Artemisinin Cancer Research Results

ART/DHA, Artemisinin: Click to Expand ⟱
Features:

Artemisinin — a plant-derived sesquiterpene lactone endoperoxide (from Artemisia annua) best known as the parent scaffold for artemisinin-class antimalarials and widely investigated as a tumor-selective redox/iron-reactive cytotoxic agent. It is a small-molecule natural product (drug-like phytochemical) whose major clinical derivatives include artesunate (water-soluble), artemether/arteether (lipophilic), and the active metabolite dihydroartemisinin (DHA). In oncology literature the abbreviation set commonly includes ART (artemisinin), AS (artesunate), and DHA (dihydroartemisinin); many mechanistic claims are derivative-specific and exposure/iron-context dependent.

Primary mechanisms (ranked):

  1. Iron-dependent activation of the endoperoxide bridge causing ROS/lipid peroxidation stress and tumor-selective cytotoxicity (iron-high contexts)
  2. Ferroptosis sensitization/induction via iron handling and lipid peroxidation programs (often linked to ferritin/lysosome biology; context-dependent)
  3. Mitochondrial dysfunction with ΔΨm loss and intrinsic apoptosis signaling (downstream of oxidative stress)
  4. ER stress / UPR activation (stress-amplification axis)
  5. Hypoxia–metabolism suppression (HIF-1α and glycolysis program attenuation; model-dependent)
  6. Pro-survival inflammatory signaling suppression (e.g., NF-κB / STAT3 axes; model-dependent)

Bioavailability / PK relevance: Oral artemisinin has variable and generally limited systemic exposure with a short half-life on the order of hours; many anticancer in-vitro concentrations exceed typical achievable free-plasma levels without formulation strategies. Artesunate is rapidly converted to DHA; in an FDA label dataset (IV artesunate for severe malaria), artesunate has a very short half-life (~0.3 h) and DHA ~1.3 h, emphasizing exposure-time constraints and the need to interpret “ART/AS/DHA” PK separately.

In-vitro vs systemic exposure relevance: Many reported anticancer effects are driven by oxidative stress at micromolar in-vitro conditions and may be difficult to reproduce systemically without targeted delivery, local administration, or combination strategies that increase intratumoral iron/ROS burden (context-dependent).

Clinical evidence status: Cancer use remains investigational (preclinical-dominant with small/early human studies). Multiple registered clinical studies have evaluated artesunate/derivatives in oncology settings (e.g., phase I solid tumor IV artesunate; small/phase II-style neoadjuvant/adjunct trials), but there is no major regulatory approval for cancer indications; artesunate is approved/used clinically for severe malaria.

Artemisinin a compound in a Chinese herb that may inhibit tumor growth and metastasis Artemisinin (antimalarial drugs)
Artesunic acid (Artesunate) , Dihydroartemisinin (DHA), artesunate, arteether, and artemether, SM735, SM905, SM933, SM934, and SM1044

The induction of OS in tumor cells via the production of ROS is the key mechanism of ART against cancer.
combination of ART and Nrf2 inhibitors to promote ferroptosis may have more efficient anticancer effects without damaging normal cells.

Summary:
- One of the strongest tumor-selective pro-oxidants, mechanism related with iron. Synergizes with iron-rich tumors
-ROS seems to affect both cancer and normal cells
- Delivery of artemisinin in conjugate form with transferrin or holotransferrin (serum iron transport proteins) have been shown to greatly improve its effectiveness.
- Potential direct inhibitor of STAT3
- Artemisinin synergized with the glycolysis inhibitor 2DG (2-deoxy- D -glucose)
ART Combined Therapy: Allicin, Resveratrol, Curcumin, VitC (but not orally at same time), Butyrate , 2-DG, Aminolevulinic AcidG
-possible problems with liver toxicity??

-Artesunate (ART), an artemisinin compound, is known for lysosomal degradation of ferritin, inducing oxidative stress and promoting cancer cell death.

