Named Bioactive Compounds · Compound
Vicenin-2 (Flavone C-glycoside)
Moderate Evidenceflavonoid4 PubMed Studies
Hermetica Superfood Encyclopedia
Vicenin-2 is a flavone C-glycoside compound found in certain plants that exhibits anti-cancer properties through apoptosis induction. This bioactive flavonoid demonstrates selective cytotoxicity against colon and prostate cancer cells by targeting multiple cellular pathways.
Vicenin-2 is a flavone C-glycoside (apigenin-6,8-di-C-glucoside) found in medicinal plants including Ocimum sanctum (holy basil) and Urtica circularis (stinging nettle). It is extracted from plant sources using solvent extraction followed by chromatographic isolation. As a dietary flavonoid, it belongs to the C-glycosylflavones class, characterized by sugar moieties directly bound to the flavone backbone via carbon linkages.
No human clinical trials, RCTs, or meta-analyses have been conducted on Vicenin-2. All available evidence comes from preclinical studies including in vitro cell lines and animal models (PMID: 29849451, 21803027). In prostate cancer xenograft models, oral Vicenin-2 achieved serum levels of 2.6 µmol/L and showed synergistic effects with docetaxel chemotherapy.
No clinically studied human dosages exist. Preclinical studies used 50 µM concentrations in cell cultures and oral administration achieving 2.6±0.3 µmol/L serum levels in mice. No standardized extract forms or human dosing data are available. Consult a healthcare provider before starting any new supplement.
Vicenin-2 (apigenin-6,8-di-C-glucoside) is a flavone C-glycoside with molecular formula C27H30O15 and molecular weight 594.52 g/mol. It is not a macronutrient source and does not contribute calories, protein, fat, or fiber in physiologically relevant amounts. As a bioactive polyphenolic compound, it is found naturally in various plant sources including: Ocimum sanctum (holy basil) at approximately 0.5–2.0 mg/g dry weight, Cyclopia subternata (honeybush tea) at roughly 1.0–4.5 mg/g dry weight, Dendrobium officinale at approximately 0.3–1.5 mg/g dry weight, mung bean sprouts (Vigna radiata) at approximately 0.1–0.8 mg/g dry weight, and in lesser concentrations in fenugreek, chamomile, and passionflower. Unlike flavone O-glycosides, the C-glycosidic bond in vicenin-2 is resistant to hydrolysis by mammalian β-glucosidases and most gut microbial enzymes, resulting in the compound being absorbed largely intact. Oral bioavailability is generally considered low to moderate (estimated <10–15% in rodent models), with absorption occurring primarily in the small intestine via passive diffusion and possibly sodium-dependent glucose transporter (SGLT1)-mediated pathways. Peak plasma concentrations (Tmax) are typically reached within 1–3 hours post-ingestion. The compound exhibits strong antioxidant capacity (ORAC values comparable to other apigenin glycosides), with notable free radical scavenging of superoxide, hydroxyl, and DPPH radicals (IC50 values in the range of 20–80 µM depending on assay). It contains no vitamins or minerals intrinsically but co-occurs in plant matrices alongside vitamin C, B-vitamins, potassium, magnesium, iron, and dietary fiber. The C-glycoside linkage confers greater metabolic stability and a longer plasma half-life (estimated 4–8 hours) compared to corresponding O-glycosides such as apigenin-7-O-glucoside. No significant interactions with major drug-metabolizing enzymes (CYP450 family) have been reported at dietary intake levels, though in vitro data suggest mild inhibition of CYP1A2 and CYP3A4 at high concentrations (>100 µM). Typical dietary intake from food sources is estimated at 1–10 mg/day depending on consumption patterns of source plants.
Vicenin-2 induces apoptosis in cancer cells through mitochondrial pathway activation and caspase cascade stimulation. The compound inhibits angiogenesis by suppressing VEGF signaling and reduces tumor cell proliferation by modulating cell cycle regulatory proteins. Its flavone structure allows interaction with multiple molecular targets involved in cancer progression.
Current evidence for vicenin-2 comes primarily from in vitro cell studies and animal xenograft models. Cell studies showed 50 µM IC50 against HT-29 colon cancer cells and apoptosis induction. Mouse xenograft studies demonstrated tumor growth reduction in PC-3 and DU145 prostate cancer models. No human clinical trials have been conducted to establish therapeutic efficacy or optimal dosing.
Safety data for vicenin-2 supplementation in humans is currently unavailable due to lack of clinical studies. Potential interactions with chemotherapy drugs or blood thinners remain unknown and require investigation. Pregnancy and breastfeeding safety has not been established. Individuals with hormone-sensitive cancers should exercise caution due to unknown effects on hormonal pathways.
