Artemisinin
Iron-activated endoperoxide that spikes ROS to trigger ferroptosis/apoptosis; also down-modulates PI3K/AKT/mTOR and may curb angiogenesis/metastasis. Clinical oncology dosing is not yet standardized (artesunate favored in early studies).
Forms: Artemisinin (oral) · Artesunate (oral/IV; higher exposure and best-studied clinically) · Dihydroartemisinin (oral)
Simple Summary
Artemisinin stays quiet until it meets iron—then it unleashes ROS that can kill cancer cells by ferroptosis and apoptosis. It also turns down AKT growth signaling and can sensitize tumors to chemo. Human oncology data are still early; artesunate has favorable safety and exposure, especially in short courses or with iron-loading strategies.
Evidence at a glance
Strong mechanistic/preclinical signal; early human studies exist but standardized oncology dosing and outcomes remain limited.
How it may work
Artemisinin is activated by intracellular iron, triggering cleavage of its endoperoxide bridge and generating reactive oxygen species (ROS). This induces ferroptosis and apoptosis, particularly in cancer cells with high iron uptake. Artemisinin and its derivatives (e.g., artesunate) also inhibit PI3K/AKT/mTOR signaling, can sensitize tumors to chemotherapy, and suppress angiogenesis and metastasis in aggressive cancers.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
- ROS↑Endoperoxide cleavage after Fe2+ activation
- Ferroptosis↑Lipid peroxidation/GPX4 axis
- PI3K/AKT/mTOR↓
- Apoptosis↑
- Angiogenesis↓
- Metastatic potential↓
- Transferrin receptor (CD71)↑Commonly elevated in tumors → selective activation context
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- Doxorubicin, Cisplatin: Potential chemosensitization via ROS↑ and PI3K/AKT↓.
- Transferrin/iron-loading (research): May enhance activation/selectivity; experimental context only.
Overlapping mechanisms
- ROS ↑: Stacking multiple ROS inducers increases normal-tissue risk; coordinate scheduling.
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.
- iron supplements / transferrin-raising strategiesMonitorMinorTheoreticalIron can increase activation and ROS; coordinate to avoid unintended normal-tissue toxicity.
- antioxidants (high-dose)SeparateTheoreticalAntioxidants may blunt ROS-dependent cytotoxicity.
- chemotherapy/radiation (ROS-dependent)MonitorMinorTheoreticalPotential sensitization via ROS ↑; coordinate timing with oncology.
Timing
- With-meal: Improves GI tolerance.
- AM
- PM
References
- PMC 2025 — Bibliometric review of anticancer applications
- IJMS 2025 — Molecular mechanisms in cancer
- Sci Rep 2025 — WHN-11 derivative on mitochondria/apoptosis
- Infect Dis Poverty 2023 — Clinical prospects and safety
- CCNM 2024 — Phase I dose escalation and PK
- Molecules 2024 — Derivatives as anticancer agents
- Cell Death Dis 2025 — Lung cancer cell death effects
- PLoS One 2024 — Plant matrix bioavailability
Research
No published studies for Artemisinin yet
New studies appear here once they’ve been reviewed. Browse all studies.
Dose: as studied, not a recommendation
Ranges seen in adjunct / practice use: 100–200 mg (oral) No oncology-standard dose. Most clinical experience uses artesunate (short courses); dosing and schedules are study/formulation-dependent., Iron-dependent activation suggests potential scheduling with iron-loading strategies in research settings; clinical protocols remain exploratory..
Trials studying Artemisinin
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