Pathways:
- Increasing reactive oxygen species (ROS) production. This oxidative stress can cause the loss of mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspase cascades.
- Downregulate HIF-1α
- By impairing glycolysis, artemisinin might force cells to rely on oxidative phosphorylation (OXPHOS) for energy production.
- Inhibit GLUT1 (glucose uptake), HK2, PKM2 (slow the glycolytic flux, thereby reducing the energy supply)
- Minimal NRF2 activation

-Artemisinin has a half-life of about 3-4 hours, Artesunate 40 minutes and Artemether 12 hours. Peak plasma levels occur in 1-2 hour.
BioAv 21%, poor-good solubility. Artesunate (ART), a water soluble derivative of artemisinin. concentrations higher in blood, colon, liver, kidney (highly perfused organs)
Pathways:
- induce ROS production, iron dependent (affect both cancer and normal cells)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓,
- Both Lowers (and raises) AntiOxidant defense in Cancer Cells: NRF2↓(contary), SOD↓, GSH↓ Catalase↓ GPx↓
- Small evidence of Raising AntiOxidant defense in Normal Cells: ROS↓(contary), NRF2↑, SOD↑(contary), GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, NF-κB↓, TGF-β↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, ECAR↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓, Integrins↓,
- some small indication of inhibiting Cancer Stem Cells : CSC↓, Hh↓, β-catenin↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, RadioSensitizer, Others(review target notes),

- Selectivity: Cancer Cells vs Normal Cells
Often synergistic with ROS-based chemo

Artemisinin-class (ART/AS/DHA) mechanisms relevant to cancer biology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Iron-activated endoperoxide chemistry and ROS burden ROS↑, lipid peroxidation↑, macromolecular damage↑ (iron-high contexts) ROS↔ to ↑ (dose-dependent) P Pro-oxidant, tumor-biased cytotoxic stress Core premise: iron availability (labile iron pool, heme/Fe²⁺ context) gates potency and selectivity; derivative and formulation matter.
2 Ferroptosis susceptibility Ferroptosis↑ (context-dependent), lipid-ROS↑ Ferroptosis↔ (context-dependent) R Non-apoptotic death program engagement or sensitization Evidence supports artemisinin-compounds as ferroptosis sensitizers/inducers in multiple models; often tied to iron handling and lipid peroxidation control nodes.
3 Ferritin and lysosome axis Ferritin turnover↑ / lysosomal iron↑ (model-dependent) → ROS↑ ↔ (model-dependent) R Iron mobilization that amplifies oxidative injury DHA/derivatives have been reported to engage ferritin/lysosome-related processes that increase reactive iron, supporting ferroptotic and apoptotic stress amplification.
4 Mitochondria and MPTP ΔΨm↓, mitochondrial ROS↑, Cyt-c release↑, apoptosis↑ Stress responses↔ to ↑ (dose-dependent) R Intrinsic apoptosis downstream of redox injury Mitochondrial impairment is commonly reported as a downstream execution route after ROS/iron activation; can intersect with ferroptosis via redox spillover.
5 ER stress and UPR ER stress↑, UPR↑ ↔ to ↑ (stress-dose dependent) R Proteostasis collapse / stress signaling Often co-occurs with ROS-driven injury; may contribute to growth arrest and death pathway crosstalk.
6 HIF-1α axis HIF-1α↓ (model-dependent) ↔ G Anti-hypoxic adaptation Reported suppression of hypoxia programs may reduce angiogenic and glycolytic adaptation in some tumors.
7 Glycolysis and glucose transport Glycolysis↓, GLUT1/HK2/PKM2↓ (model-dependent) ↔ (context-dependent) G Metabolic constraint Metabolic effects vary by cell state; can synergize with glycolysis inhibitors in model systems.
8 STAT3 axis STAT3↓ (model-dependent) ↔ G Pro-survival transcriptional attenuation Reported in subsets of studies; may contribute to reduced proliferation/survival signaling.
9 NF-κB and inflammatory signaling NF-κB↓, inflammatory cytokine programs↓ (model-dependent) Inflammation↓ (context-dependent) G Anti-inflammatory / pro-differentiation pressure Can be beneficial for tumor microenvironment modulation, but directionality and net effect depend on immune context.
10 NRF2 axis NRF2↔ (model-dependent; adaptive resistance possible) NRF2↔ to ↑ (context-dependent) G Redox adaptation gatekeeper NRF2 status can determine sensitivity vs resistance to ROS/ferroptosis; combinations that blunt NRF2 defenses are often proposed experimentally.
11 Clinical Translation Constraint Short exposure window; achievable concentrations may be below many in-vitro active ranges; heterogeneity in iron/redox state; derivative-specific PK Off-target oxidative stress risk (dose/formulation dependent) G Limits systemic reproducibility Interpret ART vs AS vs DHA separately; artesunate→DHA conversion is rapid and half-lives are short (route-dependent). Targeted delivery and combination strategies are common translational approaches.

