Verbascoside

• CAS: 22323-52-0
• Catalog Number: ACM22323520
• Category: Main Products
• Molecular Weight: 624.59
• Molecular Formula: C₂₉H₃₆O₁₅
• IUPAC Name: [(2R,3R,4R,5R,6R)-6-[2-(3,4-dihydroxyphenyl)ethoxy]-5-hydroxy-2-(hydroxymethyl)-4-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-3-yl](E)-3-(3,4-dihydroxyphenyl)prop-2-enoate
• Canonical SMILES: CC1C(C(C(C(O1)OC2C(C(OC(C2OC(=O)C=CC3=CC(=C(C=C3)O)O)CO)OCCC4=CC(=C(C=C4)O)O)O)O)O)O
• InChI Key: FBSKJMQYURKNSU-ZLSOWSIRSA-N
• EC Number: 612-110-1

Case Study

Verbascoside Inhibits Oral Squamous Cell Carcinoma Progression by Targeting METTL3-Regulated miR-31-5p/HIPK2 Axis

Huang Y, et al. Archives of Oral Biology, 2024, 164, 105979.

Verbascoside demonstrates potent anti-cancer properties, particularly in oral squamous cell carcinoma (OSCC). This study investigates its functional and molecular roles in suppressing OSCC progression.
Functional assays revealed that verbascoside significantly inhibits OSCC cell proliferation, migration, and invasion in SCC9 and UM1 cell lines. Mechanistically, verbascoside downregulates methyltransferase-3 (METTL3) expression, disrupting the METTL3-regulated miR-31-5p/HIPK2 axis. METTL3, which is overexpressed in OSCC, facilitates the N6-methyladenosine (m6A)-dependent processing of miR-31-5p, a microRNA implicated in promoting cellular migration and invasion. Verbascoside-mediated inhibition of METTL3 reduces miR-31-5p levels, thereby preserving the tumor-suppressive activity of its target, homeodomain interacting protein kinase-2 (HIPK2).
Overexpression of METTL3 or miR-31-5p, as well as HIPK2 knockdown, reverses the inhibitory effects of verbascoside, underscoring the compound's role in this regulatory pathway. These findings highlight verbascoside's therapeutic potential in OSCC treatment by targeting critical molecular drivers of tumor progression.

Verbascoside: A Multifaceted Therapeutic for Gut-Brain Axis Modulation in Depression Treatment

Mao Q, et al. Phytomedicine, 2024, 129, 155510.

Verbascoside demonstrates significant therapeutic potential in addressing depression through its modulation of the gut-brain axis (GMBA). Studies reveal its pivotal role in mitigating depression-like behaviors by restoring GMBA homeostasis. Verbascoside enhances gut and brain health, alleviating neuronal damage and synaptic dysfunction caused by chronic stress.
In preclinical models, verbascoside reversed gut microbiota disturbances by promoting beneficial strains such as Lactobacillus, Parabacteroides, Bifidobacterium, and Ruminococcus. This modulation reduced intestinal permeability and blood-brain barrier leakiness, curbing systemic and central inflammation. Furthermore, in vitro studies highlighted verbascoside's neuroprotective properties against corticosterone-induced cytotoxicity, preserving neuronal integrity.
Faecal microbiota transplantation (FMT) experiments confirmed the causality between verbascoside's modulation of gut microbiota and its antidepressant efficacy. The compound restored neurotransmitter and brain-gut peptide levels in the prefrontal cortex, underscoring its multi-pathway mechanism.

Verbascoside: A Multifaceted Antidepressant with Diverse Mechanisms of Action

Zhao Y, et al. Phytomedicine, 2023, 120, 155027.

Mechanistically, verbascoside enhances dopamine biosynthesis by upregulating tyrosine hydroxylase mRNA and protein levels and modulates serotoninergic activity via the 5-hydroxytryptamine receptor 1B (5-HT1B). It also increases the expression of neuroprotective and autophagy-related markers such as microtubule-associated protein 2 (MAP2), hemeoxygenase-1 (HO-1), and Beclin-1 while suppressing apoptosis by downregulating caspase-3 and α-synuclein. Key molecular targets like CCL2, FOS, and GABARAPL1, and pathways such as glutathione metabolism and cytochrome P450-mediated xenobiotic metabolism, further elucidate its pharmacological profile.
Applications of verbascoside extend to in vivo and in vitro depression models, where it effectively combats oxidative stress, mitigates neuroinflammation, and restores neural homeostasis. While its preclinical efficacy is well-documented, advancing its clinical application will require multicenter studies to validate these findings and explore its full therapeutic potential.