Acetylsalicylic acid
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: Acetylsalicylic acid
Examples of brand names: Aspirin [DE]
ATC code: B01AC06
Main use (for orientation): Platelet inhibition; pain
Documented research summary
Direct human surrogate experiment: CBD reduced intestinal permeability induced by acetylsalicylic acid 600 mg; no conclusion about bleeding, ulcers or acetylsalicylic-acid pharmacokinetics. Preclinically, aspirin alters various THC effects, while chronic THC reduces aspirin antinociception in a mouse model. No clinical dose recommendation or general bleeding risk can be inferred.
Uncertainties and limitations
75 mg label, but the cannabinoid intestinal experiment used 600 mg aspirin; result not validated for chronic low-dose secondary prevention.
Shared enzymes must not be equated with clinical evidence of an interaction; CBD/THC findings cannot be extrapolated to other cannabinoids.
Separately recorded findings
7 separately recorded findings. Each statement applies to its documented study context.
CBD – clinically studied
Finding ID: B0256
Type of result: Clinically controlled, surrogate
Observation: CBD reduced the aspirin-induced increase in lactulose/mannitol absorption.
Mechanism: Intestinal-barrier surrogate during aspirin challenge
Study type: Randomised double-blind placebo-controlled, with additional in-vitro/ex-vivo work
Context studied: Aspirin 600 mg, PEA in a separate arm; PEA is not CBD.
Clinical interpretation: Direct human combination experiment; not a bleeding endpoint
Limitations and uncertainties: No aspirin pharmacokinetics, ulcer/bleeding reduction or long-term safety demonstrated; full-text access blocked, sample/CBD dose not inferred from abstract.
Original sources for this finding: Palmitoylethanolamide and Cannabidiol Prevent Inflammation-induced Hyperpermeability of the Human Gut In Vitro and In Vivo-A Randomized, Placebo-controlled, Double-blind Controlled Trial. [BMED31054246]
Δ9-THC – laboratory and animal studies
Finding ID: B0257
Type of result: Preclinical
Observation: Aspirin did not show effective antinociception as in controls in the chronically THC-treated mouse model.
Mechanism: Chronic cannabinoid exposure/COX-dependent antinociception
Study type: Mouse PPQ pain test
Context studied: Oral aspirin; other NSAIDs differed.
Clinical interpretation: Not a prediction of clinical analgesic failure
Limitations and uncertainties: Authors' hypothesis for humans not clinically assessed; not an antiplatelet endpoint.
Original sources for this finding: Decrease in efficacy and potency of nonsteroidal anti-inflammatory drugs by chronic delta(9)-tetrahydrocannabinol administration. [BMED12235269]
Δ8-THC – laboratory and animal studies
Finding ID: B0258
Type of result: Preclinical
Observation: Aspirin antagonised THC-induced suppression of lever pressing.
Mechanism: COX/arachidonic-acid cascade
Study type: Rat behaviour
Context studied: Aspirin 10 mg/kg intraperitoneally.
Clinical interpretation: Experimental
Limitations and uncertainties: Not a prediction of human dose, driving ability or safety.
Original sources for this finding: Behavioral suppression induced by cannabinoids is due to activation of the arachidonic acid cascade in rats. [BMED11166698]
THC (historical delta1/delta′-trans nomenclature) – laboratory and animal studies
Finding ID: B0259
Type of result: Preclinical
Observation: Aspirin reduced sedating/cataleptic THC responses in mice; PGE2 could restore the response; fibroblast PGE2 signalling also inhibited.
Mechanism: Prostaglandin-dependent behavioural and cellular responses
Study type: Mouse/cell models
Context studied: Historical nomenclature and extracts in original papers.
Clinical interpretation: Experimental
Limitations and uncertainties: Do not present as an antidote or clinically tested attenuation of THC.
Original sources for this finding: Sedative activity of cannabis in relation to its delta'-trans-tetrahydrocannabinol and cannabidiol content. [BMED6269680]; The oral activity of delta'-tetrahydrocannabinol and its dependence on prostaglandin E2. [BMED574040]; Prostaglandins and cannabis--IX. Stimulation of prostaglandin E2 synthesis in human lung fibroblasts by delta 1-tetrahydrocannabinol. [BMED6289843]
Δ9-THC – laboratory and animal studies
Finding ID: B0260
Type of result: Preclinical
Observation: Aspirin reduced THC-induced responses in isolated kidneys/lungs and neuronal toxicity in a culture model.
Mechanism: Prostanoid-dependent tissue response
Study type: Isolated organs/cell culture
Context studied: Rabbit kidney, guinea-pig lung, hippocampal neurons/slices.
Clinical interpretation: Experimental
Limitations and uncertainties: No clinical neuroprotection or evidence of THC-induced neuronal loss at usual human doses.
Original sources for this finding: The evidence of the release of prostaglandin-like material from rabbit kidney and guinea-pig lung by (minus)-trans-delta9-tetrahydrocannabinol. [BMED239170]; Hippocampal neurotoxicity of Delta9-tetrahydrocannabinol. [BMED9651215]
Cannabis extract; cannabinoid contributions not separated – laboratory and animal studies
Finding ID: B0261
Type of result: Preclinical
Observation: Chronic extract increased aspirin esterase activity in a rat laboratory experiment.
Mechanism: Induction of hepatic hydrolases
Study type: Animal exposure with ex-vivo enzyme measurement
Context studied: High extract amounts of 158–500 mg/kg over 3 weeks; aspirin as an esterase probe substrate.
Clinical interpretation: LABORATORY FINDING, NOT a drug-interaction prediction
Limitations and uncertainties: No clinical aspirin AUC/platelet effect or attribution to CBD or THC alone.
