Kaempferol / ROS Cancer Research Results

KAE, Kaempferol: Click to Expand ⟱
Features:

Kaempferol — a naturally occurring dietary flavonol polyphenol (3,4′,5,7-tetrahydroxyflavone) found in vegetables, fruits, tea, legumes, and medicinal plants, where it commonly occurs as glycosides rather than free aglycone. It is classified as a bioactive dietary flavonoid/flavonol and experimental natural-product therapeutic; common abbreviations include KMP, KPF, KF, and KAE. Major food sources include kale and other leafy vegetables, tea, broccoli, beans, onions, capers, and some fruits. Kaempferol is a multi-target compound with substantial preclinical anticancer and neuroprotective evidence, but it is not an approved anticancer or Alzheimer’s disease drug.

Primary mechanisms (ranked):

  1. PI3K/AKT/mTOR inhibition → suppression of proliferation and survival signaling, with induction of apoptosis and autophagy.
  2. Mitochondrial and death-receptor apoptosis → ↑ Bax/Bad/Bik, ↓ Bcl-2/Bcl-xL, ↑ mitochondrial permeability and cytochrome-c release, and activation of caspase-8/9/3 pathways.
  3. Cell-cycle suppression → G0/G1 or G2/M arrest depending on tumor model, with altered cyclins/CDKs and frequent participation of p53 signaling.
  4. MAPK and STAT signaling modulation → generally ↓ proliferative ERK/STAT3 signaling, while JNK/p38 effects are strongly model- and dose-dependent.
  5. NF-κB and inflammatory signaling suppression → ↓ pro-survival and inflammatory transcription, including context-dependent reductions in COX-2 and inflammatory mediators.
  6. ROS/redox modulation → frequently ↑ oxidative/mitochondrial stress in cancer cells at cytotoxic concentrations, while lower exposures in normal tissues commonly produce antioxidant and NRF2-dependent cytoprotection.
  7. Migration, EMT, invasion and angiogenesis inhibition → ↓ EGFR/Src/FAK signaling, MMP activity, HIF-1α/VEGF signaling and other metastatic programs in selected models.
  8. Metabolic suppression → inhibition of glycolysis, including PKM2-linked glycolytic metabolism in some tumor models, which can contribute to reversal of chemotherapy resistance.
  9. Ferroptosis modulation → emerging evidence indicates that kaempferol can promote ferroptotic tumor-cell death in selected cancers, while conversely suppressing pathological ferroptosis in non-cancer tissues; direction is therefore highly context-dependent.
  10. Epigenetic modulation → direct broad HDAC inhibition has been demonstrated experimentally at micromolar concentrations and may contribute to altered transcription and growth suppression.
  11. Therapy sensitization → increased responsiveness to radiation, cisplatin, TRAIL and other anticancer treatments has been demonstrated preclinically through PI3K/AKT, mitochondrial apoptosis, metabolic and drug-resistance mechanisms.

Bioavailability / PK relevance: Oral kaempferol is absorbed but undergoes extensive intestinal and hepatic conjugation, particularly glucuronidation and sulfation, so circulating material is predominantly metabolites rather than free aglycone. In a human study using 9 mg dietary kaempferol, mean plasma Cmax was approximately 0.1 µM at about 5.8 hours, with kaempferol-3-glucuronide the major circulating form. Food matrix, glycoside structure, microbiota and formulation substantially influence exposure. Nanoformulations, lipid carriers and related delivery approaches are being investigated to improve systemic exposure but remain experimental for oncology.
-research options to improve bioavailability include: take with oil (not water soluble), add Lecithin. Examples: extra virgin olive oil, nuts, egg yolk
-consuming kaempferol from kale, broccoli, onions or similar foods, most of it is present as glycosides, so mostly dependent on gut microbiota (not oil, etc)

