Fisetin / ROS Cancer Research Results

FIS, Fisetin: Click to Expand ⟱

Features:

Fisetin is a plant based flavonoid. Found in strawberries(160ug/g), apples, persimmons, onions, cucumbers, grapes.

-Note half-life 3-4hrs
- Oral BioAv low (40-50%)
Pathways:
- induce ROS production in cancer cells, but also known to reduce it.
Also a claim Fisetin-Induced Reactive Oxygen Species Production Has No Effect on Apoptosis in RCC cells
Also one claim (NAC 10-20mM levels) that NAC enhances ROS/apoptosis
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Does not appear to lower antioxidants in cancer cells
- Raises AntiOxidant defense in Normal Cells: ROS↓">ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits HIF-1α↓, cMyc↓, LDH↓, GRP78↑,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells : CD133↓, β-catenin↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Fisetin — a naturally occurring plant flavonol and polyphenolic bioactive compound, chemically identified as 3,3′,4′,7-tetrahydroxyflavone. It is classified as a dietary flavonoid, experimental senotherapeutic and preclinical anticancer agent; Fisetin occurs in strawberries, apples, persimmons, grapes, onions and cucumbers, with strawberries providing one of the higher concentrations among commonly consumed foods. Its reported anticancer, neuroprotective and senolytic actions remain predominantly preclinical, and it is not an approved cancer or Alzheimer’s disease therapy.

Primary mechanisms (ranked):

Suppression of PI3K/AKT/mTOR and related survival signaling, reducing tumor-cell proliferation, stress tolerance and treatment resistance.
Induction of intrinsic mitochondrial apoptosis through BAX/Bcl-2 rebalancing, mitochondrial membrane-potential loss, cytochrome-c release and caspase activation.
Inhibition of NF-κB, STAT3 and inflammatory survival transcription, with reductions in COX-2 and tumor-supportive cytokine signaling.
Cell-cycle arrest through reduced cyclin D1, cyclin E, CDK2, CDK4 and CDK6, accompanied in some models by increased p21 or p27.
Suppression of Wnt/β-catenin, EMT, matrix metalloproteinases and focal-adhesion signaling, reducing cancer stemness, migration and invasion.
Biphasic redox modulation: context-dependent ROS elevation and ER or mitochondrial stress in cancer cells, but antioxidant and NRF2-associated cytoprotection in many nonmalignant injury models.
Senotherapeutic activity against selected senescent-cell populations through disruption of senescent-cell anti-apoptotic pathways; selectivity varies markedly by cell type and dosing regimen.
Secondary inhibition of HIF-1α, VEGF and tumor-associated angiogenesis in responsive experimental models.

Bioavailability / PK relevance: Native fisetin has very low aqueous solubility, rapid intestinal and hepatic conjugation, and limited systemic exposure to unconjugated fisetin after conventional oral administration. Glucuronide, sulfate and methylated metabolites can predominate in circulation. Human PK evidence remains limited, although formulated preparations can produce substantially greater exposure than unformulated fisetin. Liposomal, nanoemulsion, phospholipid, cyclodextrin and other delivery systems are therefore mechanistically relevant but cannot be assumed equivalent to ordinary supplements.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM fisetin, commonly 20–80 µM. These concentrations are substantially above the free-parent concentrations expected after ordinary dietary intake and may exceed those produced by conventional oral supplements. Direct translation of cytotoxic concentrations is therefore poor unless tumor accumulation, active metabolites or an exposure-enhancing formulation is demonstrated.

Clinical evidence status: Cancer evidence is predominantly cell-culture and animal evidence. Early human studies are evaluating fisetin as a senolytic or supportive intervention in aging, frailty and cancer-survivor populations, but there is no completed randomized evidence establishing antitumor efficacy. Fisetin should be categorized as preclinical for direct cancer treatment and investigational for adjunct or senotherapeutic use.

Safety / interaction constraints: Food-level exposure is generally regarded as low risk, and small short-term human studies have not identified a clear severe toxicity signal. However, high intermittent senolytic dosing and long-term supplemental dosing remain insufficiently characterized. Mechanistic concerns include antiplatelet or anticoagulant additivity, modulation of drug-metabolizing enzymes and transporters, topoisomerase inhibition, and context-dependent interference with oxidative or cytotoxic cancer treatments. Product purity and formulation-dependent exposure are additional uncertainties.