Original sources for this finding: Influence of chronic oral intake of cannabis extract on oxidative and hydrolytic metabolism of xenobiotics in rat. [BMED1986734]
Δ9-THC – laboratory and animal studies
Finding ID: B0262
Type of result: Preclinical ex vivo
Observation: Δ9-THC did not cause aggregation in the ex-vivo system used; the positive 2-AG finding concerned an endocannabinoid.
Mechanism: Negative control in a platelet experiment
Study type: Blood aggregometry
Context studied: Healthy people (n=8) and coronary patients taking aspirin (n=12); main question 2-AG/MAGL.
Clinical interpretation: NOT a clinical bleeding/interaction prediction
Limitations and uncertainties: Do not treat as aspirin–THC safety evidence or general THC platelet neutrality.
Original sources for this finding: 2-arachidonyl glycerol activates platelets via conversion to arachidonic acid and not by direct activation of cannabinoid receptors. [BMED20653671]
References and access status
[BAWEB_ASA] Aspirin75mg tablets – Summary of Product Characteristics
Original source / bibliographic reference
Authors: G.L.Pharma UK Limited
Year: 2026
Source type: Official UK product information via emc
Source access – 23 October 2026: Source destination was accessible when checked.
Bibliographic attribution or source identity cross-checked.
[BMED31054246] Palmitoylethanolamide and Cannabidiol Prevent Inflammation-induced Hyperpermeability of the Human Gut In Vitro and In Vivo-A Randomized, Placebo-controlled, Double-blind Controlled Trial.
Original source / bibliographic reference
Authors: Couch DG, Cook H, Ortori C, Barrett D, Lund JN, O'Sullivan SE.
Year: 2019
Source type: Publication; title and abstract reviewed
DOI: 10.1093/ibd/izz017
PMID: 31054246
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)
[BMED12235269] Decrease in efficacy and potency of nonsteroidal anti-inflammatory drugs by chronic delta(9)-tetrahydrocannabinol administration.
Original source / bibliographic reference
Authors: Anikwue R, Huffman JW, Martin ZL, Welch SP.
Year: 2002
Source type: Publication; title and abstract reviewed
DOI: 10.1124/jpet.303.1.340
PMID: 12235269
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)
[BMED11166698] Behavioral suppression induced by cannabinoids is due to activation of the arachidonic acid cascade in rats.
Original source / bibliographic reference
Authors: Yamaguchi T, Shoyama Y, Watanabe S, Yamamoto T.
Year: 2001
Source type: Publication; title and abstract reviewed
DOI: 10.1016/s0006-8993(00)03127-9
PMID: 11166698
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)
[BMED6269680] Sedative activity of cannabis in relation to its delta'-trans-tetrahydrocannabinol and cannabidiol content.
Original source / bibliographic reference
Authors: Pickens JT.
Year: 1981
Source type: Publication; title and abstract reviewed
DOI: 10.1111/j.1476-5381.1981.tb09145.x
PMID: 6269680
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)
[BMED574040] The oral activity of delta'-tetrahydrocannabinol and its dependence on prostaglandin E2.
Original source / bibliographic reference
Authors: Fairbairn JW, Pickens JT.
Year: 1979
Source type: Publication; title and abstract reviewed
DOI: 10.1111/j.1476-5381.1979.tb08691.x
PMID: 574040
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)
[BMED1986734] Influence of chronic oral intake of cannabis extract on oxidative and hydrolytic metabolism of xenobiotics in rat.
Original source / bibliographic reference
Authors: Khanna P, Gupta MB, Gupta GP, Sanwal GG, Ali B.
Year: 1991
Source type: Publication; title and abstract reviewed
DOI: 10.1016/0006-2952(91)90017-y
PMID: 1986734
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)
[BMED239170] The evidence of the release of prostaglandin-like material from rabbit kidney and guinea-pig lung by (minus)-trans-delta9-tetrahydrocannabinol.
Original source / bibliographic reference
Authors: Kaymakcalan S, Türker RK.
Year: 1975
Source type: Publication; title and abstract reviewed
DOI: 10.1111/j.2042-7158.1975.tb09507.x
PMID: 239170
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)
[BMED6289843] Prostaglandins and cannabis--IX. Stimulation of prostaglandin E2 synthesis in human lung fibroblasts by delta 1-tetrahydrocannabinol.
Original source / bibliographic reference
Authors: Burstein S, Hunter SA, Sedor C, Shulman S.
Year: 1982
Source type: Publication; title and abstract reviewed
DOI: 10.1016/0006-2952(82)90530-5
PMID: 6289843
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)
[BMED9651215] Hippocampal neurotoxicity of Delta9-tetrahydrocannabinol.
Original source / bibliographic reference
Authors: Chan GC, Hinds TR, Impey S, Storm DR.
Year: 1998
Source type: Publication; title and abstract reviewed
DOI: 10.1523/jneurosci.18-14-05322.1998
PMID: 9651215
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)
[BMED20653671] 2-arachidonyl glycerol activates platelets via conversion to arachidonic acid and not by direct activation of cannabinoid receptors.
Original source / bibliographic reference
Authors: Keown OP, Winterburn TJ, Wainwright CL, Macrury SM, Neilson I, Barrett F, Leslie SJ, Megson IL.
Year: 2010
Source type: Publication; title and abstract reviewed
DOI: 10.1111/j.1365-2125.2010.03697.x
PMID: 20653671
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)
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
Acetylsalicylic acid and cannabinoids: documented findings, evidence, sources and data gaps. Research information for discussion with your doctor or pharmacist.