VILAPRISAN for endometriosis
Vilaprisan is a Phase 2 clinical candidate for endometriosis acting as a selective progesterone receptor modulator on the progesterone receptor.
Hypothesized mechanism
By modulating the progesterone receptor, vilaprisan may suppress endometrial proliferation and ectopic lesion growth in endometriosis.
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 6 of 10 overall, a moderate reading, from a pathway rated moderate 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. Evidence generated in women (female population). (band F1, ×1.00).
Corroboration
Only a single annotation line is provided (Open Targets target/MoA mapping). No independent mechanistic lines converge—just one database entry naming the progesterone receptor as target.
Rigor
The claim derives from a curated drug-target database (Open Targets) referencing a Phase 2 clinical candidate, which is human-relevant but not an experimental mechanistic study. No primary data or model is presented.
Specificity
Vilaprisan is explicitly characterized as a selective progesterone receptor modulator acting on the progesterone receptor, a well-defined molecular target.
Plausibility
Progesterone receptor modulation is a mechanistically coherent target for endometriosis, an estrogen/progesterone-responsive disease, and the candidate reached Phase 2 for this indication.
Consistency
With only one claim there is no opportunity for signals to conflict, but also no convergent corroboration; direction is internally coherent but unsupported by additional evidence.
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), VILAPRISAN (a Small molecule) is a clinical candidate for endometriosis (maximum clinical stage PHASE_2); its mechanism of action is Progesterone receptor modulator 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 →