Vitexin / IRes Cancer Research Results

VT, Vitexin: Click to Expand ⟱
Features:

Vitexin - Apigenin-8-C-Glucoside

Alternative Names: Apigenin-8-C-glucoside, apigenin-8-C-β-D-glucopyranoside

Type: Flavone C-glycoside / apigenin derivative

Function: Vitexin is a naturally occurring C-glycosylated flavone in which glucose is attached to apigenin at the C-8 position. It exhibits antioxidant, anti-inflammatory, metabolic, cardiovascular, neuroprotective, and antiproliferative activities and can modulate pathways involving NF-κB, Nrf2/HO-1, MAPK, PI3K/AKT, AMPK, HIF-1α, apoptosis, and oxidative stress.

-see also IsoVitexin

Cancer: Preclinical studies indicate antiproliferative, pro-apoptotic, anti-migratory, anti-invasive, and anti-inflammatory effects across multiple cancer models. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, HIF-1α, ROS, apoptosis, and cell-cycle signaling. Clinical anticancer efficacy has not been established.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective activity through antioxidant and anti-inflammatory effects, reduction of neuronal injury, regulation of oxidative stress and mitochondrial function, and modulation of signaling pathways relevant to cognitive impairment and amyloid-associated neurotoxicity. Clinical efficacy for Alzheimer's disease has not been established.
IRes, Insulin Resistance: Click to Expand ⟱
Source:
Type:

Insulin Resistance - Reduced Cellular Responsiveness to Insulin

Type: Metabolic phenotype / insulin-signaling dysfunction

Function: Insulin resistance is a state in which target tissues respond inadequately to insulin, resulting in impaired glucose uptake and altered metabolic signaling. It is commonly associated with compensatory hyperinsulinemia, dysregulated PI3K/AKT signaling, inflammation, oxidative stress, mitochondrial dysfunction, and altered lipid metabolism.

Cancer: ↑ Increased insulin resistance and associated hyperinsulinemia can promote a pro-tumorigenic metabolic environment through enhanced insulin/IGF signaling, inflammation, altered lipid metabolism, and increased growth-factor availability. The strength of this association varies by cancer type.

Alzheimer's Disease: ↑ Increased peripheral and brain insulin resistance is associated with impaired neuronal glucose utilization, synaptic dysfunction, neuroinflammation, oxidative stress, abnormal tau phosphorylation, and altered amyloid processing. Improved insulin sensitivity is generally considered favorable.
Scientific Papers found: Click to Expand⟱
7887- VT,  IVT,    Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention
- Review, AD, NA - Review, Var, NA
*antiOx↑, *Inflam↓, *AntiCan↑, *Bacteria↓, *neuroP↑, *Obesity↓, *cardioP↑, *ROS↓, *MMP↑, *ATP↑, *MFN2↑, *DRP1/DNM1L↓, *FOXO3↑, *NRF2↑, *Ferroptosis↓, *GPx4↑, TumCP↓, HMGB1↓, PI3K↓, Akt↓, Hif1a↓, CDK1↓, CycB/CCNB1↓, TumCCA↑, Apoptosis↑, P53↑, NF-kB↓, ERK↓, p‑PI3K↓, miR-34a↑, Apoptosis↑, CSCs?, *MAPK↓, *HO-1↑, *hepatoP↑, *AMPK↑, *Akt↑, *GSK‐3β↑, *chemoP↑, *Casp3↓, *IRes↝, *GlucoseCon↑, ChemoSen↑, *GSH↑, *SOD↑, *ATF2↑, *GPx↑, *GSTs↑, *AntiAge↑, *Stroke↓, *AChE↓, *ACE/ACE1↓, *ACE2↓, *GutMicro↑, *MPO↓, *H+/K+-ATPase↓, *AntiDiabetic↑, *GLUT4↑, *Obesity↓, *HH↓, *RenoP↑, *BioAv↓, *BioAv↝, *BioAv↑,

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:


Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 1,  

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

CSCs?, 1,   ERK↓, 1,   miR-34a↑, 1,   PI3K↓, 1,   p‑PI3K↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1,   ACE2↓, 1,   H+/K+-ATPase↓, 1,   IRes↝, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Ferroptosis↓, 1,   GPx↑, 1,   GPx4↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 1,   MFN2↑, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   DRP1/DNM1L↓, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   GlucoseCon↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   ATF2↑, 1,   Casp3↓, 1,   Ferroptosis↓, 1,   MAPK↓, 1,  

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

FOXO3↑, 1,   GSK‐3β↑, 1,   HH↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT4↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   Obesity↓, 2,   RenoP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 47

Scientific Paper Hit Count for: IRes, Insulin Resistance
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#:462  Target#:1674  State#:%  Dir#:4
  wNotes=0  sortOrder:rid,rpid

 

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