Baicalein Cancer Research Results

Ba, Baicalein: Click to Expand ⟱
Features:

Baicalein — Baicalein is a polyphenolic flavone aglycone found primarily in Scutellaria baicalensis and related botanicals, and is the active unconjugated counterpart of baicalin after intestinal/microbial deconjugation and re-conjugation cycling. It is formally classified as a small-molecule natural-product flavonoid with pleiotropic signaling, redox, metabolic, and enzyme-modulatory activity. Standard abbreviations include Ba or BE. In cancer literature it is best characterized as a multi-target preclinical anticancer scaffold rather than an established oncology drug, with relatively strong mechanistic support for apoptosis induction, survival-pathway suppression, anti-invasive signaling, and 12-lipoxygenase inhibition, but with major translational constraints from poor aqueous solubility, extensive first-pass glucuronidation/sulfation, transporter-enzyme interactions, and the likelihood that many in-vitro exposure levels exceed typical systemic aglycone exposure.

Primary mechanisms (ranked):

  1. 12-lipoxygenase inhibition with downstream suppression of pro-survival, pro-migratory, and pro-angiogenic lipid signaling.
  2. Intrinsic apoptosis induction via mitochondrial destabilization, cytochrome-c release, caspase-9/3 activation, and BAX:BCL-2 shift.
  3. PI3K/AKT survival-axis repression, often with PTEN restoration and reduced downstream anti-apoptotic signaling.
  4. Redox stress modulation with tumor-context ROS↑ and impaired antioxidant buffering, but normal-cell antioxidant protection in oxidative-injury models.
  5. ER-stress and Ca²⁺ stress coupling that amplifies mitochondrial commitment to cell death.
  6. Suppression of glycolysis / hypoxia adaptation, including HIF-1α, HK2, LDHA, PDK1, PKM2, and GLUT1 in relevant models.
  7. Anti-invasive / anti-metastatic signaling through MMP2/MMP9 and related migration programs.
  8. Anti-angiogenic signaling with VEGF reduction.
  9. Contextual chemo- and radiosensitization in selected models.

Bioavailability / PK relevance: Oral translation is constrained by very low water solubility and extensive intestinal/hepatic phase-II metabolism to glucuronide and sulfate conjugates. Human phase-I data show rapid absorption of tablet formulations with peak plasma levels around 2 hours, steady state after repeated dosing, and major circulating/excreted metabolite burden rather than sustained high parent-aglycone exposure. Microbiota, UGT-dependent reconjugation, and transporter/CYP interactions are clinically relevant variables. Intestinal microbiota are mechanistically relevant because baicalin is converted to baicalein before absorption. Poor translational PK is reinforced by very low aqueous solubility, reported around 16.82 μg/mL, and by formulation studies showing large exposure gains after cocrystal/nanodelivery approaches.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use roughly 10–50 μM and sometimes higher. That generally exceeds typical reported average human plasma exposure for parent baicalein after oral dosing, so direct translation of higher-concentration in-vitro effects should be treated cautiously unless formulation enhancement, local delivery, tissue enrichment, conjugate deconjugation, or combination use is specifically justified.

Clinical evidence status: Strong preclinical evidence across multiple tumor models; limited animal efficacy support; human clinical experience is mainly phase-I safety/PK and non-oncology development contexts. There is no established cancer indication or mainstream regulatory oncology deployment as of March 12, 2026.

