Baicalin †Botanical
Glucuronide precursor to baicalein that suppresses NF-κB/STAT3 and PI3K→mTOR, promotes apoptosis, reverses EMT, and lowers VEGF/MMPs; may reduce tumor PD-L1. Evidence is largely preclinical with limited human outcomes and PK constraints.
Forms: Baicalin (purified) powder/capsules · Baicalin sodium · Scutellaria baicalensis extract (baicalin/baicalein mixture)
Simple Summary
Baicalin—and its active form, baicalein—turns down survival/growth switches (NF-κB/STAT3 and PI3K→mTOR), nudges tumor cells toward apoptosis, and reduces invasiveness by reversing EMT and lowering VEGF/MMPs. It may also reduce PD-L1 in tumor cells and blunt IL-6→STAT3. Orally, parent baicalin is modest; effects likely come from flexible conversion to baicalein and back.
Evidence at a glance
Strong mechanistic and in-vivo preclinical signals across multiple tumor models; human oncology outcome data limited; pharmacokinetics constrain parent exposure.
How it may work
Baicalin (baicalein 7-O-glucuronide) is hydrolyzed by gut β-glucuronidase to baicalein, absorbed, and largely re-glucuronidated with enterohepatic recycling. Across models, baicalin/baicalein suppress NF-κB and JAK/STAT3 signaling, downshift PI3K/Akt→mTOR growth pathways, and induce mitochondrial apoptosis (Bax↑/Bcl-2↓, caspase-3/PARP cleavage). They curb angiogenesis and invasion via VEGF and MMP-2/9 reduction, reverse EMT (E-cadherin↑; vimentin/Slug↓; TGF-β/Smad3 blockade), and modulate autophagy in a context-dependent fashion. Immune-relevant effects include lowering tumor PD-L1 (e.g., IFN-γ–induced) and dampening IL-6→STAT3 signaling. Oral parent baicalin is low; activity likely reflects dynamic interconversion with baicalein and conjugates.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- Cisplatin: Chemosensitization in preclinical models.
- Curcumin: Convergent NF-κB/cytokine suppression.
- EGCG: EMT/CSC program interference.
Overlapping mechanisms
- NF-κB, STAT3, PI3K/Akt/mTOR, EMT, VEGF/MMP-2/9: Avoid stacking many agents with identical endpoints without rationale and monitoring.
Safety & interactions
Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.
- anticoagulants / antiplateletsMonitorMinorTheoreticalPotential additive effects on hemostasis.
- drugs with narrow therapeutic index metabolized by UGT/CYPMonitorMinorTheoreticalPossible enzyme modulation; evidence mainly preclinical.
Timing
- Anytime: Consistency > clock time; consider splitting if GI upset.
- With food: Optional for GI comfort.
References
- Wang 2018 — STAT3 targeting
- Liu 2020 — EMT via TGF-β1/Smad3
- Zhou 2017 — EMT/metastasis ↓ in vivo
- Wang 2024 — Anti-VEGF/MMPs review
- Huang 2016 — Endothelial/angiogenesis
- Ke 2019 — PD-L1 ↓ with IFN-γ
- Guo 2024 — SOCS1↑; NF-κB/STAT3↓
- Sui 2021 — PI3K/Akt & apoptosis
- Noh 2016 — PK: gut conversion/enterohepatic
- Ganguly 2022 — PK + actions review
- Zhang 2013 — Comparative PK
Research
No published studies for Baicalin †Botanical yet
New studies appear here once they’ve been reviewed. Browse all studies.
Trials studying Baicalin †Botanical
No actively-recruiting trials matched right now. Recruiting is not the same as proven. Search ClinicalTrials.gov →