tbResList Print — PEITC Phenethyl isothiocyanate

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Product

PEITC Phenethyl isothiocyanate
Description: <b>Phenethyl isothiocyanate (PEITC)</b> 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.<br>
Source: Derived from glucosinolates in cruciferous vegetables<br>
PEITC in plants exists mainly as the glucosinolate precursor (gluconasturtiin). Upon tissue disruption (chewing, chopping), myrosinase converts gluconasturtiin → PEITC.
<br>
<pre>
-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 |


</pre>
<br>






<table>
<tr>
<th>Rank</th>
<th>Pathway / Target Axis</th>
<th>Direction</th>
<th>Primary Effect</th>
<th>Notes / Cancer Relevance</th>
<th>Ref</th>
</tr>

<tr>
<td>1</td>
<td>GSH / thiol buffering (PEITC–GSH conjugation → GSH depletion)</td>
<td>↓ GSH</td>
<td>Upstream redox collapse</td>
<td>PEITC drives a GSH-iron-ROS axis; GSH depletion is upstream of multiple death programs</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7468252/">(ref)</a></td>
</tr>

<tr>
<td>2</td>
<td>ROS accumulation</td>
<td>↑ ROS</td>
<td>Oxidative stress trigger</td>
<td>PEITC increases intracellular ROS, which then drives mitochondrial disruption and apoptosis</td>
<td><a href="https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2021.673103/full">(ref)</a></td>
</tr>

<tr>
<td>3</td>
<td>Ferroptosis (lipid peroxidation; anti-ferroptotic machinery overwhelmed)</td>
<td>↑ ferroptosis</td>
<td>Iron-dependent oxidative death</td>
<td>Direct evidence that PEITC induces ferroptosis (alongside other death programs) via GSH-iron-ROS mechanisms</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7468252/">(ref)</a></td>
</tr>

<tr>
<td>4</td>
<td>Mitochondrial integrity (ΔΨm; cytochrome-c release)</td>
<td>↓ ΔΨm / ↑ cytochrome-c release</td>
<td>Mitochondrial dysfunction</td>
<td>PEITC promotes ROS, decreases ΔΨm, increases cytochrome-c release in cancer cells</td>
<td><a href="https://onlinelibrary.wiley.com/doi/10.1155/2012/718320">(ref)</a></td>
</tr>

<tr>
<td>5</td>
<td>Intrinsic apoptosis (caspase-9 → caspase-3)</td>
<td>↑ caspase activation / ↑ apoptosis</td>
<td>Execution-phase cell death</td>
<td>PEITC activates caspase-9 and caspase-3 and induces apoptosis downstream of mitochondrial dysfunction</td>
<td><a href="https://onlinelibrary.wiley.com/doi/10.1155/2012/718320">(ref)</a></td>
</tr>

<tr>
<td>6</td>
<td>Akt → JNK → Mcl-1 axis</td>
<td>↓ Akt / ↑ JNK / ↓ Mcl-1</td>
<td>Pro-survival signaling collapse</td>
<td>Leukemia study: PEITC-initiated death is linked to Akt inactivation → JNK activation → Mcl-1 downregulation</td>
<td><a href="https://www.nature.com/articles/cddis201122">(ref)</a></td>
</tr>

<tr>
<td>7</td>
<td>NF-κB signaling</td>
<td>↓ NF-κB transcriptional activity / ↓ p65 nuclear translocation</td>
<td>Reduced pro-survival / inflammatory transcription</td>
<td>PEITC inhibits NF-κB activity and NF-κB–regulated genes (e.g., cyclin D1, VEGF, Bcl-xL) in prostate cancer cells</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/15856023/">(ref)</a></td>
</tr>

<tr>
<td>8</td>
<td>JAK–STAT3 signaling</td>
<td>↓ STAT3 activation</td>
<td>Reduced survival / growth signaling</td>
<td>PEITC inhibits IL-6–driven JAK–STAT3 activation in prostate cancer cells (STAT3 signaling direction shown)</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3964815/">(ref)</a></td>
</tr>

<tr>
<td>9</td>
<td>Cell-cycle regulation</td>
<td>↑ G2/M arrest</td>
<td>Proliferation blockade</td>
<td>PEITC inhibits proliferation and induces G2/M cell-cycle arrest in prostate cancer cells</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3964815/">(ref)</a></td>
</tr>

<tr>
<td>10</td>
<td>Autophagy program</td>
<td>↑ autophagy</td>
<td>Stress response (can interact with death)</td>
<td>PEITC induces autophagy along with ferroptosis and apoptosis in osteosarcoma cells</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7468252/">(ref)</a></td>
</tr>