Here are some of the key pathways and mechanisms implicated in its anticancer effects:
-Apoptosis and Cell Cycle Regulation
-Reactive Oxygen Species ROS↑ Generation and Oxidative Stress (Context and dose dependent)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspase-3↑, Caspase-9↑, DNA damage↑,
-Baicalein’s effects on ROS are context-dependent. In some cancer cells, it promotes ROS production to a degree that overwhelms the antioxidant defenses. Elevated ROS levels can damage cellular components and promote apoptosis, essentially tipping the balance toward cell death.
-Conversely, in normal cells, baicalein may exhibit antioxidant properties and reduce ROS↓ under conditions of oxidative stress, highlighting its dual role.
- May Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓, HO-1↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑, HO-1↑,
-MAPK, ERK Pathway:
-PI3K/Akt Pathway: Inhibition of the PI3K, Akt pathway by baicalein.
-NF-κB Pathway: Baicalein can inhibit
-Inhibition of Metastasis and Invasion: Baicalein can downregulate MMPs, MMP2, MMP9
-Angiogenesis Suppression: VEGF
-Baicalein is a well-known inhibitor of 12-lipoxygenase
-inhibitor of Glycolysis↓ and HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓
- promoting PTEN
-chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, neuroprotective, Cognitive, Renoprotection, Hepatoprotective, cardioProtective,
- Selectivity: Cancer Cells vs Normal Cells
-low bioavailability but liposomal may improve bioavailability

In summary, baicalein affects cancer cells by modulating multiple pathways—promoting apoptosis, causing cell cycle arrest, generating or modulating ROS levels, inhibiting survival and proliferative signaling (such as MAPK, PI3K/Akt, and NF-κB pathways), and reducing angiogenesis and metastasis.

Many animal studies, doses have been reported in the range of approximately 10 to 200 mg/kg body weight.
For example, some studies exploring anticancer or anti-inflammatory effects in rodent models have used doses around 50–100 mg/kg.
However, these doses do not directly translate to human dosages.
Some human studies or formulations (where they are used as nutraceuticals or supplements) may suggest dosing in the range of a few hundred milligrams per day of the extract, but it is often not standardized to a specific amount of baicalein or baicalin.
-mix with oil?

-ic50 cancer cells 10-30uM, normal cells 50-100uM
-Animal studies, 10 to 100 mg/kg.
-Reported to induce apoptosis, cause cell cycle arrest, inhibit angiogenesis, and modulate various signaling pathways (e.g., STAT3, NF-κB, MAPK).

