Compound Monograph
Vitexin
Vitexin (apigenin-8-C-glucoside) is a flavone C-glycoside marker of hawthorn, passionflower and millet, with a broad but entirely preclinical antioxidant, cardioprotective, anti-inflammatory and neuroprotective profile — plus a distinctive antithyroid (goitrogen) signal. Its carbon-bonded sugar resists hydrolysis, yet its oral bioavailability is only a few percent, and there are no human trials of the isolate.
Sources · 12
Where Does It Come From?
Vitexin is a naturally occurring flavonoid (flavone c-glycoside), found in Hawthorn, Passionflower and 10 other sources. It is well tolerated orally (low toxicity).
Principal source Hawthorn Crataegus oxyacantha Herb monograph →
Source Blue Passionflower Passiflora caerulea Herb monograph →
Source Chickweed Stellaria media Herb monograph →
Source Guamura Cecropia obtusifolia Herb monograph →
Source Passion Fruit Passiflora edulis Herb monograph →
Source Passionflower Passiflora incarnata Herb monograph →
Source Stinking Passionflower Passiflora foetida Herb monograph →
Source Tick Trefoil Desmodium spp. Herb monograph →
Source Winged-Stem Passionflower Passiflora alata Herb monograph → Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Vitexin at a Glance
Vitexin is a flavone C-glycoside — specifically apigenin-8-C-glucoside, a molecule of apigenin carrying a single glucose unit joined through a carbon–carbon bond at the 8-position. It is a widespread dietary flavonoid and a pharmacopoeial marker used to standardise hawthorn and passionflower extracts, and it is one of the three major C-glucosylflavones of pearl millet. In each of these it usually sits as one of several co-occurring C-glycosylflavones (with isovitexin, orientin, isoorientin and schaftoside) rather than a dominant constituent 1Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study →.
Its preclinical profile is genuine and broad — cardioprotective, anti-inflammatory, neuroprotective/anxiolytic, antihypertensive and anticancer effects are each reported in cell and rodent models 1,
Two features make vitexin worth its own page. First, its carbon-bonded sugar resists hydrolysis, yet its oral bioavailability is only a few percent — the isolate caveat that runs through the pharmacology 1,
Vitexin vs. Isovitexin, Orientin & the C-Glycosides
Vitexin is easy to confuse with three near-identical siblings, and the herbal literature routinely lists them together as the “flavone C-glycosides” of a plant. The distinctions are small but consequential:
| Compound | Aglycone | Sugar position |
|---|---|---|
| Vitexin | apigenin (4’-OH B-ring) | glucose at C-8 |
| Isovitexin (saponaretin) | apigenin | glucose at C-6 |
| Orientin | luteolin (3’,4’-diOH B-ring) | glucose at C-8 |
| Isoorientin (homoorientin) | luteolin | glucose at C-6 |
Two axes separate them: the aglycone (apigenin, with a single B-ring hydroxyl, versus luteolin, with a catechol) and the position of C-glycosylation (C-8 versus C-6). Vitexin and isovitexin are positional isomers — apigenin-8-C-glucoside versus apigenin-6-C-glucoside.
The instructive twist is antioxidant activity. In the classic study of C-glycosylflavones from chickweed (Stellaria media), antioxidative activity was found only for orientin and isoorientin — the two luteolin-based (catechol) glycosides — and not for the apigenin-based vitexin and isovitexin 2Reference 2Studies on antioxidative activity of some C-glycosylflavonesView study →. The extra B-ring hydroxyl of luteolin is the usual explanation. So among the quartet, vitexin is the weaker direct antioxidant twin: much of its own pharmacology therefore rests less on raw radical-scavenging and more on signalling effects (kinase, NF-κB, apoptotic and calcium pathways) than orientin’s does.
C-Glycoside Stability & Bioavailability
The single most important thing to understand about vitexin’s pharmacology is what its carbon–carbon bond does — and does not — buy it.
In an ordinary flavonoid O-glycoside, the sugar hangs off an oxygen atom and is readily cleaved: stomach acid, intestinal glycosidases and gut bacteria hydrolyse it, releasing the free aglycone that is often the truly absorbed species. Vitexin is a C-glycoside — the glucose is bolted directly to the flavone carbon skeleton — so it resists that hydrolysis and travels largely as the intact glycoside 1Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study →. This stability is real and is part of why C-glycosylflavones are robust dietary and pharmacopoeial markers.