TSF legend: P: 0–30 min    R: 30 min–3 hr    G: >3 hr
Scientific Papers found: Click to Expand⟱
576- ART/DHA,    Profiling of Multiple Targets of Artemisinin Activated by Hemin in Cancer Cell Proteome
- Analysis, NA, NA
GSTP1/GSTπ↓, TfR1/CD71↓,
575- ART/DHA,    Dihydroartemisinin initiates ferroptosis in glioblastoma through GPX4 inhibition
- in-vitro, GBM, U87MG
GPx4↓, xCT∅, ROS↑, Ferroptosis↑, ACSL4∅,
574- ART/DHA,    Dihydroartemisinin suppresses glioma proliferation and invasion via inhibition of the ADAM17 pathway
TumCP↓, TumCMig↓, TumCI↓, MMP17↓, p‑EGFR↓, p‑Akt↓,
573- ART/DHA,    Artesunate suppresses tumor growth and induces apoptosis through the modulation of multiple oncogenic cascades in a chronic myeloid leukemia xenograft mouse model
- vitro+vivo, NA, NA
p‑p38↓, p‑ERK↓, p‑CREB↓, p‑Chk2↓, p‑STAT5↓, p‑RSK↓, SOCS1↑, Apoptosis↑, Casp3↑,
572- ART/DHA,    High-throughput screening identifies artesunate as selective inhibitor of cancer stemness: Involvement of mitochondrial metabolism
CSCs↓, mtDam↑,
571- ART/DHA,  TMZ,    Artesunate enhances the therapeutic response of glioma cells to temozolomide by inhibition of homologous recombination and senescence
- vitro+vivo, GBM, A172 - vitro+vivo, GBM, U87MG
HR↓, RAD51↓, Apoptosis↑, necrosis↑, ROS↑, ChemoSen↑,
570- ART/DHA,    Artemisinin and its derivatives can significantly inhibit lung tumorigenesis and tumor metastasis through Wnt/β-catenin signaling
- vitro+vivo, NSCLC, A549 - vitro+vivo, NSCLC, H1299
TumCCA↑, CSCs↓, TumCI↓, TumCMig↓, TumCG↓, Wnt/(β-catenin)↓, Nanog↓, SOX2↓, OCT4↓, N-cadherin↓, Vim↓, E-cadherin↑,
569- ART/DHA,    Dihydroartemisinin exhibits anti-glioma stem cell activity through inhibiting p-AKT and activating caspase-3
- in-vitro, GBM, NA
TumCP↓, Apoptosis↑, TumCCA↑, Casp3↑, p‑Akt↓,
568- ART/DHA,    Mechanism-Guided Design and Synthesis of a Mitochondria-Targeting Artemisinin Analogue with Enhanced Anticancer Activity
- in-vitro, NA, MDA-MB-231 - in-vitro, NA, HeLa - in-vitro, NA, SkBr3 - in-vitro, NA, HCT116
Iron↝,
985- ART/DHA,    Artemisinin suppresses aerobic glycolysis in thyroid cancer cells by downregulating HIF-1a, which is increased by the XIST/miR-93/HIF-1a pathway
- in-vitro, Thyroid, TPC-1 - Human, NA, NA
XIST↓, Hif1a↓, Glycolysis↓, TumCCA↑, TumMeta↓,
566- ART/DHA,  2DG,    Dihydroartemisinin inhibits glucose uptake and cooperates with glycolysis inhibitor to induce apoptosis in non-small cell lung carcinoma cells
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
GlucoseCon↓, ATP↓, lactateProd↓, p‑S6↓, mTOR↓, GLUT1↓, Casp9↑, Casp8↑, Casp3↑, Cyt‑c↑, AIF↑, ROS↑,
565- ART/DHA,    Artesunate as an Anti-Cancer Agent Targets Stat-3 and Favorably Suppresses Hepatocellular Carcinoma
STAT↓, IL6↓, pro‑Casp3↝, Bcl-xL↝, survivin↝,
564- ART/DHA,  Cisplatin,    Dihydroartemisinin as a Putative STAT3 Inhibitor, Suppresses the Growth of Head and Neck Squamous Cell Carcinoma by Targeting Jak2/STAT3 Signaling
- in-vitro, NA, HN30
JAK2↓, STAT3↓, MMP2↓, MMP9↓, Mcl-1↓, Bcl-xL↓, cycD1/CCND1↓, VEGF↓, TumCCA↑, ChemoSen↑,
563- ART/DHA,    Artesunate down-regulates immunosuppression from colorectal cancer Colon26 and RKO cells in vitro by decreasing transforming growth factor β1 and interleukin-10