Mechanistic table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 12-Lipoxygenase axis ↓ 12-LOX, ↓ 12-HETE-linked survival / migration signaling ↔ or modest effect P, R Direct target-level antitumor leverage One of the more mechanistically specific baicalein actions. Supports anti-proliferative, anti-migratory, and anti-angiogenic behavior in susceptible tumors.
2 Mitochondria / MPTP ↓ ΔΨm, ↑ mitochondrial dysfunction, ↑ Cyt-c release ↔ or protected in oxidative-injury models R, G Intrinsic apoptosis commitment Mitochondrial collapse is a major convergence point downstream of redox, ER-stress, and survival-pathway suppression.
3 Caspase apoptosis program ↑ BAX, ↓ Bcl-2, ↑ Casp9, ↑ Casp3, ↑ apoptosis ↔ minimal activation G Cell-death execution Widely reported across tumor models; often follows mitochondrial injury rather than representing the earliest event.
4 PI3K / AKT / PTEN axis ↓ PI3K, ↓ p-AKT, ↑ PTEN ↔ or context-dependent R, G Survival suppression A central non-redox pathway that helps explain apoptosis sensitization, cell-cycle arrest, and metabolic downshift.
5 ROS balance ↑ ROS (dose-dependent) or ROS⇅ depending on model ↓ ROS under oxidative challenge P, R, G Tumor-selective redox stress Dual behavior is important: pro-oxidant pressure is common in malignant cells, whereas antioxidant cytoprotection is well documented in stressed non-malignant cells.
6 NRF2 / HO-1 / GSH antioxidant buffering ↓ NRF2, ↓ HO-1, ↓ GSH (context-dependent) ↑ NRF2, ↑ HO-1, ↑ GSH, ↑ SOD / catalase R, G Selectivity gate This divergent redox-buffer response likely contributes to cancer-versus-normal selectivity, but it is model-dependent and should not be overstated as universal.
7 ER stress and Ca²⁺ stress coupling ↑ ER stress, ↑ CHOP, ↑ UPR, ↑ Ca²⁺ dysregulation ↔ buffered homeostasis R, G Stress amplification Likely helps transmit redox/survival perturbation into irreversible mitochondrial death signaling.
8 Glycolysis / HIF-1α adaptation ↓ HIF-1α, ↓ HK2, ↓ LDHA, ↓ PDK1, ↓ PKM2, ↓ GLUT1, ↓ glycolysis ↔ G Metabolic constraint Most convincing in hypoxia-adaptation and gastric / radioresistance models. Usually reflects later transcriptional or adaptation-level effects.
9 NF-κB and MAPK / ERK signaling ↓ NF-κB, MAPK / ERK modulation (often ↓ ERK tone) ↔ or context-dependent P, R, G Signal reprogramming Supports lower inflammatory-survival tone, apoptosis sensitization, and reduced proliferation, but exact direction within MAPK branches can vary by tumor model.
10 Invasion / metastasis axis ↓ MMP2, ↓ MMP9, ↓ migration / invasion ↔ G Anti-invasive phenotype Phenotypically important and relatively consistent, though usually secondary to broader signaling reprogramming.
11 Angiogenesis axis ↓ VEGF, ↓ microvessel support ↔ G Anti-angiogenic support Supported by xenograft and lung-cancer data; best viewed as an adjunct downstream effect rather than sole primary mechanism.
12 Radiosensitization / chemosensitization ↑ treatment sensitivity (context-dependent) Potential normal-tissue protection in oxidative-injury contexts G Combination-use leverage Mechanistically plausible via HIF-1α/glycolysis suppression, NF-κB restraint, and apoptosis priming, but still preclinical and heterogeneous.
13 Clinical Translation Constraint Low parent exposure, variable microbiota handling, rapid conjugation, likely concentration gap May favor safety but complicates efficacy extrapolation G Delivery limitation Poor solubility, strong first-pass metabolism, conjugate predominance, possible CYP/transporter interactions, and lack of oncology-grade clinical validation are the main barriers.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/physical–chemical effects; direct enzymatic or rapid signaling shifts)
  • R: 30 min–3 hr (redox signaling and acute stress-response signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
