Database Query Results : Baicalein, , RadioS

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)

RadioS, RadioSensitizer: Click to Expand ⟱

Source:

Type:

A radiosensitizer is an agent that makes cancer cells more sensitive to the damaging effects of radiation therapy. By using a radiosensitizer, clinicians aim to enhance the effectiveness of radiation treatment by either increasing the damage incurred by tumor cells or by interfering with the cancer cells’ repair mechanisms. This can potentially allow for lower doses of radiation, reduced side effects, or improved treatment outcomes.
Pathways that help Radiosensitivity: downregulating HIF-1α, increase SIRT1, Txr

List of Natural Products with radiosensitizing properties:
-Curcumin:modulate NF-κB, STAT3 and has been shown in preclinical studies to enhance the effects of radiation by inhibiting cell survival pathways.
-Resveratrol:
-EGCG:
-Quercetin:
-Genistein:
-Parthenolide:

How radiosensitizers inhibit the thioredoxin (Trx) system in cellular contexts. Notable radiosensitizers, including:
-gold nanoparticles (GNPs),
-gold triethylphosphine cyanide ([Au(SCN) (PEt3)]),
-auranofin, ceria nanoparticles (CONPs),
-curcumin and its derivatives,
-piperlongamide,
-indolequinone derivatives,
-micheliolide,
-motexafin gadolinium, and
-ethane selenide selenidazole derivatives (SeDs)

Scientific Papers found: Click to Expand⟱

5251-

Ba,

The Fascinating Effects of Baicalein on Cancer: A Review

Review,

Var,

AntiTum↑, The anti-tumor functions of baicalein are mainly due to its capacities to inhibit complexes of cyclins to regulate the cell cycle, to scavenge oxidative radicals, to attenuate mitogen activated protein kinase (MAPK), protein kinase B (Akt) or mammali
TumCCA↓,
ROS↓,
MAPK↓,
Akt↓,
mTOR↓,
Casp3↑, , to induce apoptosis by activating caspase-9/-3 and to inhibit tumorinvasion and metastasis by reducing the expression of matrix metalloproteinase-2/-9 (MMP-2/-9).
Casp9↑,
TumCI↓,
TumMeta↓,
MMP2↓,
MMP9↓,
Securin↓, Baicalein also induced cell death by reducing the expression of securin, while also inhibiting cancer cell death by affecting the expression of p-AKT and γ-H2AX [26].
γH2AX↝,
N-cadherin↓, Baicalein also decreased the expression of metastasis-associated molecules, including N-cadherin, vimentin, ZEB1, and ZEB2.
Vim↓,
Zeb1↓,
ZEB2↓,
TumCMig↓, researchers demonstrated that baiclalein inhibited cellular adhesion, migration, invasion, and growth of HCC cells both in vitro and in vivo.
TumCG↑,
12LOX↓, Baicalein is an inhibitor of 12-LOX and induced apoptosis, morphological changes, and carbonic anhydrase expression in PaCa cells.
DR5↑, Baicalein lessened this resistance to TRAIL by upregulating DR5 expression and promoting the expression of ROS, thus causing TRAIL sensitization in PC3 cells [85]
ROS↑,
RadioS↑, baicalein increased the sensitivity of prostate cancer cells to radiation without affecting this sensitivity in normal cells
ChemoSen↑, Combination therapy of baicalein with paclitaxel, which were assembled by nanoparticles, was demonstrated to have synergistic anticancer effects in A549 lung cancer cells and in mice bearing A549/PTX drug-resistant lung cancer xenografts [97].
BioAv↓, It is worth noting that the bioavailability of baicalein in vivo remains low.

5249-

Ba,

BA,

Baicalein and baicalin in cancer therapy: Multifaceted mechanisms, preclinical evidence, and translational challenges

Review,

Var,

Apoptosis↑, Mechanistically, they modulate interconnected signaling cascades governing apoptosis, inflammation, and cell cycle control, and they enhance tumor sensitivity to chemotherapy and radiotherapy.
Inflam↓,
TumCCA↑,
ChemoSen↑,
RadioS↑,
TumCG↓, In-vivo models consistently demonstrate tumor growth inhibition, while clinical data suggest a favorable safety profile, even at relatively high oral doses.
toxicity↓,
BioAv↓, their clinical translation remains hampered by limited solubility, poor oral bioavailability, and rapid metabolism,
Half-Life↓, However, baicalein showed a partial bioavailability, poor solubility and pharmacokinetics, and a short half-life [6]

2622-

Ba,

Cisplatin,

Rad,

Natural Baicalein-Rich Fraction as Radiosensitizer in Combination with Bismuth Oxide Nanoparticles and Cisplatin for Clinical Radiotherapy

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MCF-7

RadioS↑, BRF induced radiosensitization in all cells under 6 MV photon beam (SER of 1.06 to 1.35), and MDA-MB-231 cells only under 6 MeV electron beam (SER = 1.20)

2391-

Ba,

Scutellaria baicalensis and its flavonoids in the treatment of digestive system tumors

Review,

GC,

Hif1a↓, pretreatment of baicalein increased the sensitivity of tumor cells to 6Gy ray by down-regulating HIF-1A and PKM2, the key regulators of glycolysis.
PKM2↓,
RadioS↑,
Glycolysis↓,
PAK↓, baicalein dose-dependently inhibited the growth of EC in mice with a decrease in PAK4 protein

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

0, 20, 40, or 80 µmol/L

in-vitro,

ESCC,

KYSE150

12LOX↓, increased by 12-LOX upregulation but was suppressed by the well-established 12-LOX inhibitor, baicalein
RadioS↑, In prostate cancer cells, 12-LOX inhibition has been shown to increase radiation sensitivity,
Dose↝, Additionally, 12-LOX expression was significantly inhibited at 40 µmol/L
RANTES↓, post-radiotherapy protein levels of CCL5 increased in Eca109 and Kyse150 cells but were inhibited by baicalein
MCP1↓, Baicalein, a recognized inhibitor of 12-LOX, successfully inhibited CCL2 and CCL5 expression, which was verified by RT-qPCR.

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,

Glycolysis↓, baicalein to re-sensitize tamoxifen-resistant breast cancer cells in vitro and in vivo through the attenuation of aerobic glycolysis and reversion of mitochondrial dysfunction via reduced HIF-1α expression and transcriptional activity
Hif1a↓, inhibition of HIF-1α and PKM2 by baicalein resulted in the glycolysis suppression
PKM2↓, baicalein enhanced radio-sensitivity and inhibited the progression of esophageal squamous cell carcinoma by affecting HIF-1α and PKM2.
RadioS↑,

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

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

AntiTum↑, 1, toxicity↓, 1,
Total Targets: 39

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: RadioS, RadioSensitizer

6 Baicalein
2 Radiotherapy/Radiation
1 Baicalin
1 Cisplatin

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#:1107  State#:%  Dir#:%
  wNotes=onS  sortOrder:rid,rpid

Database Query Results : Baicalein, , RadioS

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

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