic injury — Usually secondary and often opposing CGA’s antioxidant and NRF2-linked profile more often argues against ferroptosis promotion unless paired with external pro-oxidant triggers or special formulations.
13 Clinical Translation Constraint Low systemic parent exposure; many in-vitro effects are high-concentration Better fit for protection than tumor killing in some settings — PK and context limitation Main constraints are oral bioavailability, metabolite-dominant disposition, model heterogeneity, and potential therapy antagonism when antioxidant protection outweighs tumor suppression.
TSF Legend: P: 0–30 min (primary/rapid effects)   R: 30 min–3 hr (acute signaling/stress)   G: >3 hr (gene-regulatory adaptation)


Alzheimer’s disease context

Chlorogenic acid — In the Alzheimer’s disease context, chlorogenic acid (CGA) is best classified as a multifunctional dietary polyphenol/neuroprotective small molecule with preclinical cholinergic, antioxidant, anti-inflammatory, and anti-amyloid activity rather than an established AD drug. Its AD relevance is supported by in vitro and animal-model evidence showing reduced acetylcholinesterase activity, lower oxidative stress, lower neuroinflammation, and improved cognitive performance in several paradigms. Standard abbreviations include CGA and 5-CQA. The strongest current interpretation is that CGA is a plausible adjunctive neuroprotective candidate with limited human cognitive-support data, but not a clinically validated treatment for Alzheimer’s disease.

Primary mechanisms (ranked):

  1. Reduction of oxidative stress and lipid peroxidation.
  2. Suppression of microglial activation and pro-inflammatory signaling.
  3. Down-modulation of acetylcholinesterase activity with support of cholinergic tone.
  4. Reduction of amyloid-related toxicity and associated neuronal injury.
  5. Support of mitochondrial and autophagy-linked neuronal homeostasis in selected models.
  6. Functional cognitive improvement in preclinical models, with limited human support for attention/executive domains rather than confirmed AD treatment.

Bioavailability / PK relevance: Oral chlorogenic acids are meaningfully absorbed but extensively metabolized; circulating exposure includes parent compound plus conjugated and gut-derived phenolic metabolites. Brain penetration has been demonstrated in animal PK work, but CNS exposure is still constrained relative to many in vitro concentrations.

In-vitro vs systemic exposure relevance: Many neuroprotection studies use pharmacologic concentrations or dosing paradigms not directly comparable to ordinary dietary intake. AD relevance is therefore biologically plausible but still translationally constrained by metabolism, CNS exposure, and model dependence.

Clinical evidence status: Strong preclinical support; limited human cognitive-support evidence; no convincing clinical evidence that CGA is an established Alzheimer’s disease therapy.

Chlorogenic Acid in Alzheimer’s Disease

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Oxidative stress and lipid peroxidation ↓ R–G Redox neuroprotection Most consistent AD-relevant signal. CGA lowers oxidative stress markers and lipid peroxidation in amnesia and amyloid-related models.
2 Microglial activation and neuroinflammation ↓ R–G Anti-inflammatory CNS protection Supported by studies showing reduced microglial activation or M1-like inflammatory polarization with improved cognition and neuronal preservation.
3 Acetylcholinesterase ↓ R–G Support of cholinergic function AChE inhibition is supported in vitro and in animal cognitive-impairment models. This helps justify AD relevance, but the effect size and clinical comparability versus approved AChE inhibitors remain uncertain.
4 Amyloid β toxicity ↓ G Reduced amyloid-associated neuronal damage Evidence supports attenuation of Aβ-linked toxicity and, in some models, lower amyloid burden or downstream injury. This is supportive but still preclinical.
5 Synaptic and neuronal survival ↑ G Preservation of neuronal integrity CGA generally trends toward improved neuronal survival and less histologic damage in AD-like or cognitive-injury models.
6 Autophagy and proteostasis ↑ (model-dependent) G Improved clearance homeostasis Some APP/PS1 work suggests restoration of autophagic flux and improved proteostatic handling. Relevant, but not yet the dominant AD axis for CGA.
7 Mitochondrial function ↑ (model-dependent) R–G Energetic stabilization Often inferred from lower oxidative injury and better neuronal viability; mechanistically plausible but less directly established than antioxidant and anti-inflammatory effects.
8 Cognitive performance ↑ G Behavioral improvement Multiple rodent studies report improved learning or memory. Human evidence is limited and currently supports mild cognitive-function benefit more than established AD efficacy.
9 Clinical Translation Constraint ↔ — Preclinical-to-clinical gap Main constraints are metabolite-dominant exposure, uncertain brain-effective concentrations in humans, heterogeneous models, and lack of definitive AD treatment trials.
TSF Legend: P: 0–30 min   R: 30 min–3 hr   G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
6027- CGA,  CUR,  EGCG,  QC,  RES  Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol
- Review, Nor, NA
*ROS↓, ROS↑,
6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,
6009- CGA,    Chlorogenic Acid: An In-Depth Review of Its Effectiveness in Cancer Treatment
- Review, Var, NA
TumCCA↑, TumCI↓, TumMeta↓, angioG↓, ROS↑, ChemoSen↑, BioAv↓, Half-Life↓, PI3K↓, Akt↓, mTOR↓, Apoptosis↑, NOTCH↓, Hif1a↓, VEGF↓, Casp3↑, MMP↓, Ferroptosis↑, ATP↓,

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 ⓘ

Ferroptosis↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   mitResp↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Bax:Bcl2↑, 1,   Casp3↑, 2,   Casp9↑, 1,   Ferroptosis↑, 1,  

DNA Damage & Repair ⓘ

p‑P53↑, 1,   PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↝, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 2,   NOTCH↓, 1,   PI3K↓, 2,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 2,   VEGF↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Half-Life↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 39

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NRF2↑, 2,   ROS↓, 2,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   glucose↓, 1,   LDH↓, 1,   PPARα↝, 1,  

Cell Death ⓘ

Casp↓, 1,   JNK↓, 1,  

Migration ⓘ

Ca+2↓, 1,   TRPC1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 2,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 35

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
3 Chlorogenic acid
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Quercetin
1 Resveratrol
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#:59  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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