Scientific Papers found: Click to Expand⟱
2289- Ba,  Rad,    Baicalein Inhibits the Progression and Promotes Radiosensitivity of Esophageal Squamous Cell Carcinoma by Targeting HIF-1A
- in-vitro, ESCC, KYSE150
TumCP↓, TumCMig↓, Glycolysis↓, cycD1/CCND1↓, CDK4↓, ECAR↓, TumCCA↑, HK1↓, ALDH↓, ALDOA↓, PKM2↓, Hif1a↓,
1535- Ba,    Baicalein May Act as a Caloric Restriction Mimetic Candidate to Improve the Antioxidant Profile in a Natural Rodent Model of Aging
- in-vivo, Nor, NA
*antiOx↑, *ROS∅, *CRM↑,
1533- Ba,    Baicalein, as a Prooxidant, Triggers Mitochondrial Apoptosis in MCF-7 Human Breast Cancer Cells Through Mobilization of Intracellular Copper and Reactive Oxygen Species Generation
- in-vitro, BrCC, MCF-7 - in-vitro, Nor, MCF10
tumCV↓, i-ROS↑, MMP↓, Bcl-2↓, BAX↑, Cyt‑c↑, Casp9↑, Casp3↑, eff↓, selectivity↑, *toxicity∅, Apoptosis↑, Fenton↑,
1532- Ba,    Baicalein as Promising Anticancer Agent: A Comprehensive Analysis on Molecular Mechanisms and Therapeutic Perspectives
- Review, NA, NA
ROS↑, ER Stress↑, Ca+2↑, MMPs↓, Cyt‑c↑, Casp3↑, ROS↑, DR5↑, ROS↑, BAX↑, Bcl-2↓, MMP↓, Casp3↑, Casp9↑, P53↑, p16↑, P21↑, p27↑, HDAC10↑, MDM2↓, Apoptosis↑, PI3K↓, Akt↓, p‑Akt↓, p‑mTOR↓, NF-kB↓, p‑IκB↓, IκB↑, BAX↑, Bcl-2↓, ROS⇅, BNIP3↑, p38↑, 12LOX↓, Mcl-1↓, Wnt?, GLI2↓, AR↓, eff↑,
1531- Ba,    Proteomic analysis of the effects of baicalein on colorectal cancer cells
- in-vitro, CRC, DLD1 - in-vitro, CRC, SW48
TumCP↓, ROS↓, Prx6↑, eff↓, TumCCA↑, ROS↝, *ROS∅,
1530- Ba,    Baicalein Decreases Hydrogen Peroxide‐Induced Damage to NG108‐15 Cells via Upregulation of Nrf2
- in-vitro, Nor, NG108-15
*12LOX↓, *ROS↓, *NRF2↑, *eff↑,
1529- Ba,    Studies on the Inhibitory Mechanisms of Baicalein in B16F10 Melanoma Cell Proliferation
- in-vitro, Melanoma, B16-F10
ROS↑, eff↓, tumCV↓, Casp3↑, necrosis↑,
1528- Ba,    Inhibiting reactive oxygen species-dependent autophagy enhanced baicalein-induced apoptosis in oral squamous cell carcinoma
- in-vitro, OS, CAL27
Apoptosis↑, ROS↑, eff↓, TumAuto↑, cl‑PARP↑, Bax:Bcl2↑, Beclin-1↑, p62↓,
1527- Ba,    Baicalein Alleviates Arsenic-induced Oxidative Stress through Activation of the Keap1/Nrf2 Signalling Pathway in Normal Human Liver Cells
- in-vitro, Nor, MIHA
*p‑NRF2↑, *ROS↓, *MDA↓, *antiOx↑,
1526- Ba,    Baicalein induces apoptosis through ROS-mediated mitochondrial dysfunction pathway in HL-60 cells
- in-vitro, AML, HL-60
Apoptosis↑, cl‑PARP↑, DNAdam↑, cl‑BID↑, Cyt‑c↑, Casp3↑, Casp8↑, Casp9?, H2O2↑, ROS↑,
2290- Ba,    Research Progress of Scutellaria baicalensis in the Treatment of Gastrointestinal Cancer
- Review, GI, NA
p‑mTOR↓, p‑Akt↓, p‑IKKα↓, NF-kB↓, PI3K↓, Akt↓, ROCK1↓, GSK‐3β↓, CycB/CCNB1↓, cycD1/CCND1↓, cycA1/CCNA1↑, CDK4↓, P53↑, P21↑, TumCCA↑, MMP2↓, MMP9↓, EMT↓, Hif1a↓, Shh↓, PD-L1↓, STAT3↓, IL1β↓, IL2↓, IL6↓, PKM2↓, HDAC10↓, P-gp↓, Bcl-xL↓, eff↓, BioAv↓, BioAv↑,
1524- Ba,    Baicalein Induces Caspase‐dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
DR5↑, FADD↑, FasL↑, Casp8↑, cFLIP↓, Casp3↑, Casp9↑, cl‑PARP↑, MMP↓, BID↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑, Apoptosis↑, TumCCA↑, DR5↑, FasL↑, DR4∅, cFLIP↓, FADD↑, MMPs↓,
1523- Ba,    Baicalein induces human osteosarcoma cell line MG-63 apoptosis via ROS-induced BNIP3 expression
- in-vitro, OS, MG63 - in-vitro, Nor, hFOB1.19
TumCD↑, Apoptosis↑, ROS↑, eff↓, Casp3↑, Bcl-2↓, selectivity↑, Cyt‑c↑, LDH?, BNIP3?, BAX↑,
1522- Ba,    Baicalein reduces lipopolysaccharide-induced inflammation via suppressing JAK/STATs activation and ROS production
- in-vitro, Nor, RAW264.7
*p‑STAT1↓, *p‑STAT3↓, *p‑JAK1↓, *p‑JAK2↓, *iNOS↓, *NO↓, *IL1β↓, *IL6↓, *TNF-α↓, *ROS↓,
1521- Ba,    Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells
- in-vitro, Bladder, 5637
TumCG↓, Apoptosis↑, IAP1↓, IAP2↓, Casp3↑, Casp9↑, BAX↑, Bcl-2↓, MMP↓, Casp8↑, BID↑, ROS?, eff↓, DR4↑, DR5↑, FasL↑, TRAIL↑,