<tr>
<td>11</td>
<td>Migration / invasion (MMPs, FAK, RhoA)</td>
<td>↓ migration &amp; invasion / ↓ MMPs</td>
<td>Anti-metastatic phenotype</td>
<td>PEITC suppresses migration/invasion and downregulates MMP-2/-7/-9 and motility regulators (FAK, RhoA)</td>
<td><a href="https://ar.iiarjournals.org/content/30/6/2135">(ref)</a></td>
</tr>

<tr>
<td>12</td>
<td>In vivo anti-tumor effect</td>
<td>↓ tumor burden / ↑ survival (model-dependent)</td>
<td>Demonstrated efficacy in animal model</td>
<td>Leukemia study reports PEITC anti-leukemic activity including mechanistic signaling changes and in vivo efficacy evidence</td>
<td><a href="https://www.nature.com/articles/cddis201122">(ref)</a></td>
</tr>

</table>

Pathway results for Effect on Cancer / Diseased Cells

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP1A1↑, 1,   CYP2E1↑, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 14,   GSH/GSSG↓, 1,   GSSG↓, 1,   GSTA1↓, 1,   GSTP1/GSTπ↑, 1,   H2O2↑, 1,   Iron↑, 1,   lipid-P↑, 2,   MDA↑, 1,   NQO1↑, 2,   Nrf1↑, 1,   p‑NRF2↑, 1,   NRF2↑, 2,   NRF2↓, 1,   OXPHOS↓, 1,   ROS↑, 24,   ROS↓, 1,   mt-ROS↑, 1,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 4,   ATP↓, 2,   CDC25↓, 2,   EGF↓, 1,   ETC↓, 1,   mitResp↓, 1,   MKK7↓, 1,   MMP↓, 8,   mtDam↑, 3,   OCR↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cAMP↓, 1,   cMyc↓, 2,   CYP3A4↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 7,   Apoptosis↑, 22,   Apoptosis↓, 1,   BAX↑, 7,   Bcl-2↓, 5,   Bcl-xL↓, 2,   cl‑BID↑, 1,   BID↑, 3,   BMP2↓, 1,   Casp↑, 1,   Casp3↑, 7,   Casp8↑, 3,   Casp9↑, 5,   Chk2↑, 1,   Cyt‑c↑, 8,   Cyt‑c↝, 1,   Diablo↑, 1,   DR4↑, 4,   DR5↑, 3,   Fas↑, 1,   Ferroptosis↑, 2,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 2,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 3,   p27↑, 1,   p38↑, 1,   survivin↓, 2,   Telomerase↓, 1,   TumCD↑, 4,   TumCD↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   other↝, 2,   TLE1↓, 1,   tumCV↓, 9,  

Protein Folding & ER Stress ⓘ

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

Autophagy & Lysosomes ⓘ

TumAuto↑, 4,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 3,   P53↓, 1,   P53↑, 8,   cl‑PARP↑, 4,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 5,   TumCCA↑, 18,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 4,   BMI1↓, 1,   CD133↓, 1,   CD24↓, 2,   CD34↓, 1,   CD44↓, 3,   CSCs↓, 10,   CSCsMark↓, 2,   EMT↓, 2,   ERK↓, 3,   HDAC↓, 2,   miR-194↑, 1,   mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   RAS↓, 1,   SAL↑, 1,   SOX2↓, 1,   STAT3↓, 3,   SUZ12↓, 1,   TumCG↓, 17,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 3,   CD11b↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   FTO↓, 1,   ITGB1↓, 1,   ITGB6↓, 1,   Ki-67↓, 2,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 1,   N-cadherin↓, 1,   PKCδ↓, 2,   PKCδ↑, 1,   Rho↓, 1,   Slug↓, 1,   Smad1↓, 1,   Smad1↑, 1,   Snail↓, 1,   TGF-β1↓, 1,   TumCI↓, 4,   TumCMig↓, 6,   TumCP↓, 14,   TumMeta↓, 5,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   α-tubulin↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 1,   Hif1a↓, 5,   NO↑, 2,   VEGF↓, 4,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↓, 1,   COX2↓, 3,   IKKα↓, 1,   Inflam↓, 2,   JAK↓, 1,   p‑JAK2↓, 1,   NF-kB↓, 8,   p65↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,   ERα/ESR1↓, 1,  

