MikroScore
Science-backed ingredient evidence
Weak Evidence Safety: Likely safe Study dose: 50 mg/day

Apigenin

Also known as: Apigenin, 4',5,7-Trihydroxyflavon, Kamillenflavonoid, CD38-Inhibitor

Summary Weak Evidence

Apigenin is a flavonoid from chamomile and parsley that inhibits CD38, an enzyme that degrades NAD+. Complements NMN/NR approaches. Early human evidence.

EU Health Claims: No approved claims

No EFSA health claims for apigenin. Available as a herbal substance in dietary supplements within the EU. Clinical trials ongoing. No novel food classification.

AI Summary

Quick verdict

Apigenin is a flavonoid from chamomile and parsley that inhibits CD38, an enzyme that degrades NAD+. Complements NMN/NR approaches. Early human evidence.

What the evidence supports

CD38 inhibition is relatively well-studied preclinically—associated with elevated NAD+ levels in mice. Early small human studies show improvements in anxiety and cognitive function.

What is NOT supported

Clinical human trials are absent or very weak. Long-term safety in humans is largely unexplored.

EU/EFSA status

Not approved. No EFSA health claims for apigenin. Available as a herbal substance in dietary supplements within…

Safety

Likely safe

This AI summary is generated from the structured data on this page.

What is Apigenin?

Apigenin is a flavone—a polyphenol naturally found in chamomile (Matricaria chamomilla), parsley, celery, thyme, and certain fruits. Historically, it is best known as the active compound in chamomile tea, whose mild calming effects have been attributed to GABA receptor binding.

In the context of healthy aging, apigenin has a second, far more compelling identity: it is a CD38 inhibitor—and this makes it an intriguing piece of the NAD+ strategy puzzle.

The CD38/NAD+ Connection

CD38 is an enzyme that degrades NAD+—and its activity increases dramatically with advancing age. Research by David Sinclair and others demonstrates that a substantial portion of age-related NAD+ decline is not caused by reduced production, but rather by increased degradation via CD38.

This is where apigenin steps in: by inhibiting CD38, it slows NAD+ degradation—without directly supplying NAD+. This is a complementary approach to NMN or NR (which elevate NAD+ from the synthesis side).

In practice, many healthy aging enthusiasts therefore combine NMN + apigenin—increasing synthesis and inhibiting degradation simultaneously.

What Do the Studies Really Say?

Relatively well-studied preclinically

  • CD38 inhibition by apigenin was associated with measurable NAD+ elevation in aged mice (~50%)
  • Improved mitochondrial function in liver and skeletal muscle
  • Anxiolytic effects via GABA receptors (without sedation)
  • Anti-inflammatory effects via NF-κB and COX-2 inhibition

Human studies: very early

  • No RCTs on NAD+ effects in humans at the time of this review
  • Small studies on anxiety and sleep (using chamomile extract)—but with mixed formulations
  • Epidemiologically: high flavone intake is associated with less cognitive decline

Not yet proven in humans

  • Direct NAD+ elevation from oral apigenin supplementation
  • Healthy aging endpoints

Bottom line: Apigenin is biologically plausible as a CD38 inhibitor, but the leap from mouse data to human effects is particularly uncertain with NAD+ strategies. If you’re supplementing NMN, there’s a rational basis for adding apigenin—but if you’re not pursuing a NAD+ strategy, you have little direct evidence for its use.

Apigenin as a Sleep/Anxiety Supplement

Separately from healthy aging: chamomile tea (an apigenin source) does have mild anxiolytic properties. RCTs using standardized chamomile extracts show reductions in anxiety scores in generalized anxiety disorder. This is a distinct, somewhat better-supported benefit.

Is Apigenin Safe?

At typical doses (25–100 mg/day), apigenin is considered likely safe. At very high doses, animal studies showed effects on thyroid hormones and reproductive function—no evidence in humans, but a signal for caution at very high dosing.

Key Studies

Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging

Gomes AP et al. (2013)

Foundational work: CD38 activity increases with age and depletes NAD+. CD38 deletion in mice was associated with elevated NAD+ levels and notable improvements in mitochondrial function.

PubMed PMID 24360282

Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome

Escande et al. (2013)

Apigenin directly inhibits CD38 and was associated with approximately 50% higher NAD+ levels in aged mice. Improved mitochondrial function in liver and muscle.

PubMed PMID 23172919

Flavones-bound in benzodiazepine site on GABA(A) receptor: Concomitant anxiolytic-like and cognitive-enhancing effects produced by Isovitexin and 6-C-glycoside-Diosmetin

Oliveira et al. (2018)

Apigenin binds to GABA-A receptors (benzodiazepine-like) with anxiolytic effects without sedation in animal models.

PubMed PMID 29738701

Apigenin and inflammation in the brain: can apigenin inhibit neuroinflammation in preclinical models?

Olasehinde et al. (2024)

Review: Apigenin inhibits NF-κB, COX-2, and pro-inflammatory cytokines across numerous preclinical models. Anti-inflammatory effects are well-documented.

PubMed PMID 39126572
Editorial notice: For most ingredients described here, no health claims are approved in the EU (Regulation (EC) 1924/2006). Evidence levels are editorial assessments of research quality — not health promises. This content is not a substitute for medical advice and does not constitute a recommendation to treat, alleviate, or prevent any disease.