Fisetin Mechanistic Ranking

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	PI3K AKT mTOR survival signaling	↓ PI3K, ↓ AKT, ↓ mTORC1 and mTORC2	↔ or adaptive modulation	R–G	Reduced proliferation and survival	A recurrent mechanistic axis across prostate, breast, colorectal, lung and other experimental cancer models.
2	Mitochondrial intrinsic apoptosis	↑ BAX and BIM, ↓ Bcl-2 and Mcl-1, ↓ mitochondrial membrane potential, ↑ cytochrome-c and caspases	↔ generally preserved or protected (model-dependent)	R–G	Apoptotic tumor-cell death	Often downstream of survival-pathway inhibition, ER stress or redox disturbance rather than a single direct mitochondrial target.
3	NF-κB inflammatory survival signaling	↓ IKK and NF-κB activity, ↓ COX-2, ↓ anti-apoptotic transcription	↓ inflammatory NF-κB signaling	R–G	Reduced inflammation and stress resistance	Potentially relevant to both cancer-cell survival and the inflammatory tumor microenvironment.
4	Cell-cycle control	↑ G1 or G2/M arrest, ↓ cyclin D1 and cyclin E, ↓ CDK2, ↓ CDK4 and ↓ CDK6, ↑ p21 or p27	↔ or transient arrest (context-dependent)	G	Cytostatic growth suppression	The arrest point varies by cancer lineage, genotype, dose and treatment duration.
5	Wnt β-catenin and cancer stemness	↓ Wnt signaling, ↓ β-catenin, ↓ CD44 and CD133 (model-dependent)	↔	G	Reduced stem-like phenotype and tumor propagation	Particularly relevant in colorectal and other tumors with active Wnt or β-catenin signaling.
6	EMT focal adhesion and matrix degradation	↓ EMT, ↓ FAK, ↓ RhoA and uPA, ↓ MMP-2 and MMP-9, ↑ E-cadherin	↔	G	Reduced migration, invasion and metastasis	Primarily preclinical phenotype data; suppression of several nodes is model-dependent.
7	ER stress and unfolded protein response	↑ PERK, ↑ eIF2α, ↑ ATF4 and CHOP, ↑ GRP78 or BiP (context-dependent)	↔ or ↓ pathological ER stress	R–G	Stress-mediated apoptosis	GRP78 induction may indicate stress activation rather than beneficial suppression; prolonged CHOP signaling favors death.
8	Mitochondrial ROS increase	↑ ROS and mtROS (dose-dependent), but ↓ or neutral ROS in some models	↓ ROS in oxidative-injury models	P–R	Biphasic redox modulation	ROS elevation is not universal or necessarily required for apoptosis. Direction depends on concentration, cell type and baseline oxidative state.
9	NRF2 antioxidant response	↑ or ↓ NRF2 (context-dependent)	↑ NRF2, ↑ HO-1, ↑ GSH, ↑ SOD and catalase	R–G	Adaptive antioxidant regulation	Predominantly protective in normal-tissue injury models; tumor-cell NRF2 activation could theoretically reduce treatment sensitivity.
10	Calcium ER mitochondrial stress	↑ cytosolic Ca²⁺ (model-dependent)	↔	P–R	Amplification of ER and mitochondrial apoptosis	Documented in selected models and should not be treated as a universal primary mechanism.
11	HIF-1α VEGF angiogenic signaling	↓ HIF-1α, ↓ VEGF and ↓ angiogenesis	↔ or vascular protection (injury-dependent)	G	Reduced hypoxic adaptation and neovascularization	Evidence is preclinical and is not equivalent to clinically validated antiangiogenic activity.
12	Glycolysis and metabolic adaptation	↓ HIF-1α, ↓ c-Myc and altered LDH or glycolytic activity (model-dependent)	↔	G	Reduced metabolic flexibility	The database claim that fisetin uniformly inhibits glycolysis is too broad; direct evidence for comprehensive HK2, GLUT1, PKM2 and LDHA suppression is not consistent across models.
13	Senescent-cell survival networks	↓ survival of selected senescent tumor or stromal cells	↓ senescent-cell burden while sparing many nonsenescent cells (model-dependent)	G	Senolytic or senomorphic activity	Activity is heterogeneous and cannot be generalized to every senescent cell type. Effects on therapy-induced tumor senescence may be beneficial or contextually complex.
14	Chemosensitization and radiosensitization	↑ treatment response through ↓ AKT, ↓ NF-κB, apoptosis priming and possible DNA-damage enhancement	↔ or tissue protection (agent-dependent)	R–G	Potential adjunct sensitization	Preclinical only. Antioxidant effects in normal or tumor cells create treatment-specific uncertainty and require schedule-dependent evaluation.
15	Clinical Translation Constraint	Common effective in-vitro concentrations exceed ordinary systemic free-fisetin exposure	Human high-dose and long-term safety remain incompletely defined	G	Limited clinical translatability	Poor solubility, rapid conjugation, formulation dependence, tumor heterogeneity, uncertain active-metabolite contribution and absence of established anticancer efficacy are major constraints.