The intuitive expectation — that a stable molecule should therefore be well absorbed — does not hold. Vitexin’s oral bioavailability is low, reported in rats at only a few percent (on the order of ~3–5%), the consequence of poor aqueous solubility, limited intestinal permeability and extensive first-pass handling 1,
What It's Used For
Vitexin’s evidence is a preclinical machine: cell and rodent studies of the isolate, plus umbrella reviews. The split that matters is which tissue (heart and vasculature dominate) and the fact that no rung of it is human.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. There is no human evidence for isolated vitexin, so every score is capped by design — these rank preclinical strength, not clinical proof.
Vitexin’s best-developed thread, and all of it the isolated molecule. In Langendorff-perfused rat hearts subjected to ischaemia/reperfusion, vitexin (50–200 µmol/L) raised coronary flow, lowered injury scores and was anti-apoptotic and anti-inflammatory — up-regulating Bcl-2 while down-regulating Bax and NF-κB-p65 and cutting myocardial TNF-α and IL-1β 5Reference 5AnimalVitexin protects against myocardial ischemia/reperfusion injury in Langendorff-perfused rat hearts by attenuating inflammatory response and apoptosisView study →.
In a separate model, vitexin from hawthorn leaf (Crataegus pinnatifida) prevented cardiac hypertrophy in cultured myocytes and in pressure-overloaded mice by inhibiting the calcium effectors calcineurin-NFATc3 and CaMKII 6Reference 6Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathwaysView study →.
This is the mechanistic backbone of hawthorn’s marker story — though the effect belongs to the isolate, not the standardised extract.
Gap: every study is rodent or cell, on the isolate; there are no human cardiac trials, and vitexin’s poor oral bioavailability 1,
A well-characterised isolate signal spanning in-vitro and in-vivo work. In LPS-stimulated cells and in a mouse peritonitis model, vitexin reduced neutrophil migration and lowered TNF-α, IL-1β and nitric oxide by down-regulating p38, ERK1/2 and JNK phosphorylation 3Reference 3Vitexin reduces neutrophil migration to inflammatory focus by down-regulating pro-inflammatory mediators via inhibition of p38, ERK1/2 and JNK pathwayView study →.
In murine ovalbumin-induced allergic asthma, vitexin cut eosinophil/neutrophil infiltration, mucus and Th2 cytokines and IgE 4Reference 4AnimalVitexin inhibits inflammation in murine ovalbumin-induced allergic asthmaView study →.
The NF-κB/MAPK axis recurs across the cardio- and reno-protective studies, making inflammation a unifying mechanism rather than a standalone claim.
Gap: isolate + rodent/cell only; no human inflammation data, and the in-vivo doses are not translated to a human-relevant oral exposure 3,
Mechanistically tidy, but especially undercut by delivery. Reviews collect neuroprotective isolate work in which vitexin restores SOD/catalase/GSH-px, curbs ROS and lipid peroxidation, engages PI3K/Akt and ERK1/2 survival signalling while inhibiting JNK/p38 apoptosis, and reduces NMDA-receptor–driven excitotoxicity 7Reference 7ReviewA Brief Review on the Neuroprotective Mechanisms of VitexinView study →.
Behaviourally, vitexin produced a GABAergic anticonvulsant and anxiolytic-like effect in mice — protecting against picrotoxin/PTZ seizures (up to 100% at the top dose) but not glutamate-agonist seizures, implicating GABA neurotransmission 8Reference 8AnimalVitexin Possesses Anticonvulsant and Anxiolytic-Like Effects in Murine Animal ModelsView study →.
Gap: isolate + rodent/cell only; brain delivery is doubtful given the low oral bioavailability 1,
A broad but wholly preclinical signal, collated in a 2025 mechanistic review 9Reference 9Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer FunctionsView study →. Across cancer cell lines and xenografts, vitexin drives cell-cycle arrest (↓cyclin D1, ↑p21/p27), caspase-dependent apoptosis (↓Bcl-2, ↑Bax, mitochondrial-membrane collapse), anti-metastatic/anti-angiogenic effects (↓MMPs, ↓VEGF via STAT3 and NF-κB), and suppression of the glycolytic Warburg phenotype 9Reference 9Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer FunctionsView study →.
