Etoposide
For an informed discussion with your doctor or pharmacist. This information collection is not a clinically validated interaction checker. Missing data do not establish safety. Do not change or stop prescribed medicines on the basis of this information. The findings apply to the specific conditions studied; laboratory and animal studies cannot be directly extrapolated to humans.
Active substance: Etoposide
Examples of brand names: Vepesid [DE]
ATC code: L01CB01
Main use (for orientation): Oncology
Documented research summary
CBD/etoposide shows antitumour synergy in lung and prostate cancer cell models; no clinical pharmacokinetics for the pair or general dose prediction.
Uncertainties and limitations
Intravenous AVOPEF etoposide, not etoposide phosphate or oral capsules.
Shared enzymes must not be equated with clinical evidence of an interaction; CBD/THC findings cannot be extrapolated to other cannabinoids.
Separately recorded findings
1 separately recorded finding. Each statement applies to its documented study context.
CBD – laboratory and animal studies
Finding ID: B0221
Type of result: Preclinical evidence
Observation: CBD enhanced etoposide-associated cell death in NSCLC or LNCaP prostate cancer models.
Mechanism: Autophagy/stress signalling pathways
Study type: Cell models
Context studied: p53/PI3K–AKT–mTOR-dependent autophagic signals or UPR/ERAD.
Clinical interpretation: Model finding, not a recommendation for use
Limitations and uncertainties: No clinical confirmation of pharmacokinetics, safety or antitumour effects.
Original sources for this finding: Cannabidiol potentiates p53-driven autophagic cell death in non-small cell lung cancer following DNA damage: a novel synergistic approach beyond canonical pathways. [BMED40307570]; Cannabidiol Enhances the Anticancer Activity of Etoposide on Prostate Cancer Cells. [BMED39161998]
References and access status
[V2_LABEL_D0408] AVOPEF (ETOPOSIDE) INJECTION [AVYXA PHARMA, LLC]
Original source / bibliographic reference
Authors: AVYXA Pharma, LLC
Year: 2026
Source type: Official US SPL / DailyMed
Source access – 23 October 2026: Source destination was accessible when checked.
Bibliographic attribution or source identity cross-checked.
[BMED40307570] Cannabidiol potentiates p53-driven autophagic cell death in non-small cell lung cancer following DNA damage: a novel synergistic approach beyond canonical pathways.
Original source / bibliographic reference
Authors: Jeon Y, Kim T, Kwon H, Park YN, Kwon TH, Hong M, Choi KC, Ham J, Kim YJ.
Year: 2025
Source type: Publication; title and abstract reviewed
DOI: 10.1038/s12276-025-01444-x
PMID: 40307570
Source access – 23 October 2026: Automated direct retrieval was restricted; this does not establish that the link is broken.
Bibliographic attribution or source identity cross-checked.
PubMed – bibliographic reference / abstract
PubMed Central – archived text
DOI – publisher access (access restrictions may apply)
[BMED39161998] Cannabidiol Enhances the Anticancer Activity of Etoposide on Prostate Cancer Cells.
Original source / bibliographic reference
Authors: Erzurumlu Y, Catakli D.
Year: 2025
Source type: Publication; title and abstract reviewed
DOI: 10.1089/can.2023.0284
PMID: 39161998
Source access – 23 October 2026: Automated direct retrieval was restricted; this does not establish that the link is broken.
Bibliographic attribution or source identity cross-checked.
PubMed – bibliographic reference / abstract
DOI – publisher access (access restrictions may apply)
Research as of 23 October 2026. Not all original full texts could be reviewed in full. Source accessibility and the strength of scientific evidence must be assessed separately. An accessible link does not establish medical approval; a bibliographic record with an abstract does not replace the original full text.
Drug search and explanation of the evidence · Guide: cannabinoids and medicines · Author and responsibility
Etoposide and cannabinoids: documented findings, evidence, sources and data gaps. Research information for discussion with your doctor or pharmacist.
