Phenethyl isothiocyanate Cancer Research Results

PEITC, Phenethyl isothiocyanate: Click to Expand ⟱
Features:
Phenethyl isothiocyanate (PEITC) is a naturally occurring small-molecule phytochemical best known for its role in cancer chemoprevention research. It belongs to the isothiocyanate class of organosulfur compounds and has the chemical formula C₉H₉NS.
Source: Derived from glucosinolates in cruciferous vegetables
PEITC in plants exists mainly as the glucosinolate precursor (gluconasturtiin). Upon tissue disruption (chewing, chopping), myrosinase converts gluconasturtiin → PEITC.
-PEITC bioavailability from fresh, chopped microgreens is high
-Co-consumption with other isothiocyanates is additive/synergistic
-Peak plasma levels: ~1–3 hours post-consumption
-Half-life: ~4–6 hours
-Generally well tolerated up to 40 mg/day (mild GI irritation at higher dose)

PEITC is best characterized for its dual role in xenobiotic metabolism:
Inhibition of Phase I enzymes
-Suppresses cytochrome P450 enzymes (e.g., CYP1A1, CYP2E1)
-Reduces activation of pro-carcinogens

-Selectively depletes GSH in cancer cells
-Directly increases ROS beyond buffering capacity

Key pathways in cancer cells
-GSH depletion
-Mitochondrial ROS amplification
-ASK1/JNK apoptosis

Chemo relevance
-Frequently chemo-sensitizing
-Opposite of NAC/GSH

Induction of Phase II enzymes
-Activates NRF2–KEAP1 signaling
-Increases expression of detoxification and antioxidant enzymes such as:
 -Glutathione S-transferases (GSTs)
 -NAD(P)H quinone oxidoreductase 1 (NQO1)
 -Heme oxygenase-1 (HMOX1)

In preclinical systems, PEITC has been shown to:
-Deplete intracellular glutathione (GSH), increasing oxidative stress in cancer cells
-Induce mitochondrial dysfunction and apoptosis
-Inhibit histone deacetylases (HDACs) (context-dependent)
-Suppress pro-survival signaling pathways (e.g., STAT3, NF-κB)
-Target cancer stem–like cells in some models

Dietary origins

PEITC present in vegetables such as:
-Watercress (the richest source)
-Broccoli
-Cabbage
-Brussels sprouts
-Radish

Bioavailability depends on:
-Food preparation
-Gut microbiota (myrosinase activity if plant enzyme is inactive)

watercress microgreens generally have higher PEITC (and/or its precursor gluconasturtiin) per gram than mature watercress.
-The enrichment is most pronounced per unit fresh weight in the 7–14 day window.
-Absolute values vary substantially with cultivar, light intensity, sulfur/nitrogen nutrition, and post-harvest handling.
| Growth stage    |      Age | PEITC potential (mg / 100 g FW) |         Relative |
| --------------- | -------: | ------------------------------: | ---------------: |
| **Microgreens** |   7–10 d |                     **3.0–6.0** | **~2–4×** mature |
| **Microgreens** |  11–14 d |                     **2.5–5.0** |            ~2–3× |
| Baby leaf       |  21–28 d |                         1.5–3.0 |            ~1–2× |
| Mature leaf     | 35–45+ d |                         0.8–1.5 |         baseline |

Dry weight basis
| Growth stage          | PEITC potential (mg / g DW) |
| --------------------- | --------------------------: |
| Microgreens (7–10 d)  |                 **1.8–3.5** |
| Microgreens (11–14 d) |                     1.5–3.0 |
| Mature leaf           |                     0.6–1.2 |

Expect 2–5× variability depending on:
-Light spectrum (blue light ↑ glucosinolates)
-Sulfur availability

Practical optimization tips
Lighting
-12–16 h/day
-150–300 µmol/m²/s PAR (typical shop LEDs at 20–30 cm distance)
Soil
-Peat or peat-blend preferred
-Avoid over-watering (dilutes concentration)
Nutrition (optional but effective)
-One light watering with ¼-strength sulfate-containing fertilizer around day 4–5 can increase PEITC ~15–30%
Harvest & use
-Cut, rest 5–10 minutes, then consume (allows myrosinase to fully convert gluconasturtiin → PEITC)

