ASPIRIN for adenomyosis
Aspirin is listed in Open Targets as an early-phase (EARLY_PHASE_1) clinical candidate for adenomyosis acting via cyclooxygenase (PTGS2/COX-2) inhibition.
Hypothesized mechanism
Aspirin inhibits cyclooxygenase (PTGS2/COX-2), reducing prostaglandin synthesis that may drive inflammation and pain in adenomyosis.
This is the model’s proposed mechanism from the sources on file, not a demonstrated causal pathway. How well the published record supports it is reflected in the rigor and plausibility dimensions of the score, and traced to the verbatim sources at the foot of the page.
How the score was reached, for this pair
The composite score is the sum of five dimensions, each scored 0 to 2 by the model from the evidence on file. Below is the sub-score this specific pair received on each, with what that dimension measures. It scored 3 of 10 overall, a exploratory reading, from a pathway rated exploratory in strength.
The model’s overall reasoning for this pair is the summary at the top of the page, and the mechanism it proposed is in the section above.
Scored for women. Female representation not stated — applicability to women uncertain (flagged for full text). (band F4, ×0.75).
Corroboration
Only a single Open Targets database entry is provided, describing one mechanistic line (COX inhibition on PTGS2). No independent converging lines of evidence are present in the claims.
Rigor
The claim references a clinical candidate at EARLY_PHASE_1 stage per Open Targets, which implies human-relevant clinical context but at the earliest stage. There is no experimental data, study, or model detail to assess strength.
Specificity
Aspirin's mechanism is stated as a cyclooxygenase inhibitor acting on PTGS2 (COX-2), a named target. However, aspirin is a well-known nonspecific COX inhibitor (COX-1 and COX-2), so its action on the named target is not highly specific.
Plausibility
COX-2/prostaglandin inhibition plausibly relates to inflammation and pain in adenomyosis, and the entry lists it as a candidate for adenomyosis. The claim asserts a target-phenotype association but provides no phenotypic or mechanistic detail linking PTGS2 inhibition to adenomyosis pathology.
Consistency
There is only one mechanistic signal (COX/PTGS2 inhibition), so there is no conflict, but also no multiple signals to corroborate directional agreement. Consistency cannot be strongly established from a single database entry.
Independent reading, reported beside the score
One outside model cross-reference is reported alongside the composite score. It is recorded separately and is not combined into the score.
MATRIX cross-reference Top 1%
Every Cure’smachine-learned treatment-probability model, drawn from a biomedical knowledge graph across roughly 1,800 drugs and 22,000 diseases. It provides a model-based estimate of how plausible a drug-disease link is given the structure of biomedical knowledge, reported alongside the substrate’s own evidence.
For this pair. MATRIX places this pair at Top 1%, with a treat-score of 3.98 (higher is better; across the pairs we cover, scores span about 3.1 to 4.5).
Scored over MATRIX’s own entities, confirming the same drug and disease: CHEBI:15365 (drug) and MONDO:0010888 (disease). Validate against the source: Every Cure’s MATRIX dataset ↗.
More on the MATRIX cross-reference and its provenance →Layers not covered for this pair
Not covered for this pair. This layer holds documented sex-specific pharmacokinetics for a limited set of drugs, and this compound is not among them yet. A blank here means the drug is not covered by the layer, not that no sex difference exists.
More on the sex-specific pharmacokinetics layer and its sources →Not covered for this pair. The cycle-phase layer is seeded for the strongest-evidence cases so far (PMDD), and this pair is not among them yet. A blank here means the pair is not covered by the layer, not that the effect was found to be phase-independent.
More on the cycle-phase layer and its sources →Source evidence · what the pipeline ingested
These are the sources the pipeline ingested to detect and score this signal, the published literature the model actually read, each tagged by study type. Where the model combined findings the claim is marked as a synthesis (S), and where the literature disagrees the contradiction is shown (!).
Every source below belongs to this signal’s evidence arm, Pathway insights. Whel reads each drug-condition pair through four such arms, each held to its own inclusion bar; a signal is surfaced through one of them.
- 1Per Open Targets (retrieved 2026-06-16), ASPIRIN (a Small molecule) is a clinical candidate for adenomyosis (maximum clinical stage EARLY_PHASE_1); its mechanism of action is Cyclooxygenase inhibitor on target prostaglandin-endoperoxide synthase 2. Open Targets · mechanistic ↗
- 2In FDA AEMS (the FDA Adverse Event Reporting System, formerly FAERS; retrieved 2026-06-16), 4647 report(s) of ABDOMINAL PAIN were recorded for ASPIRIN among female patients (of 256523 female reports for ASPIRIN in the analysed sample). This is a raw adverse-event report count, not a disproportionality statistic or evidence of causation, and is subject to reporting bias and confounding. Read two ways: as a safety consideration, and — because it suggests ASPIRIN acts on a system relevant to adenomyosis — as a mechanistic lead for further investigation, not evidence of benefit. AEMS · adverse-event report ↗
These are the verbatim sources the pipeline surfaced and read; they may not be the full published record for a pair, and the score reflects the strength and agreement of the evidence rather than its volume. The strength of these source types is what the rigor dimension of the score reads off. MATRIX, sex-specific pharmacokinetics, and cycle phase are separate layers the pipeline does not ingest, external cross-references reported beside the score, and they link to their own sources in their sections above.
The primary sources and pipelines this evidence is drawn from →