Drug Metabolism & Resistance ⓘ

ABC↓, 1,   BioAv↝, 1,   BioAv↑, 2,   ChemoSen↑, 8,   CYP1A2↑, 1,   CYP2A3/CYP2A6↓, 1,   Dose↓, 1,   Dose↝, 5,   Dose⇅, 1,   eff↑, 6,   eff↓, 11,   Half-Life↓, 1,   P450↓, 1,   selectivity↑, 11,  

Clinical Biomarkers ⓘ

ALC∅, 1,   AR↓, 1,   EGFR↓, 1,   ERα/ESR1↓, 1,   EZH2↓, 1,   HER2/EBBR2↓, 1,   Ki-67↓, 2,   SUZ12↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 6,   AntiCan↓, 1,   chemoP↑, 1,   chemoPv↑, 5,   OS↑, 4,   QoL↑, 1,   Risk↓, 5,   toxicity↓, 1,   TumW↓, 1,   Weight↑, 1,  
Total Targets: 200

Pathway results for Effect on Normal Cells

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP2E1↓, 1,   GPx1↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 6,   Dose↝, 3,   Half-Life↝, 1,   P450↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 2,   Risk↑, 1,   toxicity↝, 2,   toxicity↓, 1,   Weight↓, 1,  
Total Targets: 20

