MIFEPRISTONE for adenomyosis
Mifepristone is documented as a Phase 2/3 clinical candidate for adenomyosis acting as a progesterone receptor antagonist.
Hypothesized mechanism
Mifepristone antagonizes the progesterone receptor, counteracting progesterone-driven proliferation and growth of adenomyotic tissue.
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 5.3 of 10 overall, a emerging reading, from a pathway rated emerging 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
A single line of evidence connects MIFEPRISTONE to adenomyosis via progesterone receptor antagonism (Open Targets, claim 1). No independent mechanistic converging lines are presented, but the drug-target-condition link is documented through a curated database with clinical stage information.
Rigor
The evidence is from Open Targets indicating a PHASE_2_3 clinical candidate status (claim 1), implying human-relevant clinical development rather than purely in-vitro work. However, no actual clinical or experimental data are cited—only a database annotation of clinical stage.
Specificity
The claim specifies a defined mechanism of action: progesterone receptor antagonist acting on the progesterone receptor target (claim 1). This is a precise, named molecular target rather than a diffuse or unspecified effect.
Plausibility
Adenomyosis is a progesterone/estrogen-dependent condition, so a progesterone receptor antagonist (claim 1) fits the target-phenotype relationship well. The PHASE_2_3 staging further supports biological plausibility of this target for this condition.
Consistency
Only one mechanistic signal is present (claim 1), so there is no opportunity for multiple signals to agree or conflict. The single signal points coherently toward PR antagonism being relevant to adenomyosis.
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), MIFEPRISTONE (a Small molecule) is a clinical candidate for adenomyosis (maximum clinical stage PHASE_2_3); its mechanism of action is Progesterone receptor antagonist on target progesterone receptor. Open Targets · mechanistic ↗
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 →