Dose: (100 g fresh microgreens ≈ 2–4 mg bioavailable PEITC)
-ie below doses are not really acheivable from fresh microgreens
Minimum biologically active dose (humans): ~10–15 mg PEITC/day
Common efficacy range used in human trials: 20–40 mg/day
Upper short-term doses studied (generally tolerated): 60 mg/day
Diet-achievable with watercress microgreens: Yes, at realistic portions
These doses are chemopreventive / pathway-modulating, not cytotoxic chemotherapy.
| PEITC dose (mg/day) | Dominant biological effects                     |
| ------------------: | ----------------------------------------------- |
|         **5–10 mg** | Phase II enzymes, mild NRF2                     |
|        **10–20 mg** | HDAC inhibition, ROS signaling                  |
|        **20–40 mg** | Apoptosis, cell-cycle arrest, anti-inflammatory |
|        **40–60 mg** | Strong redox stress in cancer cells             |
|              >60 mg | Limited data; GI irritation risk                |



Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 GSH / thiol buffering (PEITC–GSH conjugation → GSH depletion) ↓ GSH Upstream redox collapse PEITC drives a GSH-iron-ROS axis; GSH depletion is upstream of multiple death programs (ref)
2 ROS accumulation ↑ ROS Oxidative stress trigger PEITC increases intracellular ROS, which then drives mitochondrial disruption and apoptosis (ref)
3 Ferroptosis (lipid peroxidation; anti-ferroptotic machinery overwhelmed) ↑ ferroptosis Iron-dependent oxidative death Direct evidence that PEITC induces ferroptosis (alongside other death programs) via GSH-iron-ROS mechanisms (ref)
4 Mitochondrial integrity (ΔΨm; cytochrome-c release) ↓ ΔΨm / ↑ cytochrome-c release Mitochondrial dysfunction PEITC promotes ROS, decreases ΔΨm, increases cytochrome-c release in cancer cells (ref)
5 Intrinsic apoptosis (caspase-9 → caspase-3) ↑ caspase activation / ↑ apoptosis Execution-phase cell death PEITC activates caspase-9 and caspase-3 and induces apoptosis downstream of mitochondrial dysfunction (ref)
6 Akt → JNK → Mcl-1 axis ↓ Akt / ↑ JNK / ↓ Mcl-1 Pro-survival signaling collapse Leukemia study: PEITC-initiated death is linked to Akt inactivation → JNK activation → Mcl-1 downregulation (ref)
7 NF-κB signaling ↓ NF-κB transcriptional activity / ↓ p65 nuclear translocation Reduced pro-survival / inflammatory transcription PEITC inhibits NF-κB activity and NF-κB–regulated genes (e.g., cyclin D1, VEGF, Bcl-xL) in prostate cancer cells (ref)
8 JAK–STAT3 signaling ↓ STAT3 activation Reduced survival / growth signaling PEITC inhibits IL-6–driven JAK–STAT3 activation in prostate cancer cells (STAT3 signaling direction shown) (ref)
9 Cell-cycle regulation ↑ G2/M arrest Proliferation blockade PEITC inhibits proliferation and induces G2/M cell-cycle arrest in prostate cancer cells (ref)
10 Autophagy program ↑ autophagy Stress response (can interact with death) PEITC induces autophagy along with ferroptosis and apoptosis in osteosarcoma cells (ref)
11 Migration / invasion (MMPs, FAK, RhoA) ↓ migration & invasion / ↓ MMPs Anti-metastatic phenotype PEITC suppresses migration/invasion and downregulates MMP-2/-7/-9 and motility regulators (FAK, RhoA) (ref)
12 In vivo anti-tumor effect ↓ tumor burden / ↑ survival (model-dependent) Demonstrated efficacy in animal model Leukemia study reports PEITC anti-leukemic activity including mechanistic signaling changes and in vivo efficacy evidence (ref)