Research papers

Year Title Authors PMID Link Flag
2025Natural compound PEITC inhibits gain of function of p53 mutants in cancer cells by switching YAP-binding partners between p53 and p73Yi-xuan Wang—https://www.nature.com/articles/s41401-025-01474-10
2025PEITC restores chemosensitivity in cisplatin-resistant non-small cell lung cancer by targeting c-Myc/miR-424-5pHao Ding—https://link.springer.com/article/10.1007/s12672-025-03824-10
2025Phenethyl Isothiocyanate (PEITC) interaction with Keap1 activates the Nrf2 pathway and inhibits lipid accumulation in adipocytesHae-Sun Ko—https://www.sciencedirect.com/science/article/abs/pii/S09552863250012630
2025Targeting ferroptosis in osteosarcoma—https://www.sciencedirect.com/topics/medicine-and-dentistry/phenethyl-isothiocyanate0
2024Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosisXiaoshu Dong—https://www.nature.com/articles/s41420-024-02225-70
2024Nutritional Sources and Anticancer Potential of Phenethyl Isothiocyanate: Molecular Mechanisms and Therapeutic InsightsShahira M Ezzat38600885https://pubmed.ncbi.nlm.nih.gov/38600885/0
2024Targeted anti-cancer therapy: Co-delivery of VEGF siRNA and Phenethyl isothiocyanate (PEITC) via cRGD-modified lipid nanoparticles for enhanced anti-angiogenic efficacyBao Li—https://www.sciencedirect.com/science/article/pii/S18180876240000840
2023The Potential Use of Phenethyl Isothiocyanate for Cancer PreventionTsu-Hsiang Kuo—https://www.researchgate.net/publication/371564440_The_Potential_Use_of_Phenethyl_Isothiocyanate_for_Cancer_Prevention0
2023Targeting Breast Cancer Stem CellsLu ZhangPMC9830502https://pmc.ncbi.nlm.nih.gov/articles/PMC9830502/0
2023Nutri-PEITC Jelly Significantly Improves Progression-Free Survival and Quality of Life in Patients with Advanced Oral and Oropharyngeal Cancer: A Blinded Randomized Placebo-Controlled TrialAroonwan Lam-Ubol—https://www.mdpi.com/1422-0067/24/9/78240
2023Phenethyl isothiocyanate inhibits metastasis potential of non-small cell lung cancer cells through FTO mediated TLE1 m6A modificationQi-cheng Zhang—https://www.nature.com/articles/s41401-023-01178-40
2022PEITC: A resounding molecule averts metastasis in breast cancer cells in vitro by regulating PKCδ/Aurora A interplaySouvick BiswasPMC9706142https://pmc.ncbi.nlm.nih.gov/articles/PMC9706142/0
2021Cancer-preventive effect of phenethyl isothiocyanate through tumor microenvironment regulation in a colorectal cancer stem cell xenograft modelJi Min Shin33626429https://pubmed.ncbi.nlm.nih.gov/33626429/0
2021Cancer-preventive effect of phenethyl isothiocyanate through tumor microenvironment regulation in a colorectal cancer stem cell xenograft modelJi Min Shin—https://www.sciencedirect.com/science/article/abs/pii/S09447113210003500
2021Phenethyl Isothiocyanate Induces Apoptosis Through ROS Generation and Caspase-3 Activation in Cervical Cancer CellsShoaib Shoaib—https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2021.673103/full0
2020Combination of xanthohumol and phenethyl isothiocyanate inhibits NF-κB and activates Nrf2 in pancreatic cancer cellsVioletta Krajka-Kuźniak—https://www.sciencedirect.com/science/article/abs/pii/S088723331930949X0
2020PEITC: Functional Compound for Primary and Tertiary Chemoprevention of CancerDunyaporn Trachootham's Lab—https://www.researchgate.net/publication/338449539_PEITC_Functional_Compound_for_Primary_and_Tertiary_Chemoprevention_of_Cancer0
2020PEITC inhibits the invasion and migration of colorectal cancer cells by blocking TGF-β-induced EMTJian Xiao—https://www.sciencedirect.com/science/article/pii/S07533322203093670
2020PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cellsHuan-huan Lv—https://www.nature.com/articles/s41401-020-0376-80
2019Phenethyl isothiocyanate hampers growth and progression of HER2-positive breast and ovarian carcinoma by targeting their stem cell compartmentAda Koschorke31376137https://pubmed.ncbi.nlm.nih.gov/31376137/0
2019Phenethyl Isothiocyanate Exposure Promotes Oxidative Stress and Suppresses Sp1 Transcription Factor in Cancer Stem CellsBijaya UpadhyayaPMC6429440https://pmc.ncbi.nlm.nih.gov/articles/PMC6429440/0
2018Sensory Acceptable Equivalent Doses of β - Phenylethyl isothiocyanate (PEITC) Induce Cell Cycle Arrest and Retard Growth of p53 Mutated Oral Cancer In Vitro and In VivoAroonwan Lam-ubol—https://www.researchgate.net/publication/325705484_Sensory_Acceptable_Equivalent_Doses_of_b_-_Phenylethyl_isothiocyanate_PEITC_Induce_Cell_Cycle_Arrest_and_Retard_Growth_of_p53_Mutated_Oral_Cancer_In_Vitro_and_In_Vivo0
2018Sensory 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 vivoAroonwan Lam-ubo—https://pubs.rsc.org/en/content/articlelanding/2018/fo/c8fo00865e0
2017Phenethyl isothiocyanate (PEITC) suppresses prostate cancer cell invasion epigenetically through regulating microRNA-194Chengyue ZhangPMC5495185https://pmc.ncbi.nlm.nih.gov/articles/PMC5495185/0
2017Phenethyl isothiocyanate suppresses cancer stem cell properties in vitro and in a xenograft modelJi Ho Yun—https://www.sciencedirect.com/science/article/abs/pii/S09447113173003140
2017Inhibition of cancer growth in vitro and in vivo by a novel ROS-modulating agent with ability to eliminate stem-like cancer cellsJiankang WangPMC5520927https://pmc.ncbi.nlm.nih.gov/articles/PMC5520927/0
2017Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasersJung Eun ParkPMC5228035https://pmc.ncbi.nlm.nih.gov/articles/PMC5228035/0
