Wogonin.

Wogonin and baicalin occur together in Scutellaria baicalensis root and are absorbed as a set after gut bacterial deglucuronidation. They share the same beta-glucuronidase step and the same UGT conjugation on the way out.

Baicalein is the aglycone that travels with wogonin in the same root extract. Both are flavones handled by the same conjugating enzymes, so exposure to one tracks the other in practice.

Wogonin is delivered in supplements as part of the standardised Scutellaria root flavone profile. The whole extract carries the glycoside forms that gut bacteria convert into the circulating aglycones.

Quercetin and wogonin are both cleared by UGT and sulfotransferase conjugation in gut wall and liver. Taken together they compete for the same enzymes, which raises the free fraction of each.

Wogonin undergoes heavy first-pass glucuronidation. Piperine inhibits UGT activity in the intestinal wall, which is why it is added to flavone extracts to raise systemic exposure.

Ascorbate can reduce a flavonoid phenoxyl radical back to the parent phenol, which extends how long the flavone stays in its reduced form. This is the standard flavonoid and ascorbate recycling relationship.

Flavones carry hydroxyl and keto groups that chelate ferrous and ferric iron in the gut lumen and lower non-heme iron uptake. Separating a flavone-rich extract from an iron dose by a couple of hours keeps both intact.

A 2025 animal study paired ferulic acid with wogonin and reported changes in gut microbiota composition and bile acid handling that neither compound produced alone to the same degree. Both are plant phenolics with overlapping effects on inflammatory signalling. The finding is preclinical and describes markers in rodents. It does not establish a human effect.

Wogonin is a lipophilic flavone with low aqueous solubility, which limits how much dissolves in the gut lumen. Complexing a flavonoid with phosphatidylcholine forms a phytosome that disperses more readily and improves measured plasma exposure for several flavonoids. The improvement is in pharmacokinetics, a marker. Formulation, not dose alone, governs what is absorbed.

Lecithin phospholipids emulsify poorly soluble compounds and support micelle formation in the small intestine. Wogonin depends on that dispersion because it is barely soluble in water. This is a formulation mechanism common to most flavone actives. It changes absorption, not the compound's activity.

Medium-chain triglycerides provide a lipid phase that keeps lipophilic actives in solution through gastric transit and into bile-salt micelles. Wogonin's low aqueous solubility makes it dependent on that phase. Taking the extract with a fat-containing meal does the same thing. The effect is on absorption.

Skullcap root, the source of wogonin, is combined with licorice across classical formula construction, where licorice is used as a harmonising component. Glycyrrhizin also inhibits 11-beta-hydroxysteroid dehydrogenase type 2, which affects sodium and potassium handling at higher intakes and over longer periods. The pairing is traditional rather than measured. The licorice consideration is independent of the wogonin.

Gan cao appears alongside huang qin, the skullcap root that supplies wogonin, in classical multi-herb formulas. The pairing is a convention of formula construction rather than a demonstrated pharmacological synergy. Glycyrrhizin content carries its own dose and duration considerations. The basis here is traditional use.

Dang gui and huang qin appear together across traditional formulas, and combination effects have been described mainly in preclinical work on whole formulas rather than on isolated wogonin. Attributing anything to the flavone alone from a multi-herb study is not possible. The pairing is recorded as convention. Read it as traditional rather than mechanistic.

Schisandra lignans induce several hepatic drug-metabolising enzymes in animal and cell work, which can accelerate clearance of co-administered compounds. Wogonin is cleared largely by glucuronidation. The two are combined in traditional formulas, but the enzyme effect points in the opposite direction to a bioavailability enhancer. Anyone taking prescribed medicines should raise the combination with their prescriber.

Silybin and wogonin are both cleared largely by UDP-glucuronosyltransferase conjugation in the gut wall and liver. High doses of one flavonoid can occupy the same conjugating capacity that the other depends on. Competition for a shared clearance route can raise exposure to either, which is a pharmacokinetic consideration rather than a benefit. It is worth stating in a formula that stacks several flavonoids.

Resveratrol is conjugated so rapidly that most circulating material is glucuronide or sulfate. Wogonin uses the same conjugating enzymes. Stacking several polyphenols at high dose loads a shared, saturable clearance route. The consequence is unpredictable exposure rather than an established interaction outcome.

Luteolin and wogonin are both flavones acting on overlapping inflammatory signalling nodes in cell work, and both are conjugated by the same phase II enzymes. Combining them raises total flavone load through one clearance route. The overlap cuts both ways, adding signalling input while competing for elimination. Preclinical, not human.

Apigenin is the closest common flavone relative to wogonin in structure, differing in methoxylation pattern. Both are poorly soluble, both are heavily glucuronidated, and both act on similar signalling targets in cell models. A formula carrying several flavones should be read as one flavone dose split across molecules. Human data on the combination is not cited here.

Curcuminoids and wogonin share the same two practical constraints: very low aqueous solubility and rapid glucuronidation before they reach the circulation. A formulation that solves one, whether a phospholipid complex or a lipid vehicle, tends to help the other. They also compete for the same conjugating capacity. State the delivery system rather than the raw milligrams.

EGCG is conjugated by catechol-O-methyltransferase, UGT and sulfotransferases, the same phase II machinery that clears flavones. Co-dosing at high polyphenol loads means the enzymes are shared. Exposure to either compound can rise unpredictably as a result. Green tea extract also carries its own dosing considerations at concentrated intakes.

Intracellular glutathione buffers the reactive oxygen species that carry several wogonin signalling effects in cell systems. Raising thiol capacity reduces those effects in the same models. Whether oral glutathione changes intracellular redox enough to matter in people is a separate and unresolved question. The pairing is recorded as a laboratory antagonism, not a dosing instruction.

Alpha-tocopherol terminates lipid peroxidation chains in membranes, the compartment a lipophilic flavone sits in. Where a flavone effect depends on a membrane-level oxidative signal, a lipid-phase antioxidant can blunt it. This reasoning comes from cell systems and is not established for oral intake. Regard it as mechanistic.

Wogonin is cleared predominantly by UGT-mediated glucuronidation at the gut wall and in the liver. Piperine inhibits that step, which raises measured plasma concentrations of several similarly handled flavonoids. Piperine can appear in a formula under more than one name, so a formula should not count it twice. The change is in exposure, a marker.