P: 0–30 min R: 30 min–3 hr G: >3 hr

Alzheimer’s disease relevance: Fisetin has significant but predominantly preclinical relevance to Alzheimer’s disease and related neurodegenerative disorders. Experimental studies report preservation of synaptic function and cognition, suppression of microglial inflammatory signaling, reduction of oxidative stress, promotion of autophagic clearance of phosphorylated tau, and modulation of amyloid-associated toxicity. Senescent-cell clearance provides an additional emerging rationale, but the relative contribution of senolysis versus direct neuroprotective signaling is unresolved. A pilot clinical study in mild cognitive impairment or mild Alzheimer’s disease is registered, but no completed trial currently establishes cognitive efficacy.

Exposure constraint: Most neurological evidence comes from cell and animal models. Native fisetin’s poor solubility, rapid conjugation and uncertain free-brain exposure materially limit direct translation. CMS121 and other fisetin-derived compounds are being developed partly to improve potency, metabolic stability and neuroprotective exposure.

Fisetin in Alzheimer’s Disease

Rank	Pathway / Axis	Modulation	TSF	Primary Effect	Notes / Interpretation
1	Neuroinflammation and microglial activation	↓ NF-κB, ↓ inflammatory microglial activation, ↓ pro-inflammatory mediators	R–G	Reduced chronic neuroinflammatory stress	One of the more consistent neuroprotective mechanisms in cellular and animal models.
2	Synaptic plasticity and ERK CREB signaling	↑ ERK-dependent synaptic signaling and long-term potentiation (context-dependent)	R–G	Preservation of learning and memory	Neuronal ERK activation differs from the ERK suppression reported in many cancer models.
3	Tau autophagic clearance	↑ TFEB and autophagic processing, ↓ phosphorylated tau accumulation	G	Improved proteostasis	Demonstrated preclinically; human relevance and required brain exposure remain unknown.
4	Amyloid β toxicity and aggregation	↓ amyloid-associated oxidative injury and fibril formation (model-dependent)	G	Reduced amyloid-mediated neuronal stress	Evidence does not establish clinically meaningful plaque removal.
5	NRF2 antioxidant defense	↑ NRF2, ↑ HO-1 and endogenous antioxidant capacity	R–G	Protection from oxidative neuronal injury	Protective signaling may cooperate with TFEB-mediated proteostasis.
6	Neuronal mitochondria and apoptosis	↓ mitochondrial dysfunction, ↓ ROS and ↓ apoptotic signaling	R–G	Improved neuronal survival	Direction is opposite to the pro-oxidant mitochondrial stress sought in many cancer models.
7	Cellular senescence and SASP	↓ selected senescent-cell burden and ↓ senescence-associated inflammatory signaling	G	Potential reduction of age-related neuroinflammation	Mechanistically plausible but not yet clinically validated in Alzheimer’s disease.
8	Clinical Translation Constraint	Limited and formulation-dependent systemic and brain exposure; no established therapeutic dose	G	Uncertain human efficacy	Registered pilot testing does not yet constitute efficacy evidence. Native fisetin may not reproduce the exposure or pharmacology of optimized derivatives.

