HISTRELIN for endometriosis
Open Targets annotates HISTRELIN as an approved-stage GnRH receptor agonist clinical candidate for endometriosis acting on the gonadotropin-releasing hormone receptor.
Hypothesized mechanism
As a GnRH receptor agonist, histrelin causes downregulation of pituitary GnRH receptors, suppressing gonadotropin and ovarian estrogen production, thereby reducing estrogen-dependent endometriotic lesion activity.
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 4.5 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
Only a single line of evidence is present: an Open Targets annotation stating HISTRELIN is a GnRH receptor agonist clinical candidate for endometriosis. No independent mechanistic studies or convergent data lines are cited.
Rigor
The claim derives from a curated database annotation (Open Targets) indicating maximum clinical stage of APPROVAL, which implies human-relevant clinical development, but no actual study models, data, or trial results are presented in the claims.
Specificity
The mechanism is precisely specified: HISTRELIN acts as a gonadotropin-releasing hormone receptor agonist on the named target (gonadotropin releasing hormone receptor), a well-defined molecular action.
Plausibility
GnRH receptor agonism is a mechanistically well-established approach for endometriosis, suppressing gonadotropin/estrogen signaling that drives endometriotic lesion growth; the target-phenotype fit is strong and consistent with the APPROVAL stage noted.
Consistency
There is only one mechanistic signal (the GnRH receptor agonist annotation), so directional agreement cannot be assessed across multiple lines, but the single claim is internally consistent with the named target and indication.
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), HISTRELIN (a Protein) is a clinical candidate for endometriosis (maximum clinical stage APPROVAL); its mechanism of action is Gonadotropin-releasing hormone receptor agonist on target gonadotropin releasing hormone 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 →