Bromocriptine for adenomyosis
Bromocriptine is annotated as a Phase 1 clinical candidate for adenomyosis acting as a D2-like dopamine receptor agonist on DRD2.
Hypothesized mechanism
Bromocriptine activates dopamine receptor D2 (D2-like agonism), which may suppress prolactin and dopaminergic pathways relevant to 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 2.3 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 mechanistic line is provided: BROMOCRIPTINE as a D2-like dopamine receptor agonist on DRD2 (claim 1). No independent converging lines are presented.
Rigor
The only evidence is a database annotation from Open Targets listing a maximum clinical stage of PHASE_1, with no described study, model, or human outcome data. There is no mechanistic or experimental model evidence to assess relevance or recency.
Specificity
The claim names a defined target (dopamine receptor D2) and a defined action (D2-like agonist), giving moderate target specificity. However, 'D2-like' agonism implies action across the broader D2-family, limiting true selectivity.
Plausibility
Bromocriptine being a listed Phase 1 clinical candidate for adenomyosis (claim 1) suggests a presumed target-phenotype link, plausibly via prolactin suppression. But no mechanistic data connecting DRD2 agonism to adenomyosis pathology is provided.
Consistency
With only one annotation there is nothing contradictory, but also no multiple signals to confirm directional agreement. Consistency cannot be meaningfully demonstrated from a single source.
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. We read its public dataset release, which covers 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 3.77 (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:3181 (drug) and MONDO:0010888 (disease). Validate against the source: Every Cure’s MATRIX dataset ↗.
More on the MATRIX cross-reference and its provenance →Regulatory & development status
Where this candidate sits in the US regulatory landscape: whether the drug is already FDA-approved for adenomyosis (on-label) or approved for something else (off-label), whether the molecule is available as a generic or a single-source brand still under patent, and how far it has been studied as a therapy for this condition. Each fact is drawn from a public US source and reported beside the score; none of it is folded into the score.
This is descriptive context, not regulatory advice. It maps the landscape a 505(b)(2)route would build on (an already-approved active ingredient proposed for a new indication), but it is not a 505(b)(2) viability assessment, and says nothing about whether any particular development path is advisable. “Approved” means FDA-approved (US); approvals elsewhere are out of scope.
Approval relationship Off-label
Read from the drug’s FDA label via DailyMed, the US National Library of Medicine’s label repository. A label is only counted when it carries an FDA-approved marketing category (an NDA, ANDA, or biologic BLA); dietary supplements, homeopathics, and OTC-monograph products are not FDA-approved drugs and are excluded.
For this pair. The drug has an FDA-approved label, but for a different indication, so using it for this condition would be off-label.
Generic & patent supply Generic available
Read from the FDA Orange Book (Approved Drug Products with Therapeutic Equivalence Evaluations), using single-ingredient products only so that patents on novel branded combination formulations are never attributed to the base molecule.
For this molecule. A live ANDA lists this active ingredient, so the basic molecule is available as a generic (off-patent in its basic form).
Clinical-trial stage, for this condition Phase 1
Read from ClinicalTrials.gov (US National Library of Medicine). A trial only counts when the drug appears as an experimental or active-comparator intervention in an interventional study of this condition; mechanistic, drug-interaction, post-marketing (Phase 4), and comparator-background uses are excluded, so this reflects the drug being tested as a therapy for adenomyosis.
For this pair. Studied in 1 qualifying interventional trial · highest stage reached Phase 1 · completed.
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), BROMOCRIPTINE (a Small molecule) is a clinical candidate for adenomyosis (maximum clinical stage PHASE_1); its mechanism of action is D2-like dopamine receptor agonist on target dopamine receptor D2. 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 →