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)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"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
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

6895-

FIS,

Enhanced bioavailability and pharmacokinetics of a novel hybrid-hydrogel formulation of fisetin orally administered in healthy individuals: a randomised double-blinded comparative crossover study

in-vivo,

Nor,

Fifteen healthy volunteers

*neuroP↑, *cardioP↑, *chemoPv↑, *AntiDiabetic↑, *Inflam↓, *ROS↓, *BioAv↓, *BioAv↑, *eff↑, *Half-Life↓,

2861-

FIS,

The neuroprotective effects of fisetin, a natural flavonoid in neurodegenerative diseases: Focus on the role of oxidative stress

Review,

Nor,

Review,

Stroke,

Review,

Park,

*antiOx↑, *ROS↓, *neuroP↑, *NO↑, BioAv↝, *BBB↑, *toxicity↑, *eff↑, *GSH↑, *SOD↑, *Aβ↓, *12LOX↓, *COX2/PTGS2↓, *Catalase↑, *Inflam↓, *TNF-α↓, *IL6↑, *lipid-P↓, NF-kB↓, IL1β↓, NRF2↑, HO-1↑, GSTs↑, cognitive↑, *BDNF↑,

6922-

FIS,

Inhibition of Akt/mTOR signaling by the dietary flavonoid fisetin

Review,

Var,

*memory↑, *Inflam↓, *5LO↓, *lipid-P↓, *NF-kB↓, *antiOx↑, *GSH↑, *HO-1↑, *NRF2↑, *ROS↓, PI3K↓, Akt↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, TumCMig↓, MMPs↓, PSA↓,

6916-

FIS,

Fisetin regulates TPA-induced breast cell invasion by suppressing matrix metalloproteinase-9 activation via the PKC/ROS/MAPK pathways

in-vitro,

BC,

MCF7

PCK1↓, ROS↓, ERK↓, MAPK↓, p38↓, NF-kB?,

6911-

FIS,

New Mitochondria-Targeted Fisetin Derivative Compromises Mitophagy and Limits Survival of Drug-Induced Senescent Breast Cancer Cells

vitro+vivo,

BC,

MMP↓, mt-ROS↑, Apoptosis↑, p‑AMPK↑, Akt↓, HSP90↓, PI3K↓, Akt↓, mTOR↓, TumCP↓, TumMeta↓, angioG↓, TumCD↑, selectivity↑, TumVol↓,

6908-

FIS,

Modulation of p25 and inflammatory pathways by fisetin maintains cognitive function in Alzheimer's disease transgenic mice

in-vivo,

AD,

mice

*memory↑, *p‑ERK↑, *CDK5↓, *P21↓, *cognitive↑, *ROS↓, *COX2/PTGS2↓, *12LOX↓, PGD2↓,

2830-

FIS,

Biological effects and mechanisms of fisetin in cancer: a promising anti-cancer agent

Review,

Var,

TumCG↓, angioG↓, *ROS↓, TumCMig↓, VEGF↓, MAPK↑, NF-kB↓, PI3K↓, Akt↓, mTOR↓, NRF2↑, HO-1↑, ROS↓, Inflam↓, ER Stress↑, ROS↑, TumCP↓, ChemoSen↑, PTEN↑, P53↑, Casp3↑, Casp8↑, Casp9↑, COX2/PTGS2↓, Wnt↓, EGFR↓, Mcl-1↓, survivin↓, IAP1↓, IAP2/BIRC3↓, PGE2↓, β-catenin/ZEB1↓, DR5↑, MMP2↓, MMP9↓, FAK↓, uPA↓, EMT↓, ERK↓, JNK↑, p38↑, PKCδ↓, BioAv↓, BioAv↑, BioAv↑,

2842-

FIS,

Fisetin inhibits cellular proliferation and induces mitochondria-dependent apoptosis in human gastric cancer cells

in-vitro,

GC,

AGS

TumCCA↑, CDK2↓, P53↑, selectivity↑, MMP↓, DNAdam↑, cl‑PARP↑, mt-ROS↑, eff↓, survivin↓,

2840-

FIS,

Fisetin-induced cell death, apoptosis, and antimigratory effects in cholangiocarcinoma cells

NA,

CCA,

 50 μM.

