Research Radartracking 4 published studies · 1 human · 2 clinical trials · 2 cancer pages · updated Jun 2026Open the Research Map →

Apigenin

Flavonoid that suppresses PI3K/NF-κB, inhibits VEGF/angiogenesis, induces G2/M arrest & apoptosis, and can raise tumor-selective ROS; evidence mainly preclinical.

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Human-reviewed · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed

🔬⭐⭐ Preclinical — Strong cell and animal data; human trials are limited or lacking.4′,5,7-Trihydroxyflavone

Forms: Purified apigenin capsules · Chamomile/celery/parsley extracts (apigenin-rich; variable content)

Educational only, not medical advice. OncoForge makes no claim that Apigenin treats, prevents, or cures any condition, beyond what the linked studies show. Evidence levels vary; effects may not translate to people, and some compounds can cause harm. Always coordinate with your oncology team.

Simple Summary

Apigenin slows cancer-cell division, pushes them toward self-destruction, and reduces blood-vessel growth. It dials down PI3K/AKT and NF-κB and can raise ROS inside tumor cells. Most evidence is lab/animal; concentrated extracts are needed for pharmacologic effects beyond diet.

Evidence at a glance

Tier 1 · labBreast (preclinical)Prostate (preclinical)Colorectal (preclinical)

Strong mechanistic and animal data; limited human oncology evidence.

How it may work

Apigenin is a flavonoid that exerts anticancer effects by inducing G2/M cell cycle arrest, inhibiting angiogenesis (via VEGF downregulation), and acting as a topoisomerase-II poison. It modulates key signaling pathways such as PI3K/AKT, MAPK, and NF-κB, inhibits cancer cell migration and invasion, promotes apoptosis through mitochondrial disruption, and increases intracellular ROS generation selectively in cancer cells.

Targets & pathways

Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.

  • PI3K/Akt
  • NF-κB
  • Topoisomerase IIPoison/inhibitory effect in some models
  • VEGF
  • Angiogenesis
  • G2/M cell-cycle arrest
  • Apoptosis
  • ROSPreferential in tumor cells
  • MAPK/ERKContext-dependent modulation
PI3KNF-κBAngiogenesisROS

Often studied / combined with

Combinations reported in the literature, not a protocol or a recommendation.

Overlapping mechanisms

Safety & interactions

Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.

Risk categories
Diarrhea RiskPregnancy Avoid
Potential interactions
  • ROS-dependent chemotherapy/radiationSeparateModerateTheoreticalPro/antioxidant effects could blunt or alter intended ROS waves—separate timing.
  • topoisomerase II–targeting agents (e.g., doxorubicin, etoposide)MonitorMinorTheoreticalPotentially additive DNA damage/repair effects—coordinate with oncology.

Timing

References

Research

No published studies for Apigenin yet

New studies appear here once they’ve been reviewed. Browse all studies.

Dose: as studied, not a recommendation

These are doses as studied or reported, never a recommendation. The right amount of Apigenin depends on you, your other medicines, and your situation; decide it with your oncology team and pharmacist, not from a web page.

Ranges seen in adjunct / practice use: 50–200 mg (oral) Standardized apigenin; consider divided dosing with meals for GI tolerance. Higher intakes lack robust human safety/PK data., Dietary intake alone is far below pharmacologic levels; extracts are used in studies. Avoid pushing above ~200–400 mg/day without protocol-level justification and monitoring..

Trials studying Apigenin

No actively-recruiting trials matched right now. Recruiting is not the same as proven. Search ClinicalTrials.gov →

Inclusion here is not an endorsement. OncoForge makes no claim beyond what the linked studies show. Discuss anything on this page with your oncology team before acting on it.

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