Gap: the review itself stresses that the evidence “predominantly relies on in vitro and animal models,” that oral bioavailability is only ~2.8% in rats, and that “well-designed phase I/II clinical trials are needed” before any clinical claim 9Reference 9Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer FunctionsView study →.
In spontaneously hypertensive rats fed a high-sugar/high-fat diet to model hypertensive nephropathy, oral vitexin significantly lowered systolic, diastolic and mean arterial pressure, improved kidney markers (↓creatinine, ↓BUN, ↓microalbuminuria) and shifted the redox/inflammatory balance (↑SOD, ↓MDA, ↓TNF-α, ↓IL-6), with the authors implicating NF-κB suppression 12Reference 12AnimalThe Protective Effect of Vitexin on Hypertensive Nephropathy RatsView study →.
Gap: a single rodent isolate study; no human blood-pressure data, and the antihypertensive framing overlaps the general anti-inflammatory/antioxidant mechanism rather than a dedicated vascular one 12Reference 12AnimalThe Protective Effect of Vitexin on Hypertensive Nephropathy RatsView study →.
The property most often assumed and least supported for vitexin specifically. In the head-to-head chickweed assay of the four C-glycosylflavones, antioxidant activity belonged to the luteolin-based orientin and isoorientin — vitexin and isovitexin were essentially inactive 2Reference 2Studies on antioxidative activity of some C-glycosylflavonesView study →.
Vitexin does contribute to restored antioxidant-enzyme activity (SOD/catalase/GSH-px) in the tissue-protection studies above, but that is a cellular, signalling-mediated effect rather than the potent direct radical-scavenging its luteolin twins show.
Gap: direct antioxidant capacity is weak for the apigenin-based glycoside; the “antioxidant” label is better read as the antioxidant-enzyme restoration seen inside the cardio/neuro models 2,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Mitochondrial apoptotic pathway (Bcl-2 ↑, Bax ↓) | anti-apoptotic — blocks intrinsic cell-death cascade | cardioprotection; neuroprotection; anticancer (context-dependent) |
| p38 / ERK1/2 / JNK (MAPK) | phosphorylation down-regulated → ↓pro-inflammatory mediators | anti-inflammatory; neuroprotection |
| NF-κB | suppressed → ↓TNF-α, IL-1β, IL-6, iNOS/NO | anti-inflammatory; cardio/reno-protection |
| Calcineurin-NFATc3 / CaMKII | inhibited calcium-hypertrophy signalling | anti-hypertrophic cardioprotection |
| PI3K/Akt survival signalling | activated → neuronal survival | neuroprotection |
| GABAergic neurotransmission | modulated → anticonvulsant / anxiolytic-like | CNS / anxiety |
| Antioxidant enzymes (SOD, catalase, GPx) | restored inside injured tissue (not potent direct scavenging) | tissue protection |
| Thyroid peroxidase (TPO) | inhibited → impaired iodination/coupling | antithyroid / goitrogen (adverse) |
The load-bearing point is that vitexin’s benefits are mostly a signalling story — NF-κB/MAPK, calcium and apoptotic pathways — not the raw radical-scavenging that carries its luteolin twins. Almost all of it is in-vitro or rodent, on the isolate. The TPO row is the one mechanism that is a liability rather than an asset.
Pharmacokinetics
Vitexin’s pharmacokinetics are the crux of its translation problem. Because the sugar is C-linked, vitexin is not appreciably hydrolysed to free apigenin in the upper gut, so — unlike an O-glycoside — the aglycone is not the absorbed species 1Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study →. Yet the intact glycoside is poorly absorbed: rat studies put its absolute oral bioavailability at only a few percent (roughly ~3–5%, and reported as low as ~2.8%), reflecting poor aqueous solubility, limited intestinal permeability and extensive first-pass handling, with rapid elimination once in plasma 1,
Clinical Trials
There are no clinical trials of isolated vitexin. The entire evidence base is preclinical (cell and rodent). The nearest human-relevant data belong to whole Passiflora and Crataegus extracts in which vitexin is only a marker 1,
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| None(isolate) | — | — | Cardioprotection, anti-inflammatory, neuroprotection/anxiolytic, anticancer, antihypertensive (all cell/rodent) |
Last checked: July 2026.
