BENTAMAPIMOD for endometriosis
BENTAMAPIMOD is annotated as a Phase 2 clinical candidate for endometriosis acting as a JNK (MAPK8) inhibitor according to Open Targets.
Hypothesized mechanism
BENTAMAPIMOD inhibits c-Jun N-terminal kinase (JNK/MAPK8), potentially modulating MAPK signaling implicated in endometriotic tissue growth.
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 source (Open Targets) is cited, providing one annotation linking BENTAMAPIMOD to endometriosis via JNK inhibition. No independent mechanistic lines converge—there is just one drug-target-indication record.
Rigor
The claim is a database annotation of clinical candidate status (Phase 2) with no described experimental model, human or otherwise. No data, study design, or mechanistic experiments are presented to assess model quality.
Specificity
The claim names a specific target (mitogen-activated protein kinase 8 / JNK) and identifies BENTAMAPIMOD as a JNK inhibitor on that target. However, JNK has multiple isoforms and broad signaling roles, and the claim does not establish selectivity beyond the named annotation.
Plausibility
The claim asserts BENTAMAPIMOD is a Phase 2 clinical candidate for endometriosis acting via JNK inhibition, implying a target-phenotype link. But no mechanistic detail connecting JNK signaling to endometriosis pathology is provided to substantiate the fit beyond the database listing.
Consistency
There is only one signal (a single Open Targets annotation), so there is no contradiction, but also no multiple signals to corroborate directionality. Consistency cannot be strongly affirmed with a single record.
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), BENTAMAPIMOD (a Small molecule) is a clinical candidate for endometriosis (maximum clinical stage PHASE_2); its mechanism of action is c-Jun N-terminal kinase, JNK inhibitor on target mitogen-activated protein kinase 8. 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 →