ROS↑, TumCMig↓, TumCP↓,

2839-

FIS,

Dietary flavonoid fisetin for cancer prevention and treatment

Review,

Var,

DNAdam↑, ROS↑, Apoptosis↑, Bcl-2↓, BAX↑, cl‑Casp9↑, cl‑Casp3↑, Cyt‑c↑, lipid-P↓, TumCG↓, TumCA↓, TumCMig↓, TumCI↓, uPA↓, ERK↓, MMP9↓, NF-kB↓, cFos↓, cJun↓, AP-1↓, TumCCA↑, AR↓, mTORC1↓, mTORC2↓, TSC2↑, EGF↓, TGF-β↓, EMT↓, P-gp/ABCB1↓, PI3K↓, Akt↓, mTOR↓, eff↑, ROS↓, ER Stress↑, IRE1↑, ATF4↑, GRP78/BiP↑, ChemoSen↑, CDK2↓, CDK4↓, cycE/CCNE↓, cycD1/CCND1↓, P21↑, COX2/PTGS2↓, Wnt↓, EGFR↓, β-catenin/ZEB1↓, TCF-4↓, MMP7↓, RadioS↑, eff↑,

2838-

FIS,

Fisetin induces apoptosis in colorectal cancer cells by suppressing autophagy and down-regulating nuclear factor erythroid 2-related factor 2 (Nrf2)

cl‑Casp3↑, cl‑PARP↑, MMP↓, Cyt‑c↑, ROS↑, NRF2↓,

2833-

FIS,

AgNPs,

Glucose-capped fisetin silver nanoparticles induced cytotoxicity and ferroptosis in breast cancer cells: A molecular perspective

in-vitro,

BC,

MDA-MB-231

11.275 ± 0.197 μg/mL

MMP↓, ROS↑, NRF2↑, NOX↑, selectivity↑,

2832-

FIS,

Fisetin's Promising Antitumor Effects: Uncovering Mechanisms and Targeting for Future Therapies

Review,

Var,

MMP↓, mtDam↑, Cyt‑c↑, Diablo↑, Casp↑, cl‑PARP↑, Bak↑, BIM↑, Bcl-xL↓, Bcl-2↓, P53↑, ROS↑, AMPK↑, Casp9↑, Casp3↑, BID↑, AIF↑, Akt↓, mTOR↓, MAPK↓, Wnt↓, β-catenin/ZEB1↓, TumCCA↑, P21↑, p27/CDKN1B↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, TumMeta↓, uPA↓, E-cadherin↑, Vim↓, EMT↓, Twist↓, DNAdam↑, ROS↓, COX2/PTGS2↓, PGE2↓, HSF1↓, cFos↓, cJun↓, AP-1↓, Mcl-1↓, NF-kB↓, IRE1↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MMP2↓, MMP9↓, TCF-4↓, MMP7↓, RadioS↑, TOP1↓, TOP2↓,

2831-

FIS,

Fisetin as a chemoprotective and chemotherapeutic agent: mechanistic insights and future directions in cancer therapy

Review,

Var,

TumCG↓, ER Stress↑, antiOx↓, ROS↓, ChemoSen↑,

2829-

FIS,

Fisetin: An anticancer perspective

Review,

Var,

TumCP↓, TumCI↓, TumCCA↑, TumCG↓, Apoptosis↑, cl‑PARP↑, PKCδ↓, ROS↓, ERK↓, NF-kB↓, survivin↓, ROS↑, PI3K↓, Akt↓, mTOR↓, MAPK↓, p38↓, HER2/EBBR2↓, EMT↓, PTEN↑, HO-1↑, NRF2↑, MMP2↓, MMP9↓, MMP↓, Casp8↑, Casp9↑, TRAILR↑, Cyt‑c↑, XIAP↓, P53↑, CDK2↓, CDK4↓, CDC25↓, CDC2↓, VEGF↓, DNAdam↑, TET1↓, CHOP/DDIT3↑, CD44↓, CD133↓, uPA↓, CSCs↓,

2828-

FIS,

Fisetin, a Potent Anticancer Flavonol Exhibiting Cytotoxic Activity against Neoplastic Malignant Cells and Cancerous Conditions: A Scoping, Comprehensive Review

Review,

Var,

*neuroP↑, *antiOx↑, *Inflam↓, RenoP↑, COX2/PTGS2↓, Wnt↓, EGFR↓, NF-kB↓, Casp3↑, Ca+2↑, Casp8↑, TumCCA↑, CDK1↓, PI3K↓, Akt↓, mTOR↓, MAPK↓, *P53↓, *P21↓, *p16↓, mTORC1↓, mTORC2↓, P53↑, P21↑, cycD1/CCND1↓, cycA1/CCNA1↓, CDK2↓, CDK4↓, BAX↑, Bcl-2↓, PCNA↓, HER2/EBBR2↓, Cyt‑c↑, MMP↓, cl‑Casp9↑, MMP2↓, MMP9↓, cl‑PARP↑, uPA↓, DR4↑, DR5↑, ROS↓, AIF↑, CDC25↓, Dose↑, CHOP/DDIT3↑, ROS↑, cMyc↓, cardioP↑,

2827-

FIS,

The Potential Role of Fisetin, a Flavonoid in Cancer Prevention and Treatment

Review,

Var,

*antiOx↑, *Inflam↓, neuroP↑, hepatoP↑, RenoP↑, cycD1/CCND1↓, TumCCA↑, MMPs↓, VEGF↓, MAPK↓, NF-kB↓, angioG↓, Beclin-1↑, LC3s↑, ATG5↑, Bcl-2↓, BAX↑, Casp↑, TNF-α↓, Half-Life↓, MMP↓, mt-ROS↑, cl‑PARP↑, CDK2↓, CDK4↓, Cyt‑c↑, Diablo↑, DR5↑, Fas↑, PCNA↓, Ki-67↓, p‑H3↓, chemoP↑, Ca+2↑, Dose↝, CDC25↓, CDC2↓, CHK1↑, Chk2↑, ATM↑, PCK1↓, RAS↓, p‑p38↓, Rho↓, uPA↓, MMP7↓, MMP13↓, GSK‐3β↑, E-cadherin↑, survivin↓, VEGFR2/KDR/Flk1↓, IAP2/BIRC3↓, STAT3↓, JAK1↓, mTORC1↓, mTORC2↓, NRF2↑,

2825-

FIS,

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Review,

Var,

*Inflam↓, *antiOx↓, *ERK↑, *p‑cMyc↑, *NRF2↑, *GSH↑, *HO-1↑, mTOR↓, PI3K↓, Akt↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, P21↑, p27/CDKN1B↑, JNK↑, MMP2↓, MMP9↓, uPA↓, NF-kB↓, cFos↓, cJun↓, E-cadherin↑, Vim↓, N-cadherin↓, EMT↓, MMP↓, Cyt‑c↑, Diablo↑, Casp↑, cl‑PARP↑, P53↑, COX2/PTGS2↓, PGE2↓, HSP70/HSPA5↓, HSP27↓, DNAdam↑, Casp3↑, Casp9↑, ROS↑, AMPK↑, NO↑, Ca+2↑, mTORC1↓, p70S6↓, ROS↓, ER Stress↑, IRE1↑, ATF4↑, GRP78/BiP↑, eff↑, eff↑, eff↑, RadioS↑, ChemoSen↑, Half-Life↝,

2824-

FIS,

Fisetin in Cancer: Attributes, Developmental Aspects, and Nanotherapeutics

Review,

Var,

*antiOx↑, *Inflam↓, angioG↓, BioAv↓, BioAv↑, TumCP↓, TumCI↓, TumCMig↓, *neuroP↑, EMT↓, ROS↑, selectivity↑, EGFR↓, NF-kB↓, VEGF↓, MMP9↓, MMP↓, cl‑PARP↑, Casp7↑, Casp8↑, Casp9↑, *ROS↓, uPA↓, MMP1↓, Wnt↓, Akt↓, PI3K↓, ERK↓, Half-Life↝,

2844-

FIS,

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

in-vitro,

OS,

U2OS

tumCV↓, Apoptosis↑, Casp3↑, Casp8↑, Casp9↑, BAX↑, BAD↑, Bcl-2↓, Bcl-xL↓, PI3K↓, Akt↓, ERK↓, p‑JNK↑, p‑cJun↑, p‑p38↑, ROS↑, MMP↓, mTORC1↓, PTEN↑, p‑GSK‐3β↓, GSK‐3β↑, NF-kB↓, IKKα↑, Cyt‑c↑,

