Database Query Results : Baicalein, , selectivity

Ba, Baicalein: Click to Expand ⟱
Features:
Baicalein is a flavone, a type of flavonoid, originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora. It is also a constituent of Oroxylum indicum and thyme.
Baicalein, a flavonoid found in several medicinal plants (notably Scutellaria baicalensis), has been investigated for its anticancer properties. Its activities involve modulation of multiple cellular pathways, including those that regulate cell proliferation, apoptosis, metastasis, and oxidative stress. 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).

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS (tumor-selective oxidative stress) ↑ ROS (P→R); can progress to cytotoxic stress (G) ↔ or ↓ ROS under oxidative challenge (R→G) P, R, G Stress amplifier Baicalein can act as a pro-oxidant in many tumor contexts while behaving as an antioxidant in non-malignant or stressed-normal contexts; net direction is dose/model dependent.
2 Mitochondrial membrane potential (ΔΨm) / mitochondrial integrity ↓ ΔΨm (R); downstream commitment to death programs (G) ↔ preserved R, G Mitochondrial failure threshold Loss of ΔΨm is a common convergence point after sustained oxidative / stress signaling and precedes cytochrome-c release and caspase activation.
3 Cytochrome-c release → Caspase-9/3 activation (intrinsic apoptosis) ↑ Cyt-c, ↑ Caspase-9, ↑ Caspase-3 (G) ↔ minimal activation G Apoptosis execution Typically appears after upstream redox/mitochondrial stress has crossed a commitment threshold; aligns with intrinsic apoptotic signaling.
4 ER stress / UPR + Ca²⁺ dysregulation ↑ ER stress, ↑ Ca²⁺ signaling (R→G) ↔ buffered homeostasis R, G Stress-to-death coupling ER stress and Ca²⁺ transfer can amplify mitochondrial dysfunction; sustained stress favors pro-death UPR signaling.
5 DNA damage / oxidative injury markers ↑ DNA damage (R→G) ↔ or efficiently repaired (G) R, G Checkpoint stress Often interpreted as a downstream consequence of sustained ROS and impaired redox buffering rather than a primary “direct DNA” effect.
6 Antioxidant defense balance (NRF2, GSH, HO-1; SOD/Catalase) ↓ NRF2 / ↓ GSH / ↓ HO-1 (R→G) ↑ NRF2 / ↑ GSH / ↑ HO-1; ↑ SOD/Catalase (R→G) R, G Selectivity gate Reported divergence suggests tumors may fail to mount sufficient antioxidant adaptation while normal cells compensate; magnitude varies by model and baseline redox state.
7 PI3K → AKT survival axis ↓ PI3K/AKT signaling (R→G) ↔ limited effect R, G Survival suppression Reduced pro-survival signaling increases vulnerability to stress-induced apoptosis and can contribute to cell-cycle effects.
8 MAPK / ERK pathway modulation MAPK/ERK modulation (often ↓ ERK tone) (P→R→G) ↔ context-dependent P, R, G Signal re-wiring MAPK readouts often shift early (phosphorylation) and can later reshape gene programs; direction can vary across tumor types and dosing.
9 NF-κB signaling ↓ NF-κB activity (R→G) ↔ R, G Anti-survival / anti-inflammatory transcription NF-κB suppression reduces pro-survival stress responses and inflammatory tone; may support chemo-/radio-sensitization in some settings.
10 Glycolysis / hypoxia program (HIF-1α; PKM2, PDK1, GLUT1, LDHA, HK2; c-Myc) ↓ Glycolysis and associated nodes; ↓ HIF-1α / ↓ c-Myc (G) ↔ G Metabolic constraint Best interpreted as a gene-regulatory / adaptation-level effect; specific node changes are model dependent even when “glycolysis suppression” is observed.
11 Invasion / metastasis programs (MMP2/MMP9 and related MMPs) ↓ MMP2 / ↓ MMP9 (G) ↔ G Anti-invasive phenotype Usually reflected in later expression/phenotype assays (migration/invasion) rather than immediate signaling events.
12 Angiogenesis signaling (VEGF) ↓ VEGF (G) ↔ G Anti-angiogenic support Typically manifests as reduced VEGF expression/secretion and downstream angiogenic behavior over longer observation windows.
13 12-lipoxygenase (12-LOX / 12/15-LOX) inhibition ↓ 12-LOX activity (P→R) ↔ P, R Direct enzymatic target Often treated as a relatively “direct” biochemical interaction compared with downstream transcriptional programs.
14 PTEN (tumor suppressor axis) ↑ PTEN (G) ↔ G Brake on PI3K/AKT PTEN increases are generally best treated as gene-regulatory/adaptation-level outcomes that reinforce PI3K/AKT suppression.