Scientific Papers found: Click to Expand⟱
4950- PEITC,    Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential
- vitro+vivo, Pca, PC3
MMP↓, Cyt‑c↑, Smad1↑, Diablo↑, ROS↑,
4936- PEITC,    PEITC treatment suppresses myeloid derived tumor suppressor cells to inhibit breast tumor growth
- in-vivo, BC, MDA-MB-231
TumCG↓, CD34↓, CD11b↓, CSCs↓, ALC∅, CD4+↓, NF-kB↓, STAT3↓, Hif1a↓,
4937- PEITC,    PEITC: Functional Compound for Primary and Tertiary Chemoprevention of Cancer
- Review, Var, NA
chemoPv↑, tumCV↓, GSH↓, ROS↑, *toxicity↝,
4938- PEITC,    Clinical Trial of 2-Phenethyl Isothiocyanate as an Inhibitor of Metabolic Activation of a Tobacco-Specific Lung Carcinogen in Cigarette Smokers
- Trial, Nor, NA
*Risk↑, *P450↓, *BioAv↑, *BioAv↑, *BioAv↑, *Dose↝, Dose↝,
4939- PEITC,    Phenethyl Isothiocyanate Inhibits Angiogenesis In vitro and Ex vivo
- in-vitro, Pca, PC3 - ex-vivo, Nor, HUVECs
Risk↓, angioG↓, VEGF↓, TumCMig↓, Akt↓, EGF↓, TumCMig↓,
4940- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G 0/G 1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
TumCCA↑, Apoptosis↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, tumCV↓, ROS↑, Ca+2↑, CDC25↓, CDK6↓, cycD1/CCND1↓, CDK2↓, cycE/CCNE↓, P53↑, p27/CDKN1B↑, P21↑, Casp9↑, Casp3↑, GRP78/BiP↑,
4941- PEITC,    PEITC: A resounding molecule averts metastasis in breast cancer cells in vitro by regulating PKCδ/Aurora A interplay
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
PKCδ↑, Apoptosis↓, selectivity↑, tumCV↓, p‑NRF2↑, cl‑PARP1↑, TumCMig↓, ROS↓, Hif1a↓,
4942- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G(0)/G(1) Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
chemoPv↑, TumCG↓, TumCCA↑, Apoptosis↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑,
4943- PEITC,    Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activation
- in-vitro, Ovarian, OVCAR-3
TumCD↑, TumCP↓, Apoptosis↑, Casp3↑, Casp9↑, Bcl-2↓, BAX↑, Akt↓, ERK↓, cMyc↓, p38↑, JNK↑, eff↓,
4944- PEITC,    Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations
- in-vitro, Oral, NA
TumCG↓, TumCCA↑, Apoptosis↑, ROS↑, NO↑, GSH↓, MMP↓, DNAdam↑, ATM↑, Chk2↑, P53↑, eff↓,
4945- PEITC,    Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells
- in-vitro, Pca, DU145
AntiCan↑, TumCG↓, Apoptosis↑, tumCV↓, TumCCA↑, DNAdam↑, P53↑, CDC25↓, Casp9↑, Casp8↑, mtDam↑, Cyt‑c↑,
4946- PEITC,    Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑, TumAuto↑, ROS↑, OXPHOS↓, ATP↓, selectivity↑, ETC↓, eff↓, eff↓, BAX↑,
4947- PEITC,    Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1   Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- in-vitro, Oral, HSC3
AntiCan↑, chemoPv↑, TumCG↓, Apoptosis↑, TumCCA↑, P53↑, P21↑, BAX↑, BID↑, Bcl-2↓, MMP↓, Cyt‑c↑, AIF↑, ROS↑, Ca+2↑,
4948- PEITC,    Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo
- vitro+vivo, Oral, CAL27 - vitro+vivo, Oral, FaDu - vitro+vivo, Oral, SCC4 - vitro+vivo, Oral, SCC9
TumCD↑, TumCG↓, OS↑, ROS↑, P53↑, P21↑, TumCCA↑, Ki-67↓,
4949- PEITC,    Phenethyl Isothiocyanate Exposure Promotes Oxidative Stress and Suppresses Sp1 Transcription Factor in Cancer Stem Cells
- in-vitro, Cerv, HeLa
ROS↑, selectivity↑, CSCs↓, Sp1/3/4↓, P-gp/ABCB1↓, ALDH↓, GSH↓, TumCP↓, Apoptosis↑,
5015- Xan,  PEITC,    Comparison of the Impact of Xanthohumol and Phenethyl Isothiocyanate and Their Combination on Nrf2 and NF-κB Pathways in HepG2 Cells In Vitro and Tumor Burden In Vivo
- in-vitro, HCC, HepG2
NRF2↓, ROS↑, NF-kB↓, COX2/PTGS2↓, Apoptosis↑, NRF2↑, SOD↑, NQO1↑,