Vitexin, Millet & the Thyroid
Vitexin is unusual among “healthful” flavonoids in carrying a documented antithyroid action, and the story is worth stating plainly because it inverts the usual benefit framing. Diets heavy in pearl millet — a staple in parts of semi-arid Africa and India — are associated with goitre, and the C-glucosylflavones of millet are the leading suspects 11Reference 11Antithyroid and goitrogenic effects of millet: role of C-glycosylflavonesView study →. Vitexin is one of the three major C-glucosylflavones of millet, and in a dedicated study it produced antithyroid effects both in vitro and in vivo: it (and its glycoside glucosylvitexin) inhibited thyroid peroxidase (TPO) — the enzyme that iodinates tyrosine and couples iodotyrosines into thyroid hormone — and in rats interfered specifically with the coupling step, lowering T3/T4 while sparing iodide uptake 10Reference 10In vitroAntithyroid effects in vivo and in vitro of vitexin: a C-glucosylflavone in milletView study →. Millet-bran extracts inhibited TPO in proportion to their C-glycosylflavone content 11Reference 11Antithyroid and goitrogenic effects of millet: role of C-glycosylflavonesView study →.
This is a mechanistic and dietary-epidemiological signal, not an acute toxicity, and it matters most in the context of iodine deficiency (where any additional goitrogen load has a larger effect) and of heavy, chronic millet intake — not the trace exposure from a cup of hawthorn or passionflower tea. Still, it is the single most compound-specific caution here, and it is the reason the antioxidant/anti-inflammatory “good flavonoid” reading of vitexin should not be taken as unconditional.
Isolate vs. Plant Studies
The evidence divides cleanly. The mechanistic and protective work is the isolated molecule — the Langendorff ischaemia/reperfusion hearts 5Reference 5AnimalVitexin protects against myocardial ischemia/reperfusion injury in Langendorff-perfused rat hearts by attenuating inflammatory response and apoptosisView study →, the calcineurin/CaMKII anti-hypertrophy study 6Reference 6Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathwaysView study →, the neutrophil-migration and allergic-asthma anti-inflammatory work 3,
The one place a plant vitexin marks has human-relevant activity is passionflower — and there the effect is explicitly the whole extract’s: an HPLC-characterised Passiflora incarnata extract (vitexin among its C-glycoside markers) was anxiolytic via the GABAergic system, comparable to diazepam, in mice, and the mechanism is generally credited to other flavonoids (apigenin/chrysin-type) rather than vitexin 14Reference 14Anxiolytic activity of a phytochemically characterized Passiflora incarnata extract is mediated via the GABAergic systemView study →. Similarly, hawthorn’s cardiac reputation rests on the standardised leaf/flower extract, with vitexin serving as a quantitation marker, not the sole active. So the correct framing is: solid isolate mechanism in heart, vasculature and immune cells + no human isolate data + plant-level effects (passionflower anxiolysis, hawthorn cardiotonic) that are not vitexin’s alone to claim.
Its Role in Plants
Vitexin is a flavone C-glycoside built on the general flavonoid pathway. Its defining C-glycosylation is installed not on the finished flavone but on an intermediate: a 2-hydroxyflavanone (from the apigenin branch) is C-glucosylated by a C-glycosyltransferase (CGT), and dehydration then yields the flavone C-glycoside 13Reference 13Indirect and direct routes to C-glycosylated flavones in Saccharomyces cerevisiaeView study →. This “indirect” route produces mixtures of the 6-C and 8-C isomers — isovitexin and vitexin — whereas a “direct” route, in which certain CGTs glycosylate the finished flavone, tends to favour the 6-C product (isovitexin); 3’-hydroxylation of the substrate shifts the balance toward the luteolin-based 8-C glycoside (orientin) instead 13Reference 13Indirect and direct routes to C-glycosylated flavones in Saccharomyces cerevisiaeView study →.
Functionally, C-glycosylflavones like vitexin contribute to a plant’s antioxidant and UV-protective flavonoid pool and to stress and defence chemistry; in passionflower, tissue vitexin rises with mechanical wounding and silicon supplementation, consistent with a stress-responsive role. As with any constituent, this plant-biology role does not translate into a human-pharmacology claim.