- in-vitro, Colon, colon26 - in-vitro, CRC, RKO
TGF-β↓, IL10↓,
562- ART/DHA,    Artesunate exerts an anti-immunosuppressive effect on cervical cancer by inhibiting PGE2 production and Foxp3 expression
- in-vivo, NA, HeLa
CD4+↓, CD25+↓, FoxP3+↓, Treg lymp↓, PGE2↓, FOXP3↓, COX2↓,
561- ART/DHA,    Antitumor and immunomodulatory properties of artemether and its ability to reduce CD4+ CD25+ FoxP3+ T reg cells in vivo
- in-vivo, NA, NA
TumCG↓, CD4+↓, CD25+↓, FoxP3+↓, IL4↑,
560- ART/DHA,    Dihydroartemisinin shift the immune response towards Th1, inhibit the tumor growth in vitro and in vivo
- in-vivo, NA, NA
IL4↓, CD4+↓, CD25+↓, FoxP3+↓, Treg lymp↓,
559- ART/DHA,    Artemisinin and its derivatives: a promising cancer therapy
- Review, NA, NA
ROS↑,
558- ART/DHA,    Artemisinin and Its Synthetic Derivatives as a Possible Therapy for Cancer
- Review, NA, NA
ROS↑, oncosis↑, Apoptosis↑, LysoPr↑, TumAuto↑, Wnt/(β-catenin)↑, AMP↓, NF-kB↓, Myc↓, CREBBP↓, mTOR↓, E-cadherin↑,
557- ART/DHA,    Artemisinin and Its Derivatives in Cancer Care
- Review, Var, NA
*BioAv↓, *BioAv↑, Apoptosis↑, EGFR↓, CD31↓, Ki-67↓, P53↓, TfR1/CD71↑, P-gp↓, PD-1↝,
556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
IL6↓, IL1↓, TNF-α↓, TGF-β↓, NF-kB↓, MIP2↓, PGE2↓, NO↓, Hif1a↓, KDR/FLK-1↓, VEGF↓, MMP2↓, TIMP2↑, ITGB1↑, NCAM↑, p‑ATM↑, p‑ATR↑, p‑CHK1↑, p‑Chk2↑, Wnt/(β-catenin)↓, PI3K↓, Akt↓, ERK↓, cMyc↓, mTOR↓, survivin↓, cMET↓, EGFR↓, cycD1/CCND1↓, cycE1↓, CDK4/6↓, p16↑, p27↑, Apoptosis↑, TumAuto↑, Ferroptosis↑, oncosis↑, TumCCA↑, ROS↑, DNAdam↑, RAD51↓, HR↓,
1026- ART/DHA,    Artemisinin improves the efficiency of anti-PD-L1 therapy in T-cell lymphoma
Ferroptosis↑, ROS↑, ERK↓, PD-L1↓,
2576- ART/DHA,  AL,    The Synergistic Anticancer Effect of Artesunate Combined with Allicin in Osteosarcoma Cell Line in Vitro and in Vivo
- in-vitro, OS, MG63 - in-vivo, NA, NA
eff↑, tumCV↓, Casp3↑, Casp9↑, Apoptosis↑, TumCG↓,
2575- ART/DHA,  docx,    Artemisia santolinifolia-Mediated Chemosensitization via Activation of Distinct Cell Death Modes and Suppression of STAT3/Survivin-Signaling Pathways in NSCLC
- in-vitro, Lung, H23
ChemoSen↑, GPx4↓, ROS↑, Ferroptosis↑, eff↑,
2574- ART/DHA,    Artemisinin: A Promising Adjunct for Cancer Therapy
- Review, Var, NA
selectivity↑, eff↑,
2573- ART/DHA,    Cell death mechanisms induced by synergistic effects of halofuginone and artemisinin in colorectal cancer cells
- in-vitro, CRC, HCT116
eff↑,
2572- ART/DHA,  SRF,    Antileukemic efficacy of a potent artemisinin combined with sorafenib and venetoclax
- in-vitro, AML, NA
CHOP↑, Mcl-1↓, ChemoSen↑, selectivity↑,
2571- ART/DHA,    Cancer combination therapies with artemisinin-type drugs
- Review, Var, NA
AntiTum↑, ChemoSen↑, hepatoP↝,
2570- ART/DHA,    Discovery, mechanisms of action and combination therapy of artemisinin
- Review, Nor, NA
*BioAv↓, *Half-Life↓, *toxicity↓, *ROS↑, GSH↓, selectivity↑,
2569- ART/DHA,    A semiphysiological pharmacokinetic model for artemisinin in healthy subjects incorporating autoinduction of metabolism and saturable first-pass hepatic extraction
- Human, Nor, NA
*Half-Life↝, BioAv↝, *Half-Life↓, BioAv↑, *Dose↝,
