Apigenin (mainly Parsley) Cancer Research Results

Api, Apigenin (mainly Parsley): Click to Expand ⟱
Features:

Apigenin — a plant-derived flavone (4′,5,7-trihydroxyflavone) abundant in parsley/celery/chamomile and other dietary sources, often abbreviated APG (or “Api” in some indexes). It is a small-molecule polyphenol classified as a dietary phytochemical/nutraceutical candidate with broad pleiotropic signaling effects in oncology models (cell-cycle control, apoptosis, inflammatory signaling, metabolic stress, and invasion/angiogenesis programs), but with important translation constraints driven by low aqueous solubility and extensive phase-II conjugation.

Primary mechanisms (ranked):

  1. Pleiotropic pro-apoptotic / cell-cycle checkpoint engagement (mitochondrial apoptosis, caspases; CDK/cyclin suppression; p53 context-dependent)
  2. PI3K–AKT–MAPK signaling suppression with downstream anti-proliferative and anti-migration effects
  3. Inflammation axis suppression (NF-κB; COX-2 and pro-inflammatory cytokine programs)
  4. Redox stress reprogramming (often ROS↑ in cancer models; antioxidant/NRF2 effects are context-dependent and can diverge between cancer vs normal cells)
  5. HIF-1α–glycolysis downshift with ATP stress (model-dependent)
  6. Anti-invasive / anti-EMT programs (FAK/integrins; MMP/uPA; EMT markers)
  7. Epigenetic modulation (HDAC/DNMT/EZH2 axes; context-dependent)
  8. Anti-angiogenic signaling (VEGF/related programs; model-dependent)
  9. Stemness pathway pressure (Hh/GLI, CK2; model-dependent)
  10. Chemo-/death-ligand sensitization (e.g., TRAIL sensitization reported in preclinical systems)

Bioavailability / PK relevance: Oral apigenin exposure is commonly limited by poor water solubility and extensive first-pass metabolism (glucuronidation/sulfation). Human data indicate circulating apigenin is largely present as conjugated metabolites, and dietary intake can yield only low (typically sub-µM) systemic levels; lipidic/self-emulsifying formulations can increase exposure in vivo (formulation-dependent). Reported half-life/kinetic parameters vary widely across studies and matrices.

In-vitro vs systemic exposure relevance: Many anti-cancer in vitro studies use ~10–50+ µM apigenin, which can exceed typical achievable free aglycone systemic levels after oral intake; some effects may therefore be high-concentration or formulation-enabled rather than diet-achievable. Tissue-local exposure (GI lumen, local mucosa) may be higher than plasma, and conjugate biology may contribute (context-dependent).

Clinical evidence status: Predominantly preclinical oncology evidence (cell and animal models) with limited, non-definitive human cancer interventional data; at least one pilot clinical study concept exists/has been registered (status-dependent). Strongest human evidence base is for non-cancer indications and general bioactivity rather than oncology efficacy.

Apigenin present in parsley, celery, chamomile, oranges and beverages such as tea, beer and wine.
"It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways."
-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv (improves when mixed with oil/dietary fat or lipid based formulations)
-best oil might be MCT oils (medium-chain fatty acids)


Pathways:
- Often considered an antioxidant, in cancer cells it can paradoxically induce ROS production
(one report that goes against most others, by lowering ROS in cancer cells but still effective)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ (Conflicting evidence about Nrf2)
        - Combined with Metformin (reduces Nrf2) amplifies ROS production in cancer cells while sparing normal cells.
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓,
- Others: PI3K↓, AKT↓, JAK↓, 1, 2, 3, STAT↓, 1, 2, 3, 4, 5, 6, Wnt↓, β-catenin↓, AMPK↓,, α↓,, ERK↓, 5↓, JNK↓,
- Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes)
        -Ex: other flavonoids(chrysin, Luteolin, querectin) curcumin, metformin, sulforaphane, ASA
Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Apigenin exhibits biological effects (anticancer, anti-inflammatory, antioxidant, neuroprotective, etc.) typically at concentrations roughly in the range of 1–50 µM.