In-vitro vs systemic exposure relevance: Most direct anticancer studies use approximately 10–100 µM kaempferol; reported IC50 values are often around 20–60 µM depending on tumor type. These concentrations generally exceed the sub-µM systemic concentrations observed after ordinary dietary exposure. Consequently, many direct cytotoxic, HDAC-inhibitory, ROS-generating and ferroptotic effects should not be assumed to occur systemically after normal dietary intake. Local gastrointestinal exposure and specialized formulations may provide different exposure conditions.
-Human dietary exposure generally produces circulating kaempferol concentrations in the nanomolar to low-submicromolar range; plasma Cmax of approximately 0.1 µM has been reported after a 9-mg dietary dose. Therefore, in-vitro exposures of 10–20 µM are roughly two orders of magnitude above concentrations demonstrated after ordinary dietary intake.

Clinical evidence status: Preclinical. Anticancer evidence consists predominantly of cell-culture and animal studies, including xenograft studies and preclinical radiosensitization/chemosensitization. There is no established therapeutic oncology indication and no convincing cancer-treatment RCT evidence for kaempferol itself. Human evidence includes epidemiologic dietary associations, pharmacokinetic studies and a small randomized safety study in healthy adults; 50 mg/day kaempferol aglycone for four weeks was well tolerated in that study. Clinical efficacy for cancer remains unproven.


Kaempferol Mechanistic Effects

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K AKT mTOR ↓ PI3K; ↓ AKT; ↓ mTOR ↔ / context-dependent R–G ↓ survival and proliferation; ↑ apoptosis and autophagy One of the most reproducible anticancer axes; direct PI3K inhibition has been demonstrated experimentally.
2 Mitochondrial and death receptor apoptosis ↑ Bax/Bad/Bik; ↓ Bcl-2/Bcl-xL; ↑ Cyt-c; ↑ caspase-8/9/3 ↔ at lower exposure R–G ↑ programmed cell death Both intrinsic mitochondrial and extrinsic death-receptor pathways can participate.
3 Cell cycle and p53 ↑ p53 (model-dependent); ↑ G0/G1 or G2/M arrest ↔ G ↓ proliferation Exact checkpoint depends strongly on cancer type and exposure.
4 MAPK and STAT signaling ↓ ERK; ↓ STAT3; JNK/p38 ↔ (context-dependent) ↔ / protective MAPK modulation R–G ↓ proliferative signaling; ↑ apoptosis JNK and p38 direction is not uniform across models and should not be assigned a universal direction.
5 NF-κB inflammatory survival signaling ↓ NF-κB; ↓ p65; ↓ inflammatory and anti-apoptotic transcription ↓ pathological inflammation R–G Anti-inflammatory and anti-survival activity Potentially relevant to both tumor cells and the tumor microenvironment.
6 Mitochondrial ROS and NRF2 redox response ↑ ROS (dose-dependent); NRF2 ↔ (context-dependent) ↓ ROS; ↑ NRF2 (context-dependent) P–G Tumor oxidative stress versus normal-cell cytoprotection Biphasic redox behavior is important: pro-oxidant anticancer effects generally require substantially higher exposure than dietary systemic exposure.
7 EGFR EMT migration and angiogenesis ↓ EGFR/Src/ERK/AKT; ↓ FAK; ↓ MMPs; ↓ migration; ↓ VEGF ↔ G ↓ invasion, metastasis and angiogenesis Evidence is predominantly preclinical and varies among tumor types.
8 Glycolytic metabolism ↓ PKM2; ↓ glycolysis; ↓ lactate production (model-dependent) ↔ R–G ↓ tumor bioenergetics and drug resistance Particularly relevant to reported reversal of 5-FU resistance; not yet established as a universal kaempferol mechanism.
9 Ferroptosis ↑ ferroptosis (model-dependent) ↓ pathological ferroptosis (context-dependent) R–G Redox-dependent cell death modulation Emerging cancer evidence includes CA9-associated ferroptosis in oral squamous cell carcinoma; direction reverses in some neuroprotective models.
10 HDAC epigenetic regulation ↓ HDAC activity; ↑ histone acetylation ↔; toxicity at high concentration G Epigenetic growth suppression Pan-HDAC inhibition has been demonstrated in vitro; translational relevance is constrained by the micromolar exposure required.
11 Radio and chemosensitization ↑ radiation response; ↑ cisplatin/TRAIL response; ↓ resistance mechanisms ↔ / relative sparing in some models G Adjunct anticancer potential Demonstrated in cell and animal experiments but not established clinically.
12 Clinical Translation Constraint Required cytotoxic concentrations commonly exceed systemic dietary exposure Dietary and short-term supplemental exposures appear considerably better tolerated G PK and clinical-evidence limitation Rapid conjugation, low free-aglycone exposure, heterogeneous mechanisms and absence of therapeutic oncology trials remain major barriers.