1520- Ba,    Baicalein Induces G2/M Cell Cycle Arrest Associated with ROS Generation and CHK2 Activation in Highly Invasive Human Ovarian Cancer Cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, TOV-21G
TumCG↓, TumCCA↑, ROS↑, DNAdam↑, Chk2↑, Dose∅, p‑γH2AX↑, CDC25↓, CHK1↓, cycD1/CCND1↓, eff↓, 12LOX↓,
1519- Ba,    Baicalein inhibits KB oral cancer cells by inducing apoptosis via modulation of ROS
- in-vitro, Oral, KB
Apoptosis↑, Dose∅, ROS↑,
1288- Ba,    The Traditional Chinese Medicine Baicalein Potently Inhibits Gastric Cancer Cells
- in-vitro, GC, SGC-7901
TumCG↓, TumCCA↑, Apoptosis↑, MMP↓, Bcl-2↓, BAX↑,
1053- Ba,  docx,    Baicalin, a Potent Inhibitor of NF-κB Signaling Pathway, Enhances Chemosensitivity of Breast Cancer Cells to Docetaxel and Inhibits Tumor Growth and Metastasis Both In Vitro and In Vivo
- in-vivo, BC, 4T1
TumCP↓, Apoptosis↑, ROS↑, Bax:Bcl2↑, NF-kB↓, ChemoSen↑, survivin↓,
1029- Ba,  BA,    Baicalein and baicalin promote antitumor immunity by suppressing PD-L1 expression in hepatocellular carcinoma cells
- vitro+vivo, HCC, NA
PD-L1↓, T-Cell↑, STAT3↓,
999- Ba,    Baicalin Inhibits EMT through PDK1/AKT Signaling in Human Nonsmall Cell Lung Cancer
- in-vitro, Lung, H460
TumCP↓, p‑PDK1↓, p‑Akt↓, EMT↓, E-cadherin↑, Vim↓,
996- Ba,  Tam,    Baicalein resensitizes tamoxifen‐resistant breast cancer cells by reducing aerobic glycolysis and reversing mitochondrial dysfunction via inhibition of hypoxia‐inducible factor‐1α
Hif1a↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, lact/pyru↓, ROS↑, Apoptosis↑,
2476- Ba,    Baicalein Induces Caspase-dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells
- in-vitro, Lung, A549
TumCG↓, Apoptosis↑, DR5↑, FasL↑, FADD↑, Casp8↑, cFLIP↓, Casp9↑, Casp3↑, cl‑PARP↑, MMP↓, BID↑, BAX↑, Cyt‑c↑, ROS↑, eff↓, AMPK↑,
2601- Ba,    Cardioprotective effects of baicalein on heart failure via modulation of Ca2 + handling proteins in vivo and in vitro
- in-vitro, Nor, NA - in-vivo, Nor, NA
*cardioP↑, *p‑Ca+2↓,
2600- Ba,    Baicalein Induces Apoptosis and Autophagy via Endoplasmic Reticulum Stress in Hepatocellular Carcinoma Cells
- in-vitro, HCC, SMMC-7721 cell - in-vitro, HCC, Bel-7402
ER Stress↑, Bcl-2↓, Ca+2↑, JNK↑, CHOP↑, Casp9↑, Casp3↑, PARP↑, Apoptosis↑, UPR↑,
2599- Ba,    Baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting PI3K/AKT pathway in vivo and vitro
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
TumCP↓, Apoptosis↑, p‑Akt↓, p‑mTOR↓, NF-kB↓, p‑IKKα↓, IKKα↑, PI3K↓, MMP↓, TumAuto↑, TumVol↓, TumW↓,
2598- Ba,    Baicalein inhibits melanogenesis through activation of the ERK signaling pathway
- in-vitro, Melanoma, B16-F10
other↓, other?, ERK↑,
2597- Ba,    Baicalein – An Intriguing Therapeutic Phytochemical in Pancreatic Cancer
- Review, PC, NA
chemoP↑, ChemoSen↑, 12LOX?, Bcl-2↓, BAX↑, Mcl-1↓, ERK↓, Prx6↑, Dose↝, BioAv↓, eff↑,
2483- Ba,    Baicalein and 12/15-Lipoxygenase in the Ischemic Brain
- in-vivo, Stroke, NA
*12LOX↓, *antiOx↓, *neuroP↑,
2482- Ba,    Modulation of Neuroinflammation in Poststroke Rehabilitation: The Role of 12/15-Lipoxygenase Inhibition and Baicalein
- Review, Stroke, NA
*12LOX↓, *neuroP↑, *eff↑,
2481- Ba,  Rad,    Radiotherapy Increases 12-LOX and CCL5 Levels in Esophageal Cancer Cells and Promotes Cancer Metastasis via THP-1-Derived Macrophages
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, KYSE150
12LOX↓, RadioS↑, Dose↝, RANTES↓, MCP1↓,
2480- Ba,    Inhibition of 12/15 lipoxygenase by baicalein reduces myocardial ischemia/reperfusion injury via modulation of multiple signaling pathways
- in-vivo, Stroke, NA
*12LOX↓, *ROS↓, *ERK↑, *Akt↑, *p38↓, *JNK↓, *NF-kB↓, *cardioP↑,
2479- Ba,    Baicalein Overcomes Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Resistance via Two Different Cell-Specific Pathways in Cancer Cells but not in Normal Cells