Parsley microgreens can contain up to 2-3 times more apigenin than mature parsley.
Apigenin is typically measured in the range of 1-10 μM for biological activity. Assuming a molecular weight of 270 g/mol for apigenin, we can estimate the following μM concentrations:
10uM*5L(blood)*270g/mol=13.5mg apigenin (assumes 100% bioavailability)
then an estimated 10-20 mg of apigenin per 100 g of fresh weight parlsey
2.2mg/g of apigenin fresh parsley
45mg/g of apigenin in dried parsley (wikipedia)
so 100g of parsley might acheive 10uM blood serum level (100% bioavailability)
BUT bioavailability is only 1-5%
(Supplements available in 75mg liposomal)( Apigenin Pro Liposomal, 200 mg from mcsformulas.com)

A study had 2g/kg bw (meaning 160g for 80kg person) delivered a maximum 0.13uM of plasma concentration @ 7.2hrs.
Assuming parsley is 90-95% water, then that would be ~16g of dried parsley
Conclusion: to reach 10uM would seem very difficult by oral ingestion of parsley.
Other quotes:
      “4g of dried parsley will be enough for 50kg adult”
      5mg/kg BW yields 16uM, so 80Kg person means 400mg (if dried parsley is 130mg/g, then would need 3g/d)
In many cancer cell lines, concentrations in the range of approximately 20–40 µM have been reported to shift apigenin’s activity from mild antioxidant effects (or negligible ROS changes) toward a clear pro-oxidant effect with measurable ROS increases.

Low doses: At lower concentrations, apigenin is more likely to exhibit its antioxidant properties, scavenging ROS and protecting cells from oxidative stress.
In normal cells with robust antioxidant systems, apigenin’s antioxidant effects might prevail, whereas cancer cells—often characterized by an already high level of basal ROS—can be pushed over the oxidative threshold by increased ROS production induced by apigenin.
In environments with lower free copper levels, this pro-oxidant activity is less pronounced, and apigenin may tilt the balance toward its antioxidant function.

Apigenin — cancer-relevant mechanistic pathway matrix

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis program ΔΨm ↓, Cyt-c ↑, Caspase cascade ↑, apoptosis ↑ ↔ to protective (model-dependent) R Pro-apoptotic stress commitment Frequently reported core phenotype across tumor models; may be downstream of ROS and kinase-network suppression.
2 Cell-cycle control Cyclin D1/E ↓, CDK2/4/6 ↓, arrest ↑ ↔ G Anti-proliferative checkpointing Often couples to p53/p21 context and growth-factor signaling downshift.
3 PI3K / AKT / MAPK PI3K ↓, AKT ↓, ERK ↓ (model-dependent) ↔ R Growth and survival signaling suppression High industry relevance; provides a convergent explanation for anti-growth and anti-migration phenotypes.
4 NF-κB / COX-2 inflammatory axis NF-κB ↓, COX-2 ↓, inflammatory cytokine programs ↓ Inflammatory tone ↓ G Anti-inflammatory microenvironment pressure Relevant to tumor-promoting inflammation and stromal signaling (context-dependent).
5 ROS modulation ROS ↑ (often), DNA damage ↑, ER stress ↑ (model-dependent) ROS injury ↓ / antioxidant support ↑ (context-dependent) P Redox stress bifurcation (tumor vs normal) Frequently described “paradox”: pro-oxidant stress in tumors while normal cells may show antioxidant protection; not universal.
6 NRF2 / antioxidant defense NRF2 ↓, GSH ↓ (often) ↔ (conflicting) NRF2 ↑, SOD ↑, GSH ↑ (context-dependent) G Antioxidant program reprogramming Direction is context- and model-dependent; important for interpreting chemo-compatibility and ROS claims.
7 HIF-1α / glycolysis HIF-1α ↓, glycolysis ↓, ATP ↓ (model-dependent) ↔ G Metabolic stress / Warburg pressure Reported suppression of glycolysis nodes (e.g., GLUT1/LDHA/HK2/PKM2/PDK1) in some models; may be concentration-sensitive.
8 Migration / invasion and EMT EMT ↓, FAK ↓, integrin signaling ↓, MMPs ↓, uPA ↓ ↔ G Anti-metastatic phenotypes Often downstream of kinase-network suppression and inflammatory tone changes.
9 Angiogenesis programs VEGF ↓ (model-dependent) ↔ G Anti-angiogenic signaling pressure Usually indirect via HIF-1α / inflammatory signaling and tumor-stromal coupling.
10 Epigenetic regulation HDAC ↓, DNMTs ↓, EZH2 ↓ (model-dependent) ↔ G Transcriptional reprogramming Mechanistically plausible but often secondary to upstream stress/kinase changes; evidence varies by model.
11 Cancer stemness pathways Hh/GLI ↓, CK2 ↓, CSC phenotypes ↓ (model-dependent) ↔ G Stemness pressure Typically preclinical; may matter for recurrence-resistance hypotheses.
12 Chemosensitization / death-ligand sensitization Sensitization ↑ (model-dependent) ↔ R Combination leverage Examples include TRAIL sensitization in vitro; translation depends on achievable exposure and interaction risk.
13 Clinical Translation Constraint Low solubility; conjugation-heavy PK; in-vitro concentration gap; potential CYP/UGT/SULT interactions Drug–supplement interaction risk relevant to both — Delivery and interaction limitations Oral free-aglycone systemic levels are often low; formulation can change exposure. In vitro CYP inhibition is reported (notably CYP3A4/2C9); apigenin can also inhibit conjugation pathways in models—caution with narrow-therapeutic-index drugs.

