Antagonizing the corticotropin-releasing hormone receptor 1 with an orally bioavailable drug reduces endometriosis pain and associated adhesions
Clicks: 2
ID: 314632
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
0.3
/100
2 views
1 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #106 of 128 articles by views in biology of reproduction
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 128 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Abstract Estrogen stimulates corticotropin-releasing hormone (CRH) expression in endometrial tissue, and CRH signaling contributes to inflammation and pain, suggesting a mechanistic role in endometriosis pathophysiology. We previously identified elevated CRH receptor-1 (CRHR1) levels in endometriotic lesions in a rat model. Here, we tested the hypothesis that antagonizing CRHR1 with pexacerfont, an orally bioavailable small-molecule antagonist, would reduce endometriosis-associated pain and lesion activity. Beginning 25 days after disease induction, rats received pexacerfont (10 mg/kg), vehicle, or elagolix (14 mg/kg) in 7-day treatment cycles separated by 7-day drug-free intervals up to day 60 after endometriosis onset. Pexacerfont significantly reduced mechanical and inflammatory pain (34% and 38% decreases, respectