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| Baicalin is a flavone glycoside, it is a flavonoid. It is the glucuronide of baicalein.
Baicalin is a flavonoid glycoside derived from plants in the genus Scutellaria. It has anxiolytic, anti-cancer and anti-viral properties, and is used in traditional Chinese medicine. Baicalein and baicalin are chemically related, with baicalin being essentially a conjugated (sugar-attached) form of baicalein. This conjugation can modify their biological functions and impacts, making them distinct in certain aspects even though they share several pharmacological properties. baicalin is often hydrolyzed by gut β-glucuronidase to baicalein (aglycone) and then extensively converted to phase-II conjugates (glucuronides/sulfates), which constrains systemic “free” levels after oral dosing. In cancer models, baicalin/baicalein are reported to modulate NF-κB, PI3K/AKT/mTOR, MAPK, and related programs, with downstream effects on cell-cycle arrest, apoptosis, invasion/EMT, and angiogenesis (model-dependent). Baicalein appears to be antioxidant in normal cells (low Cu). In vitro, baicalein can participate in copper-dependent redox cycling under high Cu conditions, leading to ROS generation. Whether this mechanism contributes meaningfully in vivo remains model-dependent. (higher Cu levels) (May applies to other plant polyphenols as well: Ex apigenin, luteolin, EGCG, and resveratrol). Pathways: Apoptosis Pathways (Intrinsic/Mitochondrial): NF-κB Inhibition : PI3K/Akt/mTOR Signaling Pathway downregulate : MAPK/ERK and JNK Signaling Pathways: STAT3 Signaling: (inhibit) Wnt/β-Catenin Signaling Pathway: (suppress) Other Pathways and Effects: • Cell Cycle Arrests (commonly G0/G1 or G2/M) • Anti-angiogenic Effects: By inhibiting VEGF • Modulation of Oxidative Stress: Balancing reactive oxygen species (ROS) levels in cancer cells can also contribute to its antitumor effects. • In normal cells or under conditions of oxidative stress, baicalin has been shown to act as an antioxidant. • In cancer cells, baicalin may increase ROS levels, triggering apoptosis. Lower doses of baicalin might favor antioxidant responses, whereas higher concentrations could lead to ROS accumulation in cancer cells. Redox effects are concentration- and context-dependent; antioxidant behavior predominates in non-tumor oxidative stress models, whereas ROS increases have been reported in some tumor systems at higher concentrations. • If copper levels are elevated in a cancer cell, the additional ROS generated via copper-mediated reactions may synergize with baicalin’s pro-oxidant effects (if observed at higher doses) to exceed the threshold for cancer cell survival. • Conversely, in normal cells with tightly regulated copper levels, baicalin’s antioxidant properties may help in quenching excess ROS or maintaining redox balance. -IC50 in cancer cell lines: Approximately 50–200 µM (with some variability depending on the cell type). • IC50 in normal cell lines: Generally higher, often exceeding 200 µM, though values will vary with experimental conditions. Many in-vitro IC50 values exceed achievable systemic concentrations after oral dosing without advanced formulation. Low oral bioavailability: classic rat PK reports very low absolute BA bioavailability and evidence of enterohepatic cycling
Time-Scale Flag (TSF): P / R / G
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| Vimentin, a major constituent of the intermediate filament family of proteins, is ubiquitously expressed in normal mesenchymal cells and is known to maintain cellular integrity and provide resistance against stress. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. In many epithelial-derived tumors (carcinomas), elevated Vimentin expression is often observed in cancer cells that have undergone EMT. This upregulation is characteristic of a shift toward a mesenchymal state, which is associated with reduced cell–cell adhesion and increased motility. Vimentin expression is also noted in the tumor stroma, reflecting the presence and activation of mesenchymal cells such as cancer-associated fibroblasts (CAFs). This dual expression can contribute to the remodeling of the tumor microenvironment. The degree of Vimentin expression may vary depending on the tumor type, grade, and stage. More aggressive and advanced tumors tend to show higher levels of Vimentin expression. High Vimentin expression has been correlated with poor clinical outcomes in several cancers, including breast, colorectal, prostate, and lung cancers. Elevated Vimentin levels are typically associated with higher tumor grade, increased invasiveness, enhanced metastatic potential, and a greater risk of recurrence. As a component of the EMT signature, high Vimentin expression can serve as an indicator of a more aggressive tumor phenotype and is often associated with reduced overall survival. - vimentin up-regulation is often used as a marker of EMT in cancer |
| 1098- | BA, | Baicalein inhibits fibronectin-induced epithelial–mesenchymal transition by decreasing activation and upregulation of calpain-2 |
| - | in-vitro, | Nor, | MCF10 | - | in-vivo, | NA, | NA |
| 2473- | BA, | Baicalin Inhibits EMT through PDK1/AKT Signaling in Human Nonsmall Cell Lung Cancer |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B | - | in-vitro, | Lung, | H460 |
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
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