TSF

P: 0–30 min
R: 30 min–3 hr
G: >3 hr
Scientific Papers found: Click to Expand⟱
1095- Api,    Apigenin inhibits epithelial-mesenchymal transition of human colon cancer cells through NF-κB/Snail signaling pathway
- Analysis, Colon, NA
Snail↓, EMT↓, NF-kB↓,
1077- Api,    Apigenin inhibits COX-2, PGE2, and EP1 and also initiates terminal differentiation in the epidermis of tumor bearing mice
- in-vivo, NMSC, NA
*COX2↓, COX2∅,
4280- Api,    Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms
- Review, AD, NA - Review, Park, NA
*neuroP↑, *antiOx↑, *ROS↓, *Inflam↓, *TNF-α↓, *IL1β↓, *PI3K↑, *Akt↑, *BBB↑, *NRF2↑, *SOD↑, *GPx↑, *MAPK↓, *Catalase↑, *HO-1↑, *COX2↓, *PGE2↓, *PPARγ↑, *TLR4↓, *GSK‐3β↓, *Aβ↓, *NLRP3↓, *BDNF↑, *TrkB↑, *GABA↑, *AChE↓, *Ach↑, *5HT↑, *cognitive↑, *MAOA↓,
1024- Api,  CUR,    Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects
- vitro+vivo, Melanoma, A375 - in-vitro, Melanoma, A2058 - in-vitro, Melanoma, RPMI-7951
TumCG↓, Apoptosis↑, PD-L1↓, STAT1↓, tumCV↓, T-Cell↑,
1008- Api,    Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW480
Wnt/(β-catenin)↓, β-catenin/ZEB1↓, TumAuto↑, Akt↓, mTOR↓, tumCV↓, TumCCA↑, TumAuto↑, p‑Akt↓, p‑p70S6↓, p‑4E-BP1↓,
983- Api,    Apigenin acts as a partial agonist action at estrogen receptors in vivo
- in-vivo, NA, NA
ERα/ESR1↑, ERβ/ESR2↑,
958- Api,    Apigenin suppresses tumor angiogenesis and growth via inhibiting HIF-1α expression in non-small cell lung carcinoma
- in-vitro, Lung, NCIH1299
Hif1a↓, VEGF↓, VEGFR2↓, PDGF↓, angioG↓,
938- Api,  doxoR,    Apigenin and hesperidin augment the toxic effect of doxorubicin against HepG2 cells
- vitro+vivo, HCC, HepG2
LDHA↓, HK2↓,
591- Api,  doxoR,    Polyphenols act synergistically with doxorubicin and etoposide in leukaemia cell lines
- in-vitro, AML, Jurkat - in-vitro, AML, THP1
ATP↓, Casp3↑, γH2AX↑,
586- Api,  5-FU,    5-Fluorouracil combined with apigenin enhances anticancer activity through mitochondrial membrane potential (ΔΨm)-mediated apoptosis in hepatocellular carcinoma
- in-vivo, HCC, NA
ROS↑, MMP↓, Bcl-2↓, Casp3↑, PARP↑,
584- Api,  Cisplatin,    Apigenin potentiates the antitumor activity of 5-FU on solid Ehrlich carcinoma: Crosstalk between apoptotic and JNK-mediated autophagic cell death platforms
- in-vivo, Var, NA
Beclin-1↑, Casp3↑, Casp9↑, JNK↑, Mcl-1↓, Ki-67↓,
583- Api,  Cisplatin,    Apigenin suppresses GLUT-1 and p-AKT expression to enhance the chemosensitivity to cisplatin of laryngeal carcinoma Hep-2 cells: an in vitro study
- in-vitro, Laryn, HEp2
PI3K/Akt↓, GLUT1↓, Akt↓,
581- Api,  Cisplatin,    The natural flavonoid apigenin sensitizes human CD44+ prostate cancer stem cells to cisplatin therapy
- in-vitro, Pca, CD44+
Bcl-2↓, survivin↓, Casp8↑, P53↑, Sharpin↓, APAF1↑, p‑Akt↓, NF-kB↓, P21↑, Cyc↓, CDK2↓, CDK4/6↓, Snail↓, ChemoSen↑,
578- Api,  Cisplatin,    Apigenin enhances the cisplatin cytotoxic effect through p53-modulated apoptosis
- in-vitro, Lung, A549 - in-vitro, BC, MCF-7 - in-vitro, CRC, HCT116 - in-vitro, Pca, HeLa - in-vitro, Lung, H1299
p‑P53↑,
