Topotecan

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: Topotecan

Examples of brand names: Hycamtin [EU]

ATC code: L01CE01

Main use (for orientation): Relapsed small-cell lung cancer; selected ovarian cancers; cervical cancer with cisplatin

Documented research summary

An ABCG2 cell experiment with CBD/CBN/THC increased sensitivity to topotecan; no clinically demonstrated topotecan–cannabinoid interaction. The label makes the transporter pathway plausible, but does not justify extrapolating the inhibitor effect size.

Uncertainties and limitations

Oral HYCAMTIN capsule, not intravenous. The ABCG2 experiment does not predict clinical concentrations.

Shared enzymes must not be equated with clinical evidence of an interaction; CBD/THC findings cannot be extrapolated to other cannabinoids.

Separately recorded findings

3 separately recorded findings. Each statement applies to its documented study context.

CBD – laboratory and animal studies

Finding ID: B0116

Type of result: Context-specific finding; read the limitations

Observation: Resensitisation in a cell model.

Mechanism: Inhibition of ABCG2/BCRP transport

Study type: In-vitro cell assay

Context studied: Cell viability assay after cannabinoid pretreatment.

Clinical interpretation: Clinical relevance unknown

Limitations and uncertainties: No clinical chemotherapy benefit or clinical AUC increase established. Additional context from merged row B0251: overexpressing cell lines, subtoxic cannabinoid concentrations. No clinical prediction of concentration, dose or toxicity; topotecan sensitivity and mitoxantrone uptake are different measurement endpoints. In the same study, the investigated plant cannabinoids inhibited basal and substrate-stimulated ABCG2 ATPase activity; no change in ABCG2 expression was observed. Shared mechanistic study context, not additional independent evidence.

Original sources for this finding: The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids [ME06]

THC – laboratory and animal studies

Finding ID: B0118

Type of result: Context-specific finding; read the limitations

Observation: Resensitisation in a cell model.

Mechanism: Inhibition of ABCG2/BCRP transport

Study type: In-vitro cell assay

Context studied: Cell viability assay after cannabinoid pretreatment.

Clinical interpretation: Clinical relevance unknown

Limitations and uncertainties: No clinical chemotherapy benefit or clinical AUC increase established. Additional context from merged row B0251: overexpressing cell lines, subtoxic cannabinoid concentrations. No clinical prediction of concentration, dose or toxicity; topotecan sensitivity and mitoxantrone uptake are different measurement endpoints. In the same study, the investigated plant cannabinoids inhibited basal and substrate-stimulated ABCG2 ATPase activity; no change in ABCG2 expression was observed. Shared mechanistic study context, not additional independent evidence.

Original sources for this finding: The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids [ME06]

CBN – laboratory and animal studies

Finding ID: B0120

Type of result: Context-specific finding; read the limitations

Observation: Resensitisation in a cell model.

Mechanism: Inhibition of ABCG2/BCRP transport

Study type: In-vitro cell assay

Context studied: Cell viability assay after cannabinoid pretreatment.

Clinical interpretation: Clinical relevance unknown

Limitations and uncertainties: No clinical chemotherapy benefit or clinical AUC increase established. Additional context from merged row B0251: overexpressing cell lines, subtoxic cannabinoid concentrations. No clinical prediction of concentration, dose or toxicity; topotecan sensitivity and mitoxantrone uptake are different measurement endpoints. In the same study, the investigated plant cannabinoids inhibited basal and substrate-stimulated ABCG2 ATPase activity; no change in ABCG2 expression was observed. Shared mechanistic study context, not additional independent evidence.

Original sources for this finding: The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids [ME06]

References and access status

[V2_LABEL_D0454] HYCAMTIN (TOPOTECAN) CAPSULE [SANDOZ INC]

Original source / bibliographic reference

Authors: Sandoz Inc

Year: 2023

Source type: Official US SPL / DailyMed

Source access – 23 October 2026: Source destination was accessible when checked.

Bibliographic attribution or source identity cross-checked.

[ME06] The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids

Original source / bibliographic reference

Authors: Holland ML; Lau DTT; Allen JD; Arnold JC

Year: 2007

Source type: Original study: in-vitro transporters

DOI: 10.1038/sj.bjp.0707467

PMID: 17906686

Source access – 23 October 2026: Direct retrieval could not be fully verified; availability remains unresolved.

Bibliographic attribution or source identity cross-checked.

DOI – publisher access (access restrictions may apply)

PubMed Central – full-text access according to the literature database – Archive attribution confirmed by Europe PMC metadata. Direct retrieval was not fully verified here; access may require a browser check.

Europe PMC – full-text access according to the literature database – Listed as freely available HTML full text in the official Europe PMC metadata. Direct retrieval was not fully verified here.

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