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)
selectivity, selectivity: Click to Expand ⟱
Source:
Type:
The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
2615- Ba,    The Multifaceted Role of Baicalein in Cancer Management through Modulation of Cell Signalling Pathways
- Review, Var, NA
*AntiCan↓, Baicalein is known to display anticancer activity through the inhibition of inflammation and cell proliferation
*Inflam↓,
TumCP↓,
NF-kB↓, baicalein decreased the activation of nuclear factor-κB (NF-κB)
PPARγ↑, anti-inflammatory effects of baicalein might be initiated via PPARγ activation.
TumCCA↑, baicalein inhibited cell cycle progression and cell growth, and promoted apoptosis of cancer cells
JAK2↓, inactivation of the signaling pathway JAK2/STAT3 [63]
STAT3↓,
TumCMig↓, baicalein suppressed migration as well as invasion through decreasing the aerobic glycolysis and expression of MMP-2/9 proteins.
Glycolysis↓,
MMP2↓,
MMP9↓,
selectivity↑, Furthermore, baicalein and baicalin had less inhibitory effects on normal ovarian cells’ viability.
VEGF↓, baicalein is more effective in inhibiting the expressions of VEGF, HIF-1α, cMyc, and NFκB
Hif1a↓,
cMyc↓,
ChemoSen↑, baicalein enhanced the cisplatin sensitivity of SGC-7901/DDP gastric cancer cells by inducing autophagy and apoptosis through the Akt/mTOR and Keap 1/Nrf2 pathways
ROS↑, oral squamous cell carcinoma Cal27 cells. Significantly, it was noticed that baicalein activated reactive oxygen species (ROS) generation in Cal27 cells
p‑mTOR↓, results suggest that p-mTOR, p-Akt, p-IκB, and NF-κB protein expressions were decreased
PTEN↑, Baicalein upregulated PTEN expression, downregulated miR-424-3p, and downregulated PI3K and p-Akt.

5250- Ba,    Exploring baicalein: A natural flavonoid for enhancing cancer prevention and treatment
- Review, Var, NA
Apoptosis↑, Baicalein is thought to prevent cancer progression by inducing apoptosis, autophagy, and genome instability, and its ability to promote chemo-potentiation, anti-metastatic effects, and regulate specific signalling molecules and transcription factors.
TumAuto↑,
DNAdam↑,
*antiOx↑, Baicalein has already been proven to be a radical scavenger that acts as an antioxidant [14,15
Inflam↓, it can also reduce inflammation [16] and act as an E2 prostaglandin inhibitor [17].
PGE2↓,
TumCCA↑, Baicalein properties prevent cell proliferation, induce apoptosis, autophagy, cell cycle arrest, cancer cell migration and invasion, and decrease angiogenesis [18,19].
TumCMig↓,
TumCI↓,
angioG↓,
selectivity↑, Furthermore, some studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells.
ChemoSen↑, the current review emphasises baicaleins' synergistic potential with other chemotherapeutic agents
HIF-1↓, baicalein against ovarian cancer by demonstrating that it can limit tumour cell viability by downregulating the expression of cancer-promoting genes such as HIF-1, cMyc, NFkB, and VEGF
cMyc↓,
NF-kB↓,
VEGF↓,
P53↑, Baicalein has been shown to activate p53, a tumour suppressor protein that regulates cell growth and division [26].
MMP2↓, anticancer properties of baicalein are mediated through various molecular mechanisms, including inhibition of MMP-2;
CSCs↓, inhibition of cancer stem cells
Bcl-xL↓, after bladder cancer cells were treated with baicalein, the expression of antiapoptotic genes (Bcl2, Bcl-xL, XIAP, and survivin) was reduced, and cell viability was decreased [38].
XIAP↓,
survivin↓,
tumCV↓,
Casp3↑, upregulating the expression of caspase-3 and caspase-8 and decreased the BCL-2/BAX ratio [16]
Casp8↑,
Bax:Bcl2↑,
Akt↓, in lung cancer cells, apoptosis was induced through the downregulation of the Akt/mTOR signalling pathway [25].
mTOR↓,
PCNA↓, baicalein treatment promoted apoptosis in mice with U87 gliomas by downregulating PCNA expression, enhancing the expression of caspase-3 and caspase-9 and improving the Bax/Bcl-2 ratio
MMP↓, baicalein treatment of lung cancer cells caused a collapse of the mitochondrial membrane potential (MMP), an increase in ROS generation, and enhanced PARP, caspase 3, and caspase 9 cleavage,
ROS↑,
PARP↑,
Casp9↑,
BioAv↑, Baicalein has been found to enhance the cytotoxicity and bioavailability of certain cancer therapy drugs when combined [85]
eff↑, combination of baicalein with silymarin differentially decreased the viability of HepG2 cells, enhanced the proportion of cells in the G0/G1 phase, upregulated tumour suppressors such as Rb and p53 and CDK inhibitors, and downregulated cyclin D1, cyc
P-gp↓, By inhibiting P-glycoprotein (P-gp), baicalein can increase the accumulation of chemotherapeutic drugs within cancer cells [21]
BioAv↑, selenium–baicalein nanoparticles as a targeted therapeutic strategy for NSCLC. This strategy significantly improves the bioavailability of baicalein through several mechanisms.
selectivity↑, ome studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells

5248- Ba,  BA,  doxoR,    Baicalin and Baicalein Enhance Cytotoxicity, Proapoptotic Activity, and Genotoxicity of Doxorubicin and Docetaxel in MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, HUVECs
toxicity↝, We have found that baicalin and baicalein demonstrated cytotoxicity towards both cell lines, with more potent effects observed in baicalein.
ChemoSen↑, Both flavonoids, baicalin (167 µmol/L) and baicalein (95 µmol/L), synergistically enhanced the cytotoxic, proapoptotic, and genotoxic activity of doxorubicin and docetaxel in breast cancer cells.
selectivity↑, Surprisingly, low concentrations of baicalin and baicalein had a greater effect on MCF-7 viability. A
Apoptosis↑, Induction of Apoptosis and Necrosis by Baicalin and Baicalein Used alone and in Combination with Anticancer Drugs
necrosis↑,
MMP↓, After treatment with baicalin and baicalein at high concentrations (IC50), the ΔΨm of cancer cells was diminished to 30% of the control value
DNAdam↑, DNA Damage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
cl‑PARP↑, PARP Cleavage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
MRP1↓, Moreover, baicalin and baicalein reduced cisplatin resistance by inhibiting the expression of genes involved in drug resistance, such as MRP1 [30] and Bcl-2, and via the Akt/mTOR and Nrf2/Keap 1 pathway [26].
Bcl-2↓,
hepatoP↑, baicalin and baicalein can also help decrease the side effects of cisplatin treatment by protecting the liver from damage [31]
cardioP↑, Similar to baicalein, baicalin also significantly protects against doxorubicin’s cardiotoxicity.
BioAv↝, This is because baicalein has a smaller size and high lipophilicity, contributing to fast absorption and an improved ability to penetrate cells [60].

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↑, baicalein activated apoptosis through induced intracellular reactive oxygen species (ROS) generation
eff↓, and that ROS scavenger N-acetyl-cysteine (NAC), glutathione (GSH), and superoxide dismutase (SOD) apparently inhibited intracellular ROS production, consequently attenuating the baicalein-induced apoptosis.
Casp3↑, Baicalein treatment markedly increased active caspase-3 expression
Bcl-2↓,
selectivity↑, baicalein influenced little growth reduction of hFOB1.19 cells. (normal cells)
Cyt‑c↑, release of cytochrome c from mitochondrial to cytosol
LDH?, (25 and 50 μM) induced increases of LDH release (2.2- and 3.6-folds) which showed the cytotoxicity of baicalein
BNIP3?, we conclude that baicalein induces ROS production and BNIP3 expression with the subsequent activation of Bax
BAX↑,

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↑, enhancement the level of intracellular ROS exhibit pro-oxidant activity in the presence of copper ions
MMP↓,
Bcl-2↓,
BAX↑,
Cyt‑c↑, release of cytochrome C
Casp9↑,
Casp3↑,
eff↓, The pretreatment with NeoCu (I)-specific chelator) remarkably weakened these effects of baicalein exhibit pro-oxidant activity in the presence of copper ions
selectivity↑, baicalein presented little cytotoxicity to normal breast epithelial cells
*toxicity∅, baicalein presented little cytotoxicity to normal breast epithelial cells. explained by the undetectable levels of copper present in MCF-10A cells.
Apoptosis↑,
Fenton↑, results are in further support that the prooxidant action of baicalein involves the reduction of Cu (II) to Cu (I), and the consequent generation of hydroxyl radicals.

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↓, Baicalein is also known as a selective 12-lipoxygenase (12-LOX) inhibitor
DR5↑, Baicalein induces DR5 mRNA and protein expression in SW480 cells
CHOP↑, CHOP is increased by baicalein and responsible for DR5 up-regulation in SW480 cells
ROS↑, ROS are responsible for DR5 up-regulation in PC3 cells, but not in SW480 cells
*ROS∅,
selectivity↑, ROS are responsible for DR5 up-regulation in PC3 cells, but not in SW480 cells


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   ROS↑, 4,   i-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 3,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   cMyc↓, 2,   Glycolysis↓, 1,   LDH?, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp3↑, 3,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   DR5↑, 1,   necrosis↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3?, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   PTEN↑, 1,   STAT3↓, 1,  

Migration ⓘ

MMP2↓, 2,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 2,   PGE2↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 3,   eff↓, 2,   eff↑, 1,   MRP1↓, 1,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

LDH?, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   hepatoP↑, 1,   toxicity↝, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS∅, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   toxicity∅, 1,  
Total Targets: 5

Scientific Paper Hit Count for: selectivity, selectivity
6 Baicalein
1 Baicalin
1 doxorubicin
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#:1110  State#:%  Dir#:%
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