577- Api,  PacT,    Inhibition of IL-6/STAT3 axis and targeting Axl and Tyro3 receptor tyrosine kinases by apigenin circumvent taxol resistance in ovarian cancer cells
- in-vitro, Ovarian, SKOV3
p‑Akt↓, Bcl-xL↓, Bcl-2↓, AXL↓, Tyro3↓,
4281- Api,    The neurotrophic activities of brain‐derived neurotrophic factor are potentiated by binding with apigenin, a common flavone in vegetables, in stimulating the receptor signaling
- in-vitro, AD, SH-SY5Y
*BDNF↑, *TrkB↑,
421- Api,    Apigenin inhibits HeLa sphere-forming cells through inactivation of casein kinase 2α
- vitro+vivo, Cerv, HeLa
CK2↓,
419- Api,    Apigenin inhibited hypoxia induced stem cell marker expression in a head and neck squamous cell carcinoma cell line
- in-vitro, SCC, HN30 - in-vitro, SCC, HN8
CD44↓, Nanog↓, Endoglin↓, VEGF↓, CSCs↓,
418- Api,    Apigenin inhibits the proliferation and invasion of osteosarcoma cells by suppressing the Wnt/β-catenin signaling pathway
- vitro+vivo, OS, U2OS - vitro+vivo, OS, MG63
β-catenin/ZEB1↓,
416- Api,    In Vitro and In Vivo Anti-tumoral Effects of the Flavonoid Apigenin in Malignant Mesothelioma
- vitro+vivo, NA, NA
Bax:Bcl2↑, P53↑, ROS↑, Casp9↑, Casp8↑, cl‑PARP1↑, p‑ERK⇅, p‑JNK↓, p‑p38↑, p‑Akt↓, cJun↓, NF-kB↓, EGFR↓, TumCCA↑,
315- Api,    Apigenin: Selective CK2 inhibitor increases Ikaros expression and improves T cell homeostasis and function in murine pancreatic cancer
- vitro+vivo, PC, Panc02
CK2↓, CD4+↑, CD8+↑, Ikaros↑,
314- Api,    Apigenin impairs oral squamous cell carcinoma growth in vitro inducing cell cycle arrest and apoptosis
- in-vitro, SCC, HaCaT - in-vitro, SCC, SCC25
TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK1/2/5/9∅,
313- Api,    Apigenin induces autophagic cell death in human papillary thyroid carcinoma BCPAP cells
- in-vitro, Thyroid, BCPAP
LC3s↝, p62↓, ROS↑, TumCCA↑, CDC25↓, TumAuto↑, Beclin-1↑, AVOs↑, DNAdam↑,
6- Ba,  Api,  QC,    Common Botanical Compounds Inhibit the Hedgehog Signaling Pathway in Prostate Cancer
- in-vitro, Pca, PC3
HH↓, Gli1↓,
481- CUR,  CHr,  Api,    Flavonoid-induced glutathione depletion: Potential implications for cancer treatment
- in-vitro, Liver, A549 - in-vitro, Pca, PC3 - in-vitro, AML, HL-60
GSH↓, mtDam↑, MMP↓, Cyt‑c↑,
2642- Flav,  QC,  Api,  KaempF,  MCT  In Vitro–In Vivo Study of the Impact of Excipient Emulsions on the Bioavailability and Antioxidant Activity of Flavonoids: Influence of the Carrier Oil Type
- in-vitro, Nor, NA - in-vivo, Nor, NA
*BioAv↑, *eff↝, BioEnh↑,
1534- LT,  Api,  EGCG,  RES,    Plant polyphenol induced cell death in human cancer cells involves mobilization of intracellular copper ions and reactive oxygen species generation: a mechanism for cancer chemopreventive action
- in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, PC, Bxpc-3
TumCP↓, Apoptosis↑, eff↓, *toxicity↑, Dose?, eff↓, eff↓,
1025- LT,  Api,    Luteolin and its derivative apigenin suppress the inducible PD-L1 expression to improve anti-tumor immunity in KRAS-mutant lung cancer
- in-vivo, Lung, NA
TumCG↓, Apoptosis↑, PD-L1↓, p‑STAT3↓,
4665- QC,  Ash,  Api,    Targeting cancer stem cells by nutraceuticals for cancer therapy
- Review, Var, NA
CSCs↓,