- in-vitro, HCC, SW480 - in-vitro, Pca, PC3
12LOX↓, DR5↑, CHOP↑, ROS↑, *ROS∅, selectivity↑,
2478- Ba,    The role of Ca2+ in baicalein-induced apoptosis in human breast MDA-MB-231 cancer cells through mitochondria- and caspase-3-dependent pathway
- in-vitro, BC, MDA-MB-231
Bcl-2↓, BAX↓, Cyt‑c↑, Casp3↑, Ca+2↓,
2477- Ba,    Baicalein induces apoptosis via a mitochondrial-dependent caspase activation pathway in T24 bladder cancer cells
- in-vitro, CRC, T24/HTB-9
TumCG↓, TumCCA↑, MMP↓, Cyt‑c↑, Casp9↑, Casp3↑, p‑Akt↓, Bcl-2↓, BAX↑, Bax:Bcl2↑, 12LOX↓,
2291- Ba,  BA,    Baicalein and Baicalin Promote Melanoma Apoptosis and Senescence via Metabolic Inhibition
- in-vitro, Melanoma, SK-MEL-28 - in-vitro, Melanoma, A375
LDHA↓, ENO1↓, PKM2↓, GLUT1↓, GLUT3↓, HK2↓, PFK1↓, GPI↓, TPI↓, GlucoseCon↓, TumCG↓, TumCP↓, mTORC1↓, Hif1a↓, Ki-67↓,
2475- Ba,    Baicalein triggers ferroptosis in colorectal cancer cells via blocking the JAK2/STAT3/GPX4 axis
- in-vitro, CRC, HCT116 - in-vitro, CRC, DLD1 - in-vivo, NA, NA
tumCV↓, GPx4↓, STAT3↓, Ferroptosis↑,
2474- Ba,    Anticancer properties of baicalein: a review
- Review, Var, NA - in-vitro, Nor, BV2
ROS⇅, ROS↑, ER Stress↑, Ca+2↑, Apoptosis↑, eff↑, DR5↑, 12LOX↓, Cyt‑c↑, Casp7↑, Casp9↑, Casp3↑, cl‑PARP↑, TumCCA↑, cycE/CCNE↑, CDK4↓, cycD1/CCND1↓, VEGF↓, cMyc↓, Hif1a↓, NF-kB↓, BioEnh↑, BioEnh↑, P450↓, *Hif1a↓, *iNOS↓, *COX2↓, *VEGF↓, *ROS↓, *PI3K↓, *Akt↓,
2391- Ba,    Scutellaria baicalensis and its flavonoids in the treatment of digestive system tumors
- Review, GC, NA
Hif1a↓, PKM2↓, RadioS↑, Glycolysis↓, PAK↓,
2298- Ba,    Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
- Review, Var, NA
TumCG↓, TumCP↓, Hif1a↓, VEGF↓, ChemoSen↑, Glycolysis↓, HK2↓, PDK1↓, LDHA↓, p‑Akt↓, PTEN↑,
2297- Ba,    Significance of flavonoids targeting PI3K/Akt/HIF-1α signaling pathway in therapy-resistant cancer cells – A potential contribution to the predictive, preventive, and personalized medicine
- Review, Var, NA
Glycolysis↓, Hif1a↓, PKM2↓, RadioS↑,
2296- Ba,    The most recent progress of baicalein in its anti-neoplastic effects and mechanisms
- Review, Var, NA
CDK1↓, Cyc↓, p27↑, P21↑, P53↑, TumCCA↑, TumCI↓, MMP2↓, MMP9↓, E-cadherin↑, N-cadherin↓, Vim↓, LC3A↑, p62↓, p‑mTOR↓, PD-L1↓, CAFs/TAFs↓, VEGF↓, ROCK1↓, Bcl-2↓, Bcl-xL↓, BAX↑, ROS↑, cl‑PARP↑, Casp3↑, Casp9↑, PTEN↑, MMP↓, Cyt‑c↑, Ca+2↑, PERK↑, IRE1↑, CHOP↑, Copper↑, Snail↓, Vim↓, Twist↓, GSH↓, NRF2↓, HO-1↓, GPx4↓, XIAP↓, survivin↓, DR5↑,
2295- Ba,  5-FU,    Baicalein reverses hypoxia-induced 5-FU resistance in gastric cancer AGS cells through suppression of glycolysis and the PTEN/Akt/HIF-1α signaling pathway
- in-vitro, GC, AGS
ChemoSen↑, HK2↓, LDHA↓, PDK1↓, Akt↓, PTEN↑, Hif1a↓, Glycolysis↓, ROS↑, CHOP↑,
2294- Ba,    Baicalein attenuates cardiac hypertrophy in mice via suppressing oxidative stress and activating autophagy in cardiomyocytes
- in-vivo, Nor, NA
*Catalase↑, *ROS↓, *cardioP↑, *FOXO3?,
2293- Ba,    Baicalein suppresses inflammation and attenuates acute lung injury by inhibiting glycolysis via HIF‑1α signaling
- in-vitro, Nor, MH-S - in-vivo, NA, NA
*Hif1a↓, *Glycolysis↓, *Inflam↓, *HK2↓, *PFK1↓, *PKM2↓,
2292- Ba,  BA,    Baicalin and baicalein in modulating tumor microenvironment for cancer treatment: A comprehensive review with future perspectives
- Review, Var, NA
AntiCan↑, *toxicity↓, BioAv↝, BioAv↓, *ROS↓, *TLR2↓, *NF-kB↓, *NRF2↑, *antiOx↑, *Inflam↓, HDAC1↓, HDAC8↓, Wnt↓, β-catenin/ZEB1↓, PD-L1↓, Sepsis↓, NF-kB↓, LOX1↓, COX2↓, VEGF↑, PI3K↓, Akt↓, mTOR↓, MMP2↓, MMP9↓, SIRT1↑, AMPK↑,
4962- PEITC,  Ba,  PSO,    Targeting Breast Cancer Stem Cells
- Review, BC, NA
CSCs↓,
3034- RosA,  RES,  Ba,    The effect of dietary polyphenols on the epigenetic regulation of gene expression in MCF7 breast cancer cells
- in-vitro, BC, MCF-7
DNMTs↓, eff↑, eff↝,