2324- ART/DHA,    Research Progress of Warburg Effect in Hepatocellular Carcinoma
- Review, Var, NA
PKM2↓, GLUT1↓, Glycolysis↓, Akt↓, mTOR↓, Hif1a↓, HK2↓, LDH↓, NF-kB↓,
2323- ART/DHA,    Dihydroartemisinin represses esophageal cancer glycolysis by down-regulating pyruvate kinase M2
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706
PKM2↓, lactateProd↓, GlucoseCon↓, cycD1/CCND1↓, Bcl-2↓, MMP2↓, VEGF↓, Casp3↑, cl‑PARP↑, BAX↑, DNAdam↑, ROS↑,
2322- ART/DHA,    Dihydroartemisinin Regulates Self-Renewal of Human Melanoma-Initiating Cells by Targeting PKM2/LDHARelated Glycolysis
- in-vitro, Melanoma, NA
TumCP↓, PKM2↓, LDHA↓, Glycolysis↓,
2321- ART/DHA,    Dihydroartemisinin mediating PKM2-caspase-8/3-GSDME axis for pyroptosis in esophageal squamous cell carcinoma
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706
Pyro↑, PKM2↓, Casp8↑, Casp3↑, Warburg↓, TumCCA↑, Apoptosis↑,
2320- ART/DHA,    Dihydroartemisinin Inhibits the Proliferation of Leukemia Cells K562 by Suppressing PKM2 and GLUT1 Mediated Aerobic Glycolysis
- in-vitro, AML, K562 - in-vitro, Liver, HepG2
Glycolysis↓, GlucoseCon↓, lactateProd↓, GLUT1↓, PKM2↓, ECAR↓, LDHA↓, cMyc↓, other↝,
1148- ART/DHA,    Artemisinin inhibits extracellular matrix metalloproteinase inducer (EMMPRIN) and matrix metalloproteinase-9 expression via a protein kinase Cδ/p38/extracellular signal-regulated kinase pathway in phorbol myristate acetate-induced THP-1 macrophages
- in-vitro, AML, THP1
MMP9↓, EMMPRIN↓, p‑PKCδ↓, p‑JNK↓, p‑p38↓, p‑ERK↓,
1147- ART/DHA,    Inhibitory effects of artesunate on angiogenesis and on expressions of vascular endothelial growth factor and VEGF receptor KDR/flk-1
- vitro+vivo, Ovarian, HO-8910 - vitro+vivo, Nor, HUVECs
angioG↓, TumCG↓, VEGF↓, KDR/FLK-1↓, *toxicity↓,
1099- ART/DHA,    Dihydroartemisinin inhibits IL-6-induced epithelial–mesenchymal transition in laryngeal squamous cell carcinoma via the miR-130b-3p/STAT3/β-catenin signaling pathway
- in-vitro, NA, NA
EMT↓, TumCI↓, STAT3↓, β-catenin/ZEB1↓,
1079- ART/DHA,    Artesunate inhibits the growth and induces apoptosis of human gastric cancer cells by downregulating COX-2
- in-vitro, GC, BGC-823 - in-vitro, GC, HGC27 - in-vitro, GC, MGC803
TumCP↓, Apoptosis↑, COX2↓, BAX↑, Bcl-2↓, Casp3↑, Casp9↑, MMP↓,
1076- ART/DHA,    The Potential Mechanisms by which Artemisinin and Its Derivatives Induce Ferroptosis in the Treatment of Cancer
- Review, NA, NA
Ferroptosis↑, ROS↑, ER Stress↑, i-Iron↓, TumAuto↑, AMPK↑, mTOR↑, P70S6K↑, Fenton↑, lipid-P↑, ROS↑, ChemoSen↑, NRF2↑, NRF2↓,
1075- ART/DHA,    Artemisinin derivatives inactivate cancer-associated fibroblasts through suppressing TGF-β signaling in breast cancer
- in-vitro, Nor, L929
*TGF-β↓,
1074- ART/DHA,    Artemisinin attenuates lipopolysaccharide-stimulated proinflammatory responses by inhibiting NF-κB pathway in microglia cells
- in-vitro, Nor, BV2
*TNF-α↓, *IL6↓, *MCP1↓, *NO↓, *iNOS↓, *IκB↑,
2577- ART/DHA,    Artemisinin and its derivatives in cancer therapy: status of progress, mechanism of action, and future perspectives
- Review, Var, NA
eff↑, TumCCA↑, BioAv↑, eff↑, ChemoSen↑,
2579- CUR,  ART/DHA,    Curcumin-Artemisinin Combination Therapy for Malaria
- in-vivo, NA, NA
OS↑, toxicity↓,