2857-

FIS,

A review on the chemotherapeutic potential of fisetin: In vitro evidences

Review,

Var,

COX2/PTGS2↓, PGE2↓, EGFR↓, Wnt↓, β-catenin/ZEB1↓, TCF↑, Apoptosis↑, Casp3↑, cl‑PARP↑, Bcl-2↓, Mcl-1↓, BAX↑, BIM↑, BAD↑, Akt↓, mTOR↓, ACC↑, Cyt‑c↑, Diablo↑, cl‑Casp8↑, Fas↑, DR5↑, TRAIL↑, Securin↓, CDC2↓, CDC25↓, HSP70/HSPA5↓, CDK2↓, CDK4↓, cycD1/CCND1↓, MMP2↓, uPA↓, NF-kB↓, cFos↓, cJun↓, MEK↓, p‑ERK↓, N-cadherin↓, Vim↓, Snail↓, Fibronectin↓, E-cadherin↓, NF-kB↑, ROS↑, DNAdam↑, MMP↓, CHOP/DDIT3↑, eff↑, ChemoSen↑,

2856-

FIS,

N -acetyl- L -cysteine enhances fisetin-induced cytotoxicity via induction of ROS-independent apoptosis in human colonic cancer cells

in-vitro,

Colon,

COLO205

eff↑, ROS↑, tumCV↓, Casp3↑, Bcl-2↓, MMP↓, eff↑,

2855-

FIS,

Fisetin Induces Apoptosis Through p53-Mediated Up-Regulation of DR5 Expression in Human Renal Carcinoma Caki Cells

in-vitro,

RCC,

Caki-1

TumCCA↑, cl‑PARP↑, Apoptosis↑, Casp↑, P53↑, DR5↑, CHOP/DDIT3↑, ROS↑, ER Stress↑, ATF4↑, XBP-1↑, eff∅,

2853-

FIS,

Fisetin Inhibits Cell Proliferation and Induces Apoptosis via JAK/STAT3 Signaling Pathways in Human Thyroid TPC 1 Cancer Cells

in-vitro,

Thyroid,

TPC-1

Apoptosis↑, ROS↑, MMP↓, TumCCA↑, Casp3↑, Casp8↑, Casp9↑, JAK1↓, STAT3↓,

2852-

FIS,

A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms

Review,

CRC,

Risk↓, P53↑, MDM2↓, COX2/PTGS2↓, Wnt↓, NF-kB↓, CDK2↓, CDK4↓, p‑RB1↓, cycE/CCNE↓, P21↑, NRF2↓, ROS↑, Casp8↑, Fas↑, TRAIL↑, DR5↑, MMP↓, Cyt‑c↑, selectivity↑, P450↝, GSTs↝, RadioS↑, Inflam↓, β-catenin/ZEB1↓, EGFR↓, TumCCA↑, ChemoSen↑,

2851-

FIS,

Apoptosis induction in breast cancer cell lines by the dietary flavonoid fisetin

in-vitro,

BC,

MDA-MB-468

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MCF7

in-vitro,

BC,

T47D

in-vitro,

BC,

SkBr3

in-vitro,

Nor,

tumCV↓, selectivity↑, TumCCA↑, Apoptosis↑, ROS∅,

2850-

FIS,

ROSMAPK_pathways">Fisetin regulates TPA-induced breast Cancer cell invasion by suppressing matrix metalloproteinase-9 activation via the PKC/ROS/MAPK pathways

in-vitro,

BC,

MCF7

TumCI↓, PKCδ↓, ROS↓, ERK↑, p38↓, NF-kB↓, MMP9↓,

2849-

FIS,

Activation of reactive oxygen species/AMP activated protein kinase signaling mediates fisetin-induced apoptosis in multiple myeloma U266 cells

in-vitro,

Melanoma,

U266

40 μg/ml

TumCD↑, TumCCA↑, Casp3↑, Bcl-2↓, Mcl-1↓, BAX↑, BIM↑, BAD↑, AMPK↑, ACC↑, p‑Akt↓, p‑mTOR↓, ROS↑, eff↓,

2848-

FIS,

Fisetin alleviates cellular senescence through PTEN mediated inhibition of PKCδ-NOX1 pathway in vascular smooth muscle cells

in-vitro,

Nor,

*ROS↓, *PTEN↑, *PKCδ↑, *Inflam↓,

2847-

FIS,

Fisetin-induced cell death, apoptosis, and antimigratory effects in cholangiocarcinoma cells

in-vitro,

CCA,

tumCV↓, ChemoSen↑, TumCMig↓, ROS↑, TumCI↓, angioG↓, CDK2↓, PI3K↓, Akt↓, mTOR↓, EGFR↓, Casp↑, mTORC1↓, mTORC2↑, cycD1/CCND1↓, cycE/CCNE↓, MMP2↓, MMP9↓, ER Stress↑, Ca+2↑, eff↓,

