Database Query Results : Baicalein, , chemoP

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)
chemoP, ChemoProtective: Click to Expand ⟱
Source:
Type:
Protects normal cells against the effect of Chemo.
Scientific Papers found: Click to Expand⟱
2597- Ba,    Baicalein – An Intriguing Therapeutic Phytochemical in Pancreatic Cancer
- Review, PC, NA
chemoP↑, Compounds such as baicalein, offer promise in dietary chemoprevention, as chemotherapeutic adjuvants, or as targeted therapy.
ChemoSen↑,
12LOX?, LOX-12 specific inhibitor baicalein attenuates cancer cell growth
Bcl-2↓, baicalein, human pancreatic cancer cells expressed decreased anti-apoptotic proteins Bcl-2 and Mcl-1 and increased pro-apoptotic protein bax
BAX↑,
Mcl-1↓,
ERK↓, activation of the ERK pathway in melanoma
Prx6↑, up-regulation in the expression of PRDX6 in colorectal cancer
Dose↝, concentrations at which we and others have found baicalein to be anti-proliferative in vitro are between 10μM and 100μM.
BioAv↓, it is thought that only 10% of ingested dietary polyphenols or their conjugates are found in the urine or plasma.
eff↑, It is possible that the antitumor properties of baicalein in vivo are due to baicalin as opposed to baicalein, as these compounds are inter-converted in the intestine by naturally occurring microbes


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Prx6↑, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX?, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Mcl-1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: chemoP, ChemoProtective
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#:1171  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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