Showing Research Papers: 51 to 98 of 98
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 98

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Copper↑, 1,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 2,   GSH↓, 1,   H2O2↑, 1,   HK1↓, 1,   HO-1↓, 1,   NRF2↓, 1,   Prx6↑, 2,   ROS?, 1,   ROS↓, 1,   ROS↑, 17,   ROS⇅, 2,   ROS↝, 1,   i-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   MMP↓, 9,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX?, 1,   12LOX↓, 6,   ALDOA↓, 1,   AMPK↑, 3,   cMyc↓, 1,   ECAR↓, 1,   ENO1↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 6,   GPI↓, 1,   HK2↓, 3,   lact/pyru↓, 1,   lactateProd↓, 1,   LDH?, 1,   LDHA↓, 3,   PDK1↓, 2,   p‑PDK1↓, 1,   PFK1↓, 1,   PKM2↓, 5,   SIRT1↑, 1,   TPI↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 6,   Apoptosis↑, 15,   BAX↓, 1,   BAX↑, 10,   Bax:Bcl2↑, 3,   Bcl-2↓, 11,   Bcl-xL↓, 2,   BID↑, 3,   cl‑BID↑, 1,   Casp3↑, 14,   Casp7↑, 1,   Casp8↑, 4,   Casp9?, 1,   Casp9↑, 9,   cFLIP↓, 3,   Chk2↑, 1,   Cyt‑c↑, 10,   DR4↑, 1,   DR4∅, 1,   DR5↑, 8,   FADD↑, 3,   FasL↑, 4,   Ferroptosis↑, 1,   IAP1↓, 1,   IAP2↓, 1,   JNK↑, 1,   Mcl-1↓, 2,   MDM2↓, 1,   necrosis↑, 1,   p27↑, 2,   p38↑, 1,   survivin↓, 2,   TRAIL↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