Showing Research Papers: 51 to 66 of 66
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 66

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   ARE↑, 1,   GPx↓, 1,   GPx4↓, 2,   GSH↓, 16,   GSH/GSSG↓, 1,   GSSG↓, 1,   H2O2↑, 1,   HO-1↑, 1,   Iron↑, 2,   lipid-P↑, 3,   MDA↑, 2,   NQO1↑, 2,   Nrf1↑, 1,   NRF2↓, 1,   NRF2↑, 4,   p‑NRF2↑, 1,   ROS↓, 2,   ROS↑, 30,   mt-ROS↑, 1,   SOD↑, 2,   Trx↑, 2,   TrxR↑, 1,   TrxR1↑, 1,   xCT/SLC7A11↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 4,   compI↓, 1,   compIII↓, 3,   compIV↓, 1,   EGF↓, 1,   ETC↓, 2,   mitResp↓, 1,   MKK7↓, 1,   mtDam↑, 4,   OCR↓, 2,   OXPHOS↓, 2,   SDH↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATP↓, 2,   cAMP↓, 1,   Glycolysis↓, 1,   PDK1 / PDPK1↓, 1,  

Cell Death(tgid=5) ⓘ

AIF↑, 5,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 25,   BAX↑, 7,   Bcl-2↓, 6,   Bcl-xL↓, 3,   BID↑, 3,   cl‑BID↑, 1,   BIM↑, 1,   Casp↑, 2,   Casp3↑, 8,   Casp8↑, 4,   Casp9↑, 6,   Cyt‑c↑, 9,   Cyt‑c↝, 1,   Diablo↑, 1,   DR5↑, 3,   Fas↑, 1,   Ferroptosis↑, 3,   iNOS↓, 2,   Mcl-1↓, 3,   p38↓, 1,   p38↑, 1,   survivin↓, 3,   TumCD↓, 1,   TumCD↑, 5,   XIAP↓, 4,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 9,   p‑Akt↓, 1,   EGFR↓, 2,   ERK↓, 3,   HER2/EBBR2↓, 2,   IKKα↓, 1,   JAK↓, 1,   JAK2↓, 1,   p‑JAK2↓, 1,   JNK↓, 1,   JNK↑, 2,   MAPK↓, 1,   MAPK↑, 1,   mTOR↓, 4,   PI3K↓, 2,   PKCδ↓, 2,   PKCδ↑, 1,   PTEN↑, 1,   RAS↓, 1,   Sp1/3/4↓, 1,   STAT3↓, 6,  

Transcription & Epigenetics(tgid=7) ⓘ

cMyc↓, 3,   DNMTs↓, 1,   EZH2↓, 1,   FOXO1↓, 1,   FOXO3↓, 1,   HDAC↓, 5,   HDAC3↓, 1,   HDAC6↓, 1,   miR-194↑, 1,   OCT4↓, 2,   other↝, 2,   SOX2↓, 2,   SUZ12↓, 1,   TLE1↓, 1,   tumCV↓, 9,  

Protein Folding & ER Stress(tgid=8) ⓘ

ATF6↑, 1,   CHOP/DDIT3↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 2,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 4,  

DNA Damage & Repair(tgid=10) ⓘ

8-oxo-dG↓, 1,   ATM↑, 1,   DNAdam↑, 4,   P53↓, 1,   P53↑, 9,   cl‑PARP↑, 4,   cl‑PARP1↑, 1,   Telomerase↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 3,   CDK2↓, 1,   CDK4↓, 1,   CDK6↓, 2,   Chk2↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 2,   Ki-67↓, 3,   P21↑, 6,   p27/CDKN1B↑, 2,   TumCCA↑, 24,   WEE1↑, 1,  