Prevalence in Nature
Vitexin is widespread but rarely dominant. It occurs across several plant families, typically as one of a set of co-occurring C-glycosylflavones (vitexin, isovitexin, orientin, isoorientin, schaftoside). Documented sources include hawthorn (Crataegus spp., leaf and flower — the part used in standardised cardiac extracts) 6Reference 6Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathwaysView study →, passionflower (Passiflora incarnata, aerial parts, where it is a pharmacopoeial marker) 1,
Where it has been studied, vitexin is treated as a marker for standardisation rather than a headline concentration — reliable comparative content figures across these matrices are not well consolidated in the accessible literature (the holes are tracked in this compound’s gaps file). In hawthorn and passionflower it is a minor flavonoid within a larger C-glycoside set; in millet it is abundant enough to carry the goitrogen signal 11Reference 11Antithyroid and goitrogenic effects of millet: role of C-glycosylflavonesView study →.
Major Natural Sources
| Source | Plant part | Role / note |
|---|---|---|
| Hawthorn (Crataegus spp.) | leaf & flower | standardisation marker of cardiac extracts 6Reference 6Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathwaysView study → |
| Passionflower (Passiflora incarnata) | aerial parts | pharmacopoeial C-glycoside marker 1, |
| Pearl millet (Pennisetum glaucum) | grain / bran | one of three major C-glucosylflavones; goitrogen source 10, |
| Mung bean, bamboo leaf, Ficus deltoidea | seed / leaf | reported dietary/herbal sources 1Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study → |
These are qualitative source assignments, not whole-plant percentages; documented vitexin content shifts with species, plant part, processing and analytical method, and precise ranges are not consolidated here.
Discovery & Synthesis
Vitexin is a long-known flavone C-glycoside whose name derives from the genus Vitex, from which early flavone C-glycosides were characterised. The precise date and author of its first isolation are not well documented in the accessible literature, and it entered pharmacology as one of a cluster of flavone C-glycosides identified across many species through the 20th century.
Modern synthesis of vitexin is chiefly of interest for supply and study rather than commerce: because direct chemical C-glycosylation is difficult, recent work reconstructs the biosynthetic route in engineered microbes — expressing a C-glycosyltransferase (with, for the indirect route, a flavanone 2-hydroxylase) in Saccharomyces cerevisiae to build vitexin and its isomers from flavonoid precursors 13Reference 13Indirect and direct routes to C-glycosylated flavones in Saccharomyces cerevisiaeView study →. There is no large-scale commercial manufacture; material for research is obtained by extraction from rich sources (hawthorn, millet, mung bean) or by such biosynthetic routes.
Patents: not yet researched.
Toxicity & Safety
Vitexin carries a low toxicity flag. It is a constituent of ordinary foods and beverages — millet, mung bean, and hawthorn/passionflower teas — consumed for generations without an acute safety signal attached to the molecule, and its poor absorption further limits systemic exposure 1,
The one substantive caveat is the thyroid one. Vitexin is a documented thyroid-peroxidase inhibitor and goitrogen, and heavy, chronic millet intake — the dietary setting where vitexin is abundant — is associated with goitre, especially against a background of iodine deficiency 10,
- Low-toxicity dietary flavonoid. A normal constituent of millet, mung bean and herbal teas, with no acute safety signal and limited systemic absorption 1,
9Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study →Reference 9Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer FunctionsView study → . - Antithyroid / goitrogen signal. Vitexin inhibits thyroid peroxidase; heavy chronic millet intake is linked to goitre, especially with iodine deficiency 10,
11Reference 10In vitroAntithyroid effects in vivo and in vitro of vitexin: a C-glucosylflavone in milletView study →Reference 11Antithyroid and goitrogenic effects of millet: role of C-glycosylflavonesView study → . - All efficacy evidence is preclinical. No human trials of the isolate exist — efficacy and safety in people are simply unknown.
- Poor bioavailability undercuts potency. In-vitro and rodent effects occur at exposures an oral dose (~a few percent absorbed) may not reach; do not read the mechanistic results as a delivered human benefit 1,
9Reference 1ReviewA review on the pharmacological effects of vitexin and isovitexinView study →Reference 9Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer FunctionsView study → . - Marker, not proven active, in its herbs. Its presence does not make vitexin responsible for a herb’s effect — passionflower anxiolysis and hawthorn’s cardiotonic action are the whole extracts’ 14Reference 14Anxiolytic activity of a phytochemically characterized Passiflora incarnata extract is mediated via the GABAergic systemView study →.
