GOSERELIN for adenomyosis
Goserelin is annotated in Open Targets as a Phase 2/3 clinical candidate for adenomyosis acting as a gonadotropin-releasing hormone receptor agonist.
Hypothesized mechanism
As a GnRH receptor agonist, goserelin downregulates pituitary gonadotropin release and induces a hypoestrogenic state, suppressing the estrogen-dependent ectopic endometrial tissue underlying 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 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 presented—an Open Targets database entry listing goserelin as a GnRH receptor agonist clinical candidate for adenomyosis. No independent mechanistic lines converge to support the claim.
Rigor
The claim cites a clinical candidate status (maximum clinical stage PHASE_2_3), implying human-relevant development, but no actual study models, data, or outcomes are reported—only a database annotation of mechanism and clinical stage.
Specificity
The mechanism is specifically defined as a gonadotropin-releasing hormone receptor agonist acting on the named target gonadotropin releasing hormone receptor, which is a precise drug-target relationship.
Plausibility
GnRH receptor agonism inducing a hypoestrogenic state fits well with the estrogen-dependent pathophysiology of adenomyosis, and the drug is annotated as a Phase 2/3 clinical candidate for this exact condition.
Consistency
With only one claim there is no opportunity for multiple signals to align or conflict; the single annotation is internally coherent but cannot demonstrate convergence.
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), GOSERELIN (a Protein) is a clinical candidate for adenomyosis (maximum clinical stage PHASE_2_3); its mechanism of action is Gonadotropin-releasing hormone receptor agonist on target gonadotropin releasing hormone receptor. Open Targets · mechanistic ↗
- 2In FDA AEMS (the FDA Adverse Event Reporting System, formerly FAERS; retrieved 2026-06-16), 110 report(s) of ABDOMINAL PAIN were recorded for GOSERELIN among female patients (of 4439 female reports for GOSERELIN 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 GOSERELIN acts on a system relevant to adenomyosis — as a mechanistic lead for further investigation, not evidence of benefit. AEMS · adverse-event report ↗
- 3Per SIDER (the Side Effect Resource, from pre-2015 drug labels), GOSERELIN lists Abdominal pain as a labeled side effect, reported in 0%. SIDER 4.1 is a 2015 snapshot, so newer drugs may be unrepresented; this is a label-derived association, not causation in any individual. Read two ways: as a safety consideration, and — because it suggests GOSERELIN acts on a system relevant to adenomyosis — as a mechanistic lead for further investigation, not evidence of benefit. SIDER · label side-effect ↗
- 4Per SIDER (the Side Effect Resource, from pre-2015 drug labels), GOSERELIN lists Dysmenorrhoea as a labeled side effect, reported in 1–10% of participants. SIDER 4.1 is a 2015 snapshot, so newer drugs may be unrepresented; this is a label-derived association, not causation in any individual. Read two ways: as a safety consideration, and — because it suggests GOSERELIN acts on a system relevant to adenomyosis — as a mechanistic lead for further investigation, not evidence of benefit. SIDER · label side-effect ↗
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 →