Database Query Results : Myricetin, ,

Myr, Myricetin: Click to Expand ⟱
Features:
Myricetin (MYR; 3,3′,4′,5,5′,7-hexahydroxyflavone) is a dietary flavonol polyphenol abundant in berries, tea, red wine, and some medicinal plants. Its dominant biology is redox-active modulation with context-dependent pro-oxidant capacity, ranking conceptually as:
(1) ROS modulation (scavenging at low dose; pro-oxidant at higher dose or with metal redox cycling),
(2) PI3K/Akt/mTOR and MAPK pathway inhibition,
(3) NF-κB suppression and inflammatory signaling control, and
(4) mitochondrial apoptosis induction (caspase activation, ΔΨm disruption).
Bioavailability is limited by low aqueous solubility and rapid conjugation (glucuronidation/sulfation); reported human plasma levels after dietary exposure are typically sub-micromolar (<1 µM), while many in-vitro cancer studies use 10–100 µM, often exceeding realistic systemic exposure. Clinical evidence remains preclinical-dominant; no robust RCT-grade anticancer efficacy established. Redox duality implies potential chemo-sensitization in oxidative tumors but also theoretical protection of normal tissue.

-Possible inhibitory effects on mammalian TrxRs (thioredoxin reductase)

Myricetin (MYR) — Cancer-Relevant Pathway Effects

Rank Pathway / Axis Cancer Cells (↑/↓/↔ + qualifiers) Normal Cells (↑/↓/↔ + qualifiers) TSF Primary Effect Notes / Interpretation
1 ROS Modulation ↑ ROS (high conc., pro-oxidant); ↓ ROS (low conc.) ↓ ROS (protective; dose-dependent) P–R Redox stress induction or buffering Metal-chelating flavonol; can shift to pro-oxidant under tumor oxidative stress, enabling apoptosis.
2 PI3K/Akt/mTOR ↓ Akt phosphorylation (model-dependent) ↔ / mild inhibition R–G Anti-proliferative signaling Common in breast, colon, and prostate cell models; often ≥10 µM required.
3 MAPK (ERK/JNK/p38) ↓ ERK; ↑ JNK/p38 (stress-activated; context) ↔ / adaptive stress response R Pro-apoptotic signaling shift Promotes apoptotic cascades via stress kinase activation.
4 NF-κB ↓ NF-κB activation ↓ NF-κB (anti-inflammatory) R–G Anti-inflammatory modulation May reduce tumor-promoting inflammation.
5 Mitochondrial Apoptosis (Caspase / ΔΨm) ↑ Bax; ↓ Bcl-2; ↑ caspase-3 ↔ / protective at low dose R–G Intrinsic apoptosis activation Frequently observed in leukemia and solid tumor models at supra-physiologic doses.
6 NRF2 Axis ↔ / mild ↑ (context-dependent) ↑ NRF2 (cytoprotection) R–G Adaptive antioxidant response Less potent NRF2 activator than electrophilic isothiocyanates.
7 Ca²⁺ Signaling ↑ intracellular Ca²⁺ (mitochondrial stress; model-dependent) ↔ R Apoptosis facilitation Reported in some hepatoma and leukemia models.
8 Ferroptosis ↔ / potentially ↓ (iron-chelating) ↔ — Lipid peroxidation modulation Chelation may counter ferroptosis unless combined with pro-oxidant triggers.
9 Clinical Translation Constraint Low oral bioavailability; plasma <1 µM; most anticancer studies use 10–100 µM — PK limitation Conjugation and rapid metabolism limit systemic tumor exposure.
TSF Legend: P: 0–30 min   R: 30 min–3 hr   G: >3 hr
Scientific Papers found: Click to Expand⟱
1044- Myr,    Myricetin inhibits interferon-γ-induced PD-L1 and IDO1 expression in lung cancer cells
- in-vitro, Lung, NA
PD-L1↓, IDO1↓,
1128- Myr,    Myricetin suppresses TGF-β-induced epithelial-to-mesenchymal transition in ovarian cancer
- vitro+vivo, Ovarian, NA
MAPK↓, ERK↓, PI3K↓, Akt↓, p‑PARP↑, cl‑Casp3↑, Bax:Bcl2↑, TumCMig↓, SMAD3↓,
1141- Myr,    Myricetin: targeting signaling networks in cancer and its implication in chemotherapy
- Review, NA, NA
*PI3K↑, *Akt↑, p‑Akt↓, SIRT3↑, p‑ERK↓, p38↓, VEGF↓, MEK↓, MKK4↓, MMP9↓, Raf↓, F-actin↓, MMP2↓, COX2↓, BMP2↓, cycD1/CCND1↓, Bax:Bcl2↑, EMT↓, EGFR↓, TumAuto↑,
1273- Myr,    Myricetin Induces Ferroptosis and Inhibits Gastric Cancer Progression by Targeting NOX4
- vitro+vivo, GC, NA
Ferroptosis↑, MDA↑, Iron↑, GSH↓, NOX4↑, NRF2↓, GPx4↓,
1997- Myr,  QC,    Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity
- in-vitro, Lung, A549
TrxR↓, eff↑, TumCCA↑, eff↓, ROS↑,
1998- Myr,  CUR,    Thioredoxin-dependent system. Application of inhibitors
- Review, Var, NA
TrxR↓, ROS↑,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   Iron↑, 1,   MDA↑, 1,   NOX4↑, 1,   NRF2↓, 1,   ROS↑, 2,   SIRT3↑, 1,   TrxR↓, 2,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   MKK4↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

IDO1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Bax:Bcl2↑, 2,   BMP2↓, 1,   cl‑Casp3↑, 1,   Ferroptosis↑, 1,   MAPK↓, 1,   p38↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

p‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   PI3K↓, 1,  

Migration ⓘ

F-actin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   SMAD3↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   PD-L1↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   PD-L1↓, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  
Total Targets: 2

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

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