Dosage
There is no established or recommended human dose for isolated vitexin. The figures in the literature are preclinical: cell-culture concentrations (typically low micromolar, e.g. 50–200 µmol/L in isolated-heart work 5Reference 5AnimalVitexin protects against myocardial ischemia/reperfusion injury in Langendorff-perfused rat hearts by attenuating inflammatory response and apoptosisView study →) and rodent doses (e.g. 30–100 mg/kg in the cardio-, reno- and anti-inflammatory models 4,
Real human exposure is dietary and indirect — vitexin arrives as one C-glycosylflavone within hawthorn and passionflower products (whose dosing is set at the standardised-extract level, not the molecule level) and within millet-based foods. These are research figures and food-exposure notes, not a personal recommendation.
References
- He M, Min JW, Kong WL, He XH, Li JX, Peng BW (2016). A review on the pharmacological effects of vitexin and isovitexin. Fitoterapia. https://pubmed.ncbi.nlm.nih.gov/27693342/
- Budzianowski J, et al. (1991). Studies on antioxidative activity of some C-glycosylflavones. Polish Journal of Pharmacology and Pharmacy. https://pubmed.ncbi.nlm.nih.gov/1824129/
- Rosa SIG, Rios-Santos F, Balogun SO, Martins DTO (2016). Vitexin reduces neutrophil migration to inflammatory focus by down-regulating pro-inflammatory mediators via inhibition of p38, ERK1/2 and JNK pathway. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/26902402/
- Venturini CL, Macho A, Arunachalam K, et al. (2018). Vitexin inhibits inflammation in murine ovalbumin-induced allergic asthma. Biomedicine & Pharmacotherapy. https://pubmed.ncbi.nlm.nih.gov/29091859/
- Dong L, Fan Y, Shao X, Chen Z (2011). Vitexin protects against myocardial ischemia/reperfusion injury in Langendorff-perfused rat hearts by attenuating inflammatory response and apoptosis. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/22001368/
- Lu CC, Xu YQ, Wu JC, et al. (2013). Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathways. Naunyn-Schmiedeberg’s Archives of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/23624753/
- Lima LKF, Pereira SKS, Junior RDSS, et al. (2018). A Brief Review on the Neuroprotective Mechanisms of Vitexin. BioMed Research International. https://pubmed.ncbi.nlm.nih.gov/30627560/
- de Oliveira DD, da Silva CP, Iglesias BB, Beleboni RO (2020). Vitexin Possesses Anticonvulsant and Anxiolytic-Like Effects in Murine Animal Models. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/32848784/
- Lu L, Deng Y, Li J, Feng X, Zou H (2025). Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/40565318/
- Gaitan E, Cooksey RC, Legan J, Lindsay RH (1995). Antithyroid effects in vivo and in vitro of vitexin: a C-glucosylflavone in millet. Journal of Clinical Endocrinology & Metabolism. https://pubmed.ncbi.nlm.nih.gov/7714083/
- Gaitan E, Lindsay RH, Reichert RD, et al. (1989). Antithyroid and goitrogenic effects of millet: role of C-glycosylflavones. Journal of Clinical Endocrinology & Metabolism. https://pubmed.ncbi.nlm.nih.gov/2921306/
- Duan T, Li M, Lin Z, et al. (2024). The Protective Effect of Vitexin on Hypertensive Nephropathy Rats. Kidney and Blood Pressure Research. https://pubmed.ncbi.nlm.nih.gov/39079512/
- Vanegas KG, Larsen AB, Eichenberger M, Fischer D, Mortensen UH, Naesby M (2018). Indirect and direct routes to C-glycosylated flavones in Saccharomyces cerevisiae. Microbial Cell Factories. https://pubmed.ncbi.nlm.nih.gov/29986709/
- Grundmann O, Wang J, McGregor GP, Butterweck V (2008). Anxiolytic activity of a phytochemically characterized Passiflora incarnata extract is mediated via the GABAergic system. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/19006051/