TSF: P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer’s disease: Kaempferol has substantial preclinical neuroprotective evidence in cellular and animal models of Alzheimer’s disease and sporadic dementia, but no established human therapeutic efficacy. Reported mechanisms include ↓ oxidative stress and neuroinflammation, ↓ Aβ-associated toxicity and deposition, ↓ neuronal apoptosis, modulation of AChE, improvement of synaptic/neurotrophic signaling, and suppression of pathological neuronal ferroptosis. Recent evidence implicates NRF2/HO-1/GPX4-associated antioxidant and ferroptosis-control pathways. Cognitive and memory improvements have been reported in several rodent models; these findings have not yet been validated in clinical AD trials.

Kaempferol in Alzheimer’s Disease

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Oxidative stress and NRF2 defense ↓ ROS/lipid oxidation; ↑ NRF2/HO-1 antioxidant signaling Neuronal protection One of the most consistently reported mechanisms across preclinical AD models.
2 Aβ pathology ↓ Aβ toxicity/deposition ↓ amyloid-associated neuronal injury Demonstrated in cellular and animal models; clinical relevance remains unknown.
3 Neuroinflammation ↓ inflammatory signaling ↓ neuronal inflammatory stress Likely overlaps with NF-κB and oxidative-stress modulation.
4 Neuronal ferroptosis ↓ Fe²⁺; ↓ lipid ROS; ↑ GPX4/SLC7A11/AKR1C3-associated defense ↓ ferroptotic neuronal death Emerging evidence; contrasts with pro-ferroptotic effects reported in certain cancer models.
5 Tau pathology ↓ phosphorylated Tau (model-dependent) ↓ neurodegenerative pathology Recent animal evidence; replication and human validation are required.
6 Acetylcholinesterase ↓ AChE (preclinical) Potential ↑ cholinergic signaling Evidence is substantially weaker than for approved AChE inhibitors and should not imply comparable clinical efficacy.
7 Cognition and memory ↑ learning; ↑ memory performance Functional neuroprotection Observed in several rodent models; no established human AD efficacy.


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






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






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






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
8087- KAE,    Therapeutic Importance of Kaempferol in the Treatment of Cancer through the Modulation of Cell Signalling Pathways
- Review, Var, NA
TumCCA↓, ROS↝, Apoptosis↑, TumCP↑, TumMeta↓, angioG↓, PI3K↓, EMT↓, Snail↓, E-cadherin↓, N-cadherin↓, MMP2↓, Casp9↑, Casp7↑, PARP↑, Apoptosis↑, *ROS↓, Hif1a↓, p‑Akt↓, P53↑, cMyc↓, Glycolysis↓, PKM2↓, miR-339-5p↝, 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:


NA, unassigned(tgid=0) ⓘ

miR-339-5p↝, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   Glycolysis↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 2,   Casp7↑, 1,   Casp9↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↓, 1,  

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

EMT↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↓, 1,   MMP2↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCP↑, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
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#:275  State#:%  Dir#:4
  wNotes=0  sortOrder:rid,rpid

 

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