Kaempferol / Dose Cancer Research Results

KaempF, Kaempferol: Click to Expand ⟱
Features:

Kaempferol = dietary flavonol polyphenol (aglycone; often present as glycosides such as kaempferol-3-O-glucoside). Sources: tea, kale, spinach, capers, broccoli, onions. Primary mechanisms (ranked):
1) PI3K/Akt/mTOR pathway inhibition → ↓ proliferation, ↓ survival signaling (core anti-tumor axis).
2) MAPK modulation (ERK/JNK/p38) → apoptosis or growth arrest (context-dependent).
3) NF-κB suppression → ↓ inflammatory and pro-survival transcription programs.
4) Pro-oxidant ROS induction at higher concentrations → mitochondrial apoptosis signaling.
Bioavailability/PK relevance: Oral absorption modest; extensive phase II metabolism (glucuronidation/sulfation); plasma typically low µM or sub-µM after dietary intake; many in-vitro studies use 10–100 µM (often exceeding achievable systemic exposure without specialized delivery).
Clinical evidence status: largely preclinical (cell + animal); limited human cancer trial data; strongest support in epidemiologic associations rather than interventional oncology RCTs.

Kaempferol—an abundant flavonoid found in various fruits, vegetables, and medicinal herbs—affects cancer cell behavior

Pathways:
-Inhibit the PI3K/Akt signaling
-Modulation of the MAPK pathway (including ERK1/2)
-Inhibit NF-κB Signaling Pathway
-can upregulate or activate p53-dependent pathways
-Inhibitory action on STAT
-Activation of AMPK
-Reduce VEGF
-Can induce oxidative stress in cancer cells (ROS)

Kaempferol — Cancer vs Normal Pathway Effects

Rank Pathway / Axis Cancer Cells (↑ / ↓ / ↔) Normal Cells (↑ / ↓ / ↔) TSF Primary Effect Notes / Interpretation
1 PI3K/Akt/mTOR ↓ proliferation; ↓ survival signaling ↔ / mild ↓ (cytoprotective context) R→G Growth suppression Core mechanistic axis across multiple tumor models (breast, lung, colon, prostate).
2 MAPK (ERK, JNK, p38) ↑ JNK/p38 (pro-apoptotic); ↓ ERK (proliferative) ↔ (dose-dependent) R Apoptosis induction Often stress-activated signaling; balance of ERK vs JNK determines outcome.
3 NF-κB ↓ transcription of inflammatory & anti-apoptotic genes ↓ inflammatory tone R→G Anti-inflammatory / anti-survival Reduces cytokine signaling and tumor microenvironment support pathways.
4 ROS ↑ (high concentration; pro-oxidant apoptosis) ↔ / ↓ (antioxidant at low conc.) P→R Mitochondrial stress Biphasic: antioxidant at dietary levels; pro-oxidant at higher in-vitro doses.
5 NRF2 ↔ / ↓ (context-dependent) ↑ cytoprotective response G Redox adaptation May activate antioxidant genes in normal cells; persistent activation in tumors could support resistance.
6 Intrinsic apoptosis (Bax/Bcl-2, caspases) ↑ Bax; ↓ Bcl-2; ↑ caspase-3/9 ↔ R→G Mitochondrial apoptosis Common downstream convergence of ROS + PI3K suppression.
7 Ca2+ signaling ↑ mitochondrial Ca2+ (subset models) ↔ R Apoptotic amplification Not universal; observed in certain carcinoma lines.
8 HIF-1α / Angiogenesis ↓ HIF-1α; ↓ VEGF (model-dependent) ↔ G Anti-angiogenic potential Observed in hypoxia models; translational impact uncertain.
9 Ferroptosis ↔ (indirect; limited data) ↔ R Redox-linked sensitivity (theoretical) No consistent ferroptosis signature established.
10 Clinical Translation Constraint Low oral bioavailability; rapid conjugation; in-vitro concentrations commonly exceed systemic exposure; limited human interventional oncology data. — PK / Evidence Dietary intake likely below cytotoxic range; delivery systems (nano-formulations) under investigation.

TSF legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr
Dose, Dosage: Click to Expand ⟱
Source:
Type:
Drug dosage vs efficacy, and actual dosage number of research papers.
Scientific Papers found: Click to Expand⟱
7827- KaempF,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, *Learn↑, *memory↑, *antiOx↑, *Inflam↓, *Aβ↓, *cognitive↑, *BDNF↑, *TrkB↑, *CREB↑, *ERβ/ESR2↑, *ERK↑, *ROS↓, *AChE↓, *Dose↑,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Learn↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CREB↑, 1,  

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

ERK↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BDNF↑, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ERβ/ESR2↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 15

Scientific Paper Hit Count for: Dose, Dosage
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#:316  Target#:1114  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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