Showing Research Papers: 51 to 94 of 94
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 94

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   Ferroptosis↑, 5,   GPx4↓, 2,   GSH↓, 1,   GSTP1/GSTπ↓, 1,   Iron↝, 1,   i-Iron↓, 1,   lipid-P↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 11,   xCT∅, 1,  

Metal & Cofactor Biology ⓘ

TfR1/CD71↓, 1,   TfR1/CD71↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4∅, 1,   AMP↓, 1,   AMPK↑, 1,   cMyc↓, 2,   p‑CREB↓, 1,   ECAR↓, 1,   GlucoseCon↓, 3,   Glycolysis↓, 4,   HK2↓, 1,   lactateProd↓, 3,   LDH↓, 1,   LDHA↓, 2,   PKM2↓, 5,   p‑S6↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 9,   BAX↑, 2,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Bcl-xL↝, 1,   Casp3↑, 7,   pro‑Casp3↝, 1,   Casp8↑, 2,   Casp9↑, 3,   p‑Chk2↓, 1,   p‑Chk2↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 5,   p‑JNK↓, 1,   Mcl-1↓, 2,   Myc↓, 1,   necrosis↑, 1,   oncosis↑, 2,   p27↑, 1,   p‑p38↓, 2,   Pyro↑, 1,   p‑RSK↓, 1,   survivin↓, 1,   survivin↝, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 3,  

DNA Damage & Repair ⓘ

p‑ATM↑, 1,   p‑ATR↑, 1,   p‑CHK1↑, 1,   DNAdam↑, 2,   HR↓, 2,   p16↑, 1,   P53↓, 1,   cl‑PARP↑, 1,   RAD51↓, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 3,   cycE1↓, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   CREBBP↓, 1,   CSCs↓, 2,   EMT↓, 1,   ERK↓, 2,   p‑ERK↓, 2,   mTOR↓, 4,   mTOR↑, 1,   Nanog↓, 1,   OCT4↓, 1,   P70S6K↑, 1,   PI3K↓, 1,   SOX2↓, 1,   STAT↓, 1,   STAT3↓, 2,   p‑STAT5↓, 1,   TumCG↓, 4,   Wnt/(β-catenin)↓, 2,   Wnt/(β-catenin)↑, 1,  

Migration ⓘ

CD31↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 2,   EMMPRIN↓, 1,   ITGB1↑, 1,   Ki-67↓, 1,   LysoPr↑, 1,   MMP17↓, 1,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   NCAM↑, 1,   p‑PKCδ↓, 1,   TGF-β↓, 2,   TIMP2↑, 1,   Treg lymp↓, 2,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,   p‑EGFR↓, 1,   Hif1a↓, 3,   KDR/FLK-1↓, 2,   NO↓, 1,   VEGF↓, 4,  

Barriers & Transport ⓘ

GLUT1↓, 3,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 3,   CD4+↓, 3,   COX2↓, 2,   FOXP3↓, 1,   FoxP3+↓, 3,   IL1↓, 1,   IL10↓, 1,   IL4↓, 1,   IL4↑, 1,   IL6↓, 2,   JAK2↓, 1,   MIP2↓, 1,   NF-kB↓, 3,   PD-1↝, 1,   PD-L1↓, 1,   PGE2↓, 2,   SOCS1↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 7,   eff↑, 6,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   p‑EGFR↓, 1,   IL6↓, 2,   Ki-67↓, 1,   LDH↓, 1,   Myc↓, 1,   PD-L1↓, 1,   XIST↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   hepatoP↝, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 161

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Migration ⓘ

TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   IκB↑, 1,   MCP1↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   Dose↝, 1,   Half-Life↓, 2,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 15

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

 

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