Showing Research Papers: 101 to 129 of 129
Prev Page 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 129

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   ROS↑, 3,  

Metal & Cofactor Biology ⓘ

Ikaros↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   CDC25↓, 1,   MMP↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

HK2↓, 1,   LDHA↓, 1,   PI3K/Akt↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 4,   APAF1↑, 1,   Apoptosis↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp3↑, 3,   Casp8↑, 2,   Casp9↑, 2,   CK2↓, 2,   Cyt‑c↑, 1,   JNK↑, 1,   p‑JNK↓, 1,   Mcl-1↓, 1,   p‑p38↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

p‑p70S6↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   tumCV↓, 2,  

Autophagy & Lysosomes ⓘ

AVOs↑, 1,   Beclin-1↑, 2,   LC3s↝, 1,   p62↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 2,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP1↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1/2/5/9∅, 1,   CDK2↓, 1,   Cyc↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 1,   p‑ERK⇅, 1,   Gli1↓, 1,   HH↓, 1,   mTOR↓, 1,   Nanog↓, 1,   STAT1↓, 1,   p‑STAT3↓, 1,   TumCG↓, 2,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AXL↓, 1,   CDK4/6↓, 1,   Ki-67↓, 1,   PDGF↓, 1,   Sharpin↓, 1,   Snail↓, 2,   TumCP↓, 1,   Tyro3↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   Endoglin↓, 1,   Hif1a↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2∅, 1,   NF-kB↓, 3,   PD-L1↓, 2,   T-Cell↑, 1,  

Hormonal & Nuclear Receptors ⓘ

ERα/ESR1↑, 1,   ERβ/ESR2↑, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   ChemoSen↑, 1,   Dose?, 1,   eff↓, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   ERα/ESR1↑, 1,   Ki-67↓, 1,   PD-L1↓, 2,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 93

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

PPARγ↑, 1,  

Cell Death ⓘ

Akt↑, 1,   MAPK↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   PI3K↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 1,   Inflam↓, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↑, 1,   AChE↓, 1,   BDNF↑, 2,   GABA↑, 1,   MAOA↓, 1,   TrkB↑, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↝, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   neuroP↑, 1,   toxicity↑, 1,  
Total Targets: 33

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

 

Home Page