PAK↓, 1,  

Transcription & Epigenetics ⓘ

other?, 1,   other↓, 1,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

CHOP↑, 4,   ER Stress↑, 3,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   BNIP3?, 1,   BNIP3↑, 1,   LC3A↑, 1,   p62↓, 2,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↑, 2,   DNMTs↓, 1,   p16↑, 1,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 6,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↓, 3,   Cyc↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   cycE/CCNE↑, 1,   P21↑, 3,   TumCCA↑, 9,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CSCs↓, 1,   EMT↓, 2,   ERK↓, 1,   ERK↑, 1,   GSK‐3β↓, 1,   HDAC1↓, 1,   HDAC10↓, 1,   HDAC10↑, 1,   HDAC8↓, 1,   mTOR↓, 1,   p‑mTOR↓, 4,   mTORC1↓, 1,   PI3K↓, 4,   PTEN↑, 3,   Shh↓, 1,   STAT3↓, 3,   TumCG↓, 7,   Wnt?, 1,   Wnt↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 4,   CAFs/TAFs↓, 1,   E-cadherin↑, 2,   GLI2↓, 1,   Ki-67↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 2,   N-cadherin↓, 1,   ROCK1↓, 2,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 7,   Twist↓, 1,   Vim↓, 3,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 9,   LOX1↓, 1,   VEGF↓, 3,   VEGF↑, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   GLUT3↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IKKα↑, 1,   p‑IKKα↓, 2,   IL1β↓, 1,   IL2↓, 1,   IL6↓, 1,   IκB↑, 1,   p‑IκB↓, 1,   MCP1↓, 1,   NF-kB↓, 6,   PD-L1↓, 4,   RANTES↓, 1,   T-Cell↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 1,   BioAv↝, 1,   BioEnh↑, 2,   ChemoSen↑, 4,   Dose↝, 2,   Dose∅, 2,   eff↓, 10,   eff↑, 4,   eff↝, 1,   P450↓, 1,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   IL6↓, 1,   Ki-67↓, 1,   LDH?, 1,   PD-L1↓, 4,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   TumVol↓, 1,   TumW↓, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 189

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 3,   Catalase↑, 1,   MDA↓, 1,   NRF2↑, 2,   p‑NRF2↑, 1,   ROS↓, 7,   ROS∅, 3,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 4,   CRM↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   PFK1↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   iNOS↓, 2,   JNK↓, 1,   p38↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   FOXO3?, 1,   PI3K↓, 1,   p‑STAT1↓, 1,   p‑STAT3↓, 1,  

Migration ⓘ

p‑Ca+2↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,   NO↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   p‑JAK1↓, 1,   p‑JAK2↓, 1,   NF-kB↓, 2,   TLR2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 3,   neuroP↑, 2,   toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 43

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

 

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