Oseltamivir

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: Oseltamivir

Examples of brand names: Tamiflu [EU/DE]

ATC code: J05AH02

Main use (for orientation): Influenza

Documented research summary

THC, CBD, CBN and CBG/THCA inhibit CES1 in vitro. This creates a mechanistic concern about altered oseltamivir activation, but not measured clinical loss of efficacy. The original prodrug and active metabolite must not be equated.

Uncertainties and limitations

Original abstracts and available methods preview assessed; full texts of the two CES1 papers technically not fully accessible. No isolated human oseltamivir/cannabinoid pharmacokinetic study; do not infer clinical dose/risk values from Ki. Missing data do not establish safety.

Separately recorded findings

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

CBD – theoretical plausibility

Finding ID: B0451

Type of result: Pharmacokinetics/prodrug; clinical pair effect not measured

Observation: Altered activation to oseltamivir carboxylate possible; clinical loss of efficacy or exposure change not established.

Mechanism: CBD reversibly inhibited CES1 in the laboratory; CES1 participates in oseltamivir activation

Study type: Mechanistic extrapolation from in-vitro CES1 inhibition

Context studied: CES1-expressing HEK293 S9 fractions; CBD Ki 0.974 µM in the original abstract.

Clinical interpretation: Mechanistic concern, not a clinically confirmed interaction.

Limitations and uncertainties: No human pair pharmacokinetics. Full text not completely accessible; protein binding, concentration and prodrug/metabolite dynamics limit extrapolation. No dose recommendation.

Original sources for this finding: In Vitro Inhibition of Carboxylesterase 1 by Major Cannabinoids and Selected Metabolites [ME26]

THC – theoretical plausibility

Finding ID: B0452

Type of result: Pharmacokinetics/prodrug; clinical pair effect not measured

Observation: Possible influence on oseltamivir activation remains clinically unconfirmed.

Mechanism: THC reversibly inhibited CES1 in the laboratory

Study type: Mechanistic extrapolation from in-vitro CES1 inhibition

Context studied: CES1-expressing HEK293 S9 fractions; THC Ki 0.541 µM in the original abstract.

Clinical interpretation: Hypothesis-generating enzyme finding, not evidence of lost efficacy.

Limitations and uncertainties: No human combination assessment or quantified influence on active oseltamivir carboxylate. Abstract access, not complete methods verification.

Original sources for this finding: In Vitro Inhibition of Carboxylesterase 1 by Major Cannabinoids and Selected Metabolites [ME26]

CBN – theoretical plausibility

Finding ID: B0453

Type of result: Pharmacokinetics/prodrug; clinical pair effect not measured

Observation: Altered oseltamivir activation is mechanistically plausible, not clinically established.

Mechanism: CBN reversibly inhibited CES1 in the laboratory

Study type: Mechanistic extrapolation from in-vitro CES1 inhibition

Context studied: CES1-expressing HEK293 S9 fractions; CBN Ki 0.263 µM in the original abstract.

Clinical interpretation: Mechanistic plausibility, not a dose or treatment recommendation.

Limitations and uncertainties: No human pair pharmacokinetics. Despite low Ki, the authors expect only limited CES1 influence at achievable unbound CBN plasma concentrations; no clinical assurance of safety. Full-text access limited.

Original sources for this finding: In Vitro Inhibition of Carboxylesterase 1 by Major Cannabinoids and Selected Metabolites [ME26]

CBG – laboratory and animal studies

Finding ID: B0454

Type of result: Pharmacokinetics/prodrug; laboratory inhibition, not a clinical pair effect

Observation: Potential influence on oseltamivir activation; clinical effect size unknown.

Mechanism: CBG reversibly inhibited CES1 in the laboratory; oseltamivir phosphate/carboxylate serve as probe/substrate product

Study type: In-vitro enzyme study with an oseltamivir probe

Context studied: Original abstract and indexed original methods 2.1/2.5–2.8 assessed: oseltamivir phosphate (OST) in the CES1 probe assay; metabolite analysis by LC-MS/MS.

Clinical interpretation: Preclinical mechanism, not a clinically validated combination rule.

Limitations and uncertainties: Full text not completely accessible, so no unassessed quantitative CBG values. No evidence of clinical treatment impairment.

Original sources for this finding: An in vitro evaluation of common botanical extracts on carboxylesterase 1 catalytic activity [ME30]

THCA – laboratory and animal studies

Finding ID: B0455

Type of result: Pharmacokinetics/prodrug; laboratory inhibition, not a clinical pair effect

Observation: Possible influence on oseltamivir activation; no clinical exposure or efficacy measurement.

Mechanism: THCA reversibly inhibited CES1 through a mixed competitive/non-competitive mechanism

Study type: In-vitro enzyme study with an oseltamivir probe

Context studied: Original abstract and indexed original methods 2.1/2.5–2.8 assessed; oseltamivir phosphate as a probe. THCA reported as the strongest investigated inhibitor in the abstract.

Clinical interpretation: Preclinical interaction potential, not a use recommendation.

Limitations and uncertainties: Full-text access limited; do not interpret nominal in-vitro potency as a clinical risk category. Do not equate THCA with THC.

Original sources for this finding: An in vitro evaluation of common botanical extracts on carboxylesterase 1 catalytic activity [ME30]

References and access status

[VE_LABEL_D0318] OSELTAMIVIR PHOSPHATE (OSELTAMIVIR) CAPSULE [AMNEAL PHARMACEUTICALS LLC]

Original source / bibliographic reference

Authors: Respective marketing authorisation holder; regulatory product information

Year: 2026

Source type: Product information / SmPC / US Prescribing Information

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

Bibliographic attribution or source identity cross-checked.

[ME26] In Vitro Inhibition of Carboxylesterase 1 by Major Cannabinoids and Selected Metabolites

Original source / bibliographic reference

Authors: Qian Y; Wang X; Markowitz JS

Year: 2019

Source type: Original study: in-vitro CES1

DOI: 10.1124/dmd.118.086074

PMID: 30833288

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)

[ME30] An in vitro evaluation of common botanical extracts on carboxylesterase 1 catalytic activity

Original source / bibliographic reference

Authors: Melchert PW; Zhang Q; Raeuscher JM; Gurley BJ; Markowitz JS

Year: 2025

Source type: Original study: in-vitro CES1

DOI: 10.1016/j.dmd.2025.100129

PMID: 40834765

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