Myricetin / PD-L1 Cancer Research Results

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
PD-L1, Programmed Death-Ligand 1: Click to Expand ⟱
Source:
Type:
PD-L1 is a protein that plays a crucial role in the regulation of the immune system. PD-L1 helps to prevent the immune system from attacking healthy cells by binding to its receptor, PD-1, on immune cells. However, some cancer cells can exploit this mechanism by expressing high levels of PD-L1, which can help them evade immune detection.
PD-L1 has become a key target for cancer immunotherapy, particularly in the development of checkpoint inhibitors.

PD-1: Upregulated on tumor-infiltrating lymphocytes (TILs), reflecting chronic antigen exposure and an “exhausted” T cell phenotype.
PD-L1 and PD-L2: Frequently overexpressed by many tumor types (e.g., non–small cell lung cancer, melanoma, renal cell carcinoma, head and neck cancers.
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↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis ⓘ

IDO1↓, 1,  

Immune & Inflammatory Signaling ⓘ

PD-L1↓, 1,  

Clinical Biomarkers ⓘ

PD-L1↓, 1,  
Total Targets: 3

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PD-L1, Programmed Death-Ligand 1
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#:127  Target#:243  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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