2846-

FIS,

Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity

in-vitro,

Nor,

0, 5, 10, 15, 20, 30, 40, 60, 80 and 100 μM

concentration of 15 μM of fisetin in the subsequent experiments

*cardioP↑, *ROS↓, *Casp↓, *DNAdam↓,

2845-

FIS,

Fisetin: A bioactive phytochemical with potential for cancer prevention and pharmacotherapy

Review,

Var,

PI3K↓, Akt↓, mTOR↓, p38↓, *antiOx↑, *neuroP↑, Casp3↑, Bcl-2↓, Mcl-1↓, BAX↑, BIM↑, BAD↑, AMPK↑, ACC↑, DNAdam↑, MMP↓, eff↑, ROS↑, cl‑PARP↑, Cyt‑c↑, Diablo↑, P53↑, p65↓, Myc↓, HSP70/HSPA5↓, HSP27↓, COX2/PTGS2↓, Wnt↓, EGFR↓, NF-kB↓, TumCCA↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycA1/CCNA1↓, P21↑, MMP2↓, MMP9↓, TumMeta↓, MMP1↓, MMP3↓, MMP7↓, MET↓, N-cadherin↓, Vim↓, Snail↓, Fibronectin↓, E-cadherin↑, uPA↓, ChemoSen↑, EMT↓, Twist↓, Zeb1↓, cFos↓, cJun↓, EGF↓, angioG↓, VEGF↓, eNOS↓, *NRF2↑, HO-1↑, NRF2↓, GSTs↓, ATF4↓,

2843-

FIS,

Fisetin and Quercetin: Promising Flavonoids with Chemopreventive Potential

Review,

Var,

NRF2↑, Keap1↓, ChemoSen↑, BioAv↓, Cyt‑c↑, Casp3↑, Casp9↑, BAX↑, tumCV↓, Mcl-1↓, cl‑PARP↑, IGF-1↓, Akt↓, CDK6↓, TumCCA↑, P53?, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, MMP2↓, MMP9↓, MMP1↓, MMP7↓, MMP3↓, VEGF↓, PI3K↓, mTOR↓, COX2/PTGS2↓, Wnt↓, EGFR↓, NF-kB↓, ERK↓, ROS↑, angioG↓, TNF-α↓, PGE2↓, iNOS↓, NO↓, IL6↓, HSP70/HSPA5↝, HSP27↝,

3372-

QC,

FIS,

KaempF,

Anticancer Potential of Selected Flavonols: Fisetin, Kaempferol, and Quercetin on Head and Neck Cancers

Review,

HNSCC,

ROCK1↑, TumCCA↓, HSPs↓, RAS↓, ROS↑, Ca+2↑, MMP↓, Cyt‑c↑, Endon↑, MMP9↓, MMP2↓, MMP7↓, MMP-10↓, VEGF↓, NF-kB↓, p65↓, iNOS↓, COX2/PTGS2↓, uPA↓, PI3K↓, FAK↓, MEK↓, ERK↓, JNK↓, p38↓, cJun↓, FOXO3↑,

Showing Research Papers: 1 to 34 of 34

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 34

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 6, Catalase↑, 1, GSH↑, 3, HO-1↑, 2, lipid-P↓, 2, NRF2↑, 3, ROS↓, 8, SOD↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

12LOX↓, 2, p‑cMyc↑, 1,

Cell Death(tgid=5) ⓘ

Casp↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1, p16↓, 1, P53↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 2,

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

ERK↑, 1, p‑ERK↑, 1, PTEN↑, 1,

Migration(tgid=13) ⓘ

5LO↓, 1, CDK5↓, 1, PKCδ↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↑, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2, IL6↑, 1, Inflam↓, 8, NF-kB↓, 1, TNF-α↓, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

IL6↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1, cardioP↑, 2, chemoPv↑, 1, cognitive↑, 1, memory↑, 2, neuroP↑, 5, toxicity↑, 1,
Total Targets: 43

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

34 Fisetin
1 Silver-NanoParticles
1 Quercetin
1 Kaempferol

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#:78  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Fisetin / ROS Cancer Research Results

Fisetin Mechanistic Ranking

Fisetin in Alzheimer’s Disease

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

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