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

ALDH↓, 4,   BMI1↓, 1,   BMP2↓, 1,   CD133↓, 1,   CD24↓, 2,   CD34↓, 1,   CSCs↓, 13,   CSCsMark↓, 2,   Ki-67↓, 3,   Nanog↓, 2,   NOTCH↑, 1,   NOTCH2↑, 1,   SAL↑, 1,   STAT1↓, 1,   TumCG↓, 19,   TumCP↓, 17,  

Migration(tgid=13) ⓘ

AP-1↓, 2,   Ca+2↑, 4,   CD11b↓, 1,   E-cadherin↑, 2,   EMT↓, 4,   FAK↓, 1,   ITGB1↓, 1,   ITGB6↓, 1,   MMP2↓, 6,   MMP9↓, 5,   MMPs↓, 1,   N-cadherin↓, 1,   Rho↓, 1,   Slug↓, 1,   Smad1↓, 1,   Smad1↑, 1,   Snail↓, 2,   TGF-β↓, 1,   TGF-β1↓, 1,   TumCI↓, 5,   TumCMig↓, 6,   TumMeta↓, 6,   uPA↓, 1,   uPAR↓, 1,   Vim↓, 1,   Zeb1↓, 2,   ZEB2↓, 1,   α-tubulin↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 6,   CD31/PECAM-1↓, 1,   Hif1a↓, 6,   NO↑, 2,   VEGF↓, 5,  

Barriers & Transport(tgid=15) ⓘ

MMP↓, 10,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ALC∅, 1,   CD4+↓, 1,   CD44↓, 3,   COX2/PTGS2↓, 3,   CXCR4↓, 2,   DR4↑, 4,   IL6↓, 2,   Inflam↓, 4,   NF-kB↓, 11,   p65↓, 1,   PSA↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 2,   ERα/ESR1↓, 1,   SXR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABC↓, 1,   BioAv↑, 4,   BioAv↝, 1,   ChemoSen↑, 11,   CYP1A1↑, 1,   CYP1A2↑, 1,   CYP2A3/CYP2A6↓, 1,   CYP2E1↑, 1,   CYP3A4↓, 2,   Dose↓, 1,   Dose⇅, 1,   Dose↝, 5,   eff↓, 11,   eff↑, 3,   GSTA1↓, 1,   GSTP1/GSTπ↑, 1,   Half-Life↓, 1,   P-gp/ABCB1↓, 1,   P450↓, 2,   RadioS↑, 2,   selectivity↑, 13,   selectivity↝, 1,   Synergy↑, 12,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 2,   EGFR↓, 2,   ERα/ESR1↓, 1,   EZH2↓, 1,   HER2/EBBR2↓, 2,   IL6↓, 2,   Polyps↓, 1,   PSA↓, 1,   SUZ12↓, 1,   Tumccf↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1,   AntiCan↑, 7,   chemoP↑, 1,   chemoPv↑, 7,   FTO↓, 1,   OS↑, 4,   QoL↑, 1,   Risk↓, 8,   toxicity↓, 1,   TumW↓, 1,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 2,  

Ingredients & Constituents(tgid=25) ⓘ

Ingr?, 1,   Ingr↝, 1,  
Total Targets: 246

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   GPx1↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 1,   MPO↓, 1,   NQO1↑, 2,   NRF2↑, 3,   ROS↓, 2,   ROS↑, 1,   ROS⇅, 1,   SOD↑, 1,   SOD1↑, 1,   SOD2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

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

p‑4E-BP1↓, 1,   Diff↓, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD40↓, 1,   IL10↓, 1,   Inflam↓, 1,   IP-10/CXCL-10↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 8,   BioAv↝, 2,   CYP2E1↓, 1,   Dose↝, 3,   eff↑, 3,   Half-Life↝, 2,   P450↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 1,   chemoPv↑, 2,   cognitive↑, 1,   hepatoP↑, 1,   Risk↑, 1,   toxicity↓, 1,   toxicity↝, 3,   Weight↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiBio↑, 1,  
Total Targets: 44

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#:388  Target#:%  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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