2016Clinical Trial of 2-Phenethyl Isothiocyanate as an Inhibitor of Metabolic Activation of a Tobacco-Specific Lung Carcinogen in Cigarette SmokersJian-Min Yuan—https://aacrjournals.org/cancerpreventionresearch/article/9/5/396/50523/Clinical-Trial-of-2-Phenethyl-Isothiocyanate-as-an0
2016Irreversible Inhibition of Glutathione S-Transferase by Phenethyl Isothiocyanate (PEITC), a Dietary Cancer Chemopreventive PhytochemicalVandana Kumari—https://journals.plos.org/plosone/article?id=10.1371/journal.pone.01638210
2015Phenethyl Isothiocyanate (PEITC) from Cruciferous Vegetables Targets Human Cancer Stem-Like CellsBijaya Upadhyaya—https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.29.1_supplement.130.30
2015ROS accumulation by PEITC selectively kills ovarian cancer cells via UPR-mediated apoptosisYoon-Hee Hong—https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2015.00167/full0
2015PEITC treatment suppresses myeloid derived tumor suppressor cells to inhibit breast tumor growthParul GuptaPMC4404818https://pmc.ncbi.nlm.nih.gov/articles/PMC4404818/0
2014Phenethyl isothiocyanate and paclitaxel synergistically enhanced apoptosis and alpha-tubulin hyperacetylation in breast cancer cellsShundong CangPMC3927854https://pmc.ncbi.nlm.nih.gov/articles/PMC3927854/0
2014Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutationsYao-Tsung Yeh—https://www.sciencedirect.com/science/article/abs/pii/S08915849140026030
2014Phenethyl Isothiocyanate: A comprehensive review of anti-cancer mechanismsParul GuptaPMC4260992https://pmc.ncbi.nlm.nih.gov/articles/PMC4260992/0
2014Pharmacokinetics and Pharmacodynamics of Phenethyl Isothiocyanate: Implications in Breast Cancer PreventionMarilyn E. Morris—https://link.springer.com/article/10.1208/s12248-014-9610-y0
2014Phenethyl isothiocyanate upregulates death receptors 4 and 5 and inhibits proliferation in human cancer stem-like cellsDan WangPMC4148558https://pmc.ncbi.nlm.nih.gov/articles/PMC4148558/0
2013Phenethyl Isothiocyanate Suppresses Inhibitor of Apoptosis Family Protein Expression in Prostate Cancer Cells in Culture and In VivoKozue SakaoPMC3310272https://pmc.ncbi.nlm.nih.gov/articles/PMC3310272/0
2012Phenethyl isothiocyanate-induced cytoskeletal changes and cell death in lung cancer cellsAndrzej Pawlik—https://www.sciencedirect.com/science/article/abs/pii/S02786915120052120
2012Phenethyl 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 DeathPo-Yuan ChenPMC3418800https://pmc.ncbi.nlm.nih.gov/articles/PMC3418800/0
2012Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agentSharifah S Syed AlwiPMC3535168https://pmc.ncbi.nlm.nih.gov/articles/PMC3535168/0
2012Phenethyl 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 DeathPo-Yuan ChenPMC3418800https://pmc.ncbi.nlm.nih.gov/articles/PMC3418800/0
2012Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1   Phase Arrest and Mitochondria-Mediated Apoptotic Cell DeathPo-Yuan Chen—https://onlinelibrary.wiley.com/doi/10.1155/2012/7183200
2011Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathwaysN Gao—https://www.nature.com/articles/cddis2011220
2011Phenethyl 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 cellsNou-Ying Tang21617228https://pubmed.ncbi.nlm.nih.gov/21617228/0
2010Phenethyl Isothiocyanate Inhibits Migration and Invasion of Human Gastric Cancer AGS Cells through Suppressing MAPK and NF-κB Signal PathwaysMEI-DUE YANG—https://ar.iiarjournals.org/content/30/6/21350
2010Phenethyl Isothiocyanate Inhibits Oxidative Phosphorylation to Trigger Reactive Oxygen Species-mediated Death of Human Prostate Cancer CellsDong Xiao—https://www.jbc.org/article/S0021-9258(20)59619-1/fulltext0
2009Phenethyl Isothiocyanate inhibits STAT3 activation in prostate cancer cellsAiyu GongPMC3964815https://pmc.ncbi.nlm.nih.gov/articles/PMC3964815/0
2007PEITC: a natural compound effective in killing primary leukemia cells and overcoming drug resistanceDunyaporn Trachootham—https://aacrjournals.org/cancerres/article/67/9_Supplement/1842/539877/PEITC-a-natural-compound-effective-in-killing0
2007Phenethyl Isothiocyanate Inhibits Angiogenesis In vitro and Ex vivoDong Xiao—https://aacrjournals.org/cancerres/article/67/5/2239/534088/Phenethyl-Isothiocyanate-Inhibits-Angiogenesis-In0
2006Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanateDunyaporn Trachootham—https://www.cell.com/cancer-cell/fulltext/S1535-6108(06)00250-90
2006Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potentialDong Xiao—https://academic.oup.com/carcin/article-abstract/27/11/2223/2391866?redirectedFrom=fulltext&login=false0
2006Phenethyl isothiocyanate (PEITC) inhibits growth of ovarian cancer cells by inducing apoptosis: role of caspase and MAPK activationK S Satyan16624391https://pubmed.ncbi.nlm.nih.gov/16624391/0
2005Suppression of NF-kappaB and NF-kappaB-regulated gene expression by sulforaphane and PEITC through IkappaBalpha, IKK pathway in human prostate cancer PC-3 cellsChangjiang Xu15856023https://pubmed.ncbi.nlm.nih.gov/15856023/0
2001Inhibition and Inactivation of Human Cytochrome P450 Isoforms by Phenethyl IsothiocyanateMiki Nakajima—https://dmd.aspetjournals.org/article/S0090-9556(24)04273-9/abstract0
2021Comparison 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 VivoMarta Cykowiak—https://www.mdpi.com/2072-6643/13/9/30000