Benefits
CD38 Inhibition and NAD+ Preservation
CD38 is an enzyme that breaks down NAD+, a coenzyme whose levels fall with age. In laboratory work apigenin blocked CD38, and in obese mice given apigenin by injection it raised NAD+ in the liver and improved blood sugar and fat measures. In healthy men, pure apigenin taken by mouth was poorly absorbed, and no human study has shown that apigenin raises NAD+.
Calming Effects via the Benzodiazepine Receptor
In a laboratory and mouse study, apigenin competed with the drug flunitrazepam for binding at the brain's benzodiazepine receptor and reduced anxiety-like behavior in mice on a maze test. A 10-fold higher dose was mildly sedating and cut movement by 26 percent. This is often offered as one reason chamomile feels calming, but no human trial of apigenin itself for stress is cited here.
Sleep Support
Chamomile has a long traditional use as a bedtime tea. A review discusses apigenin's activity at calming brain receptors as one possible reason, citing mostly animal work, chamomile extract trials and a survey linking higher dietary apigenin with better sleep quality. No human trial of apigenin itself for sleep is cited here, so its effect on sleep in people is unknown.
Inflammatory Signaling and Free Radical Activity
In cell and animal studies summarized in a review, apigenin lowered inflammatory signals such as TNF-α, IL-6 and iNOS and affected NF-κB activity, and in chemical tests it scavenges hydroperoxide and inhibits xanthine oxidase. These are laboratory findings. No study cited here measured inflammation or antioxidant status in people taking apigenin.
Mechanism of action
CD38 Inhibition (NAD+ Pathway)
CD38 is the main NAD+-consuming enzyme in mammals. Apigenin inhibited human CD38 in a test tube with an IC50 of about 10 micromol/L, raised NAD+ in cultured cells, and lowered liver CD38 activity in obese mice injected with 100 mg/kg daily for one week. Whether oral apigenin reaches enough in the body to inhibit CD38 in people has not been tested.
Benzodiazepine Receptor Binding
Apigenin binds the central benzodiazepine receptor (Ki about 4 micromol/L) without affecting muscimol binding at the GABA-A receptor, muscarinic receptors or alpha1-adrenoceptors. In mice it reduced anxiety-like behavior without sedation at doses similar to classical benzodiazepines; only a 10-fold higher dose was mildly sedating. These effects were measured in mice, not in people.
Aromatase Inhibition
In tests on human placental and ovarian microsomes, apigenin inhibited aromatase (CYP19), the enzyme that converts androgens to estrogens, though less potently than chrysin. In immature rats given 50 mg/kg by mouth, apigenin did not change estrogen-driven or androgen-driven uterine growth, possibly because of poor absorption. No cited study measured hormone levels in people.
NF-κB and Inflammatory Pathway Inhibition
In mouse immune cells challenged with a bacterial toxin, apigenin reduced IL-1β, IL-8 and TNF production, with non-canonical regulation of NF-κB activity in vitro; in a rat study it lowered TNF-α, IL-6 and iNOS. Whether this changes inflammation in the human body has not been tested in any study cited here.
Clinical trials
Laboratory and mouse study testing binding at the brain's benzodiazepine receptor and behavior on the elevated plus maze and hole board tests (Viola et al. 1995, Planta Med)
Mice. No people were studied.
Apigenin competed with flunitrazepam for benzodiazepine receptor binding (Ki about 4 micromol/L) and reduced anxiety-like behavior on the elevated plus maze without sedation at doses similar to classical benzodiazepines. A 10-fold higher dose was mildly sedating, with 26 percent less movement and a 35 percent drop in hole board measures. This does not show an effect in people.
Laboratory, cell culture and mouse study of apigenin and quercetin as CD38 inhibitors (Escande et al. 2013, Diabetes)
Human recombinant CD38, cultured cells, and mice on a high-fat diet (6 per group). No people were studied.
Apigenin inhibited CD38 in a test tube (IC50 about 10 micromol/L) and raised NAD+ in cultured cells. Obese mice injected with 100 mg/kg apigenin daily for one week had lower liver CD38 activity, higher liver NAD+, and better glucose and lipid measures than controls. The mice received apigenin by injection, not by mouth.
Crossover absorption study (registered NCT03526081) comparing a pure apigenin capsule with a parsley drink, parsley in yogurt and chamomile tea (Borges et al. 2022, Free Radic Biol Med)
Healthy adult men (17 enrolled; eligible ages 25 to 60, per the trial registry).
Pure apigenin was poorly absorbed: urinary metabolites equaled 0.5 percent of intake over 24 hours. Apigenin glycosides from food did better, with 11.2 percent of intake from a parsley drink and 34 percent from chamomile tea recovered in urine. The study measured absorption only, not health effects.
Randomized crossover dietary study with added in vitro platelet tests (Janssen et al. 1998, Am J Clin Nutr)
18 healthy volunteers.
Volunteers ate 5 g of dried parsley a day, providing 84 mg of apigenin, for 7 days, compared with onions and a placebo. Parsley had no significant effect on platelet aggregation, thromboxane B2, factor VII or other clotting measures. In test tubes apigenin blocked platelet clumping only at 2500 micromol/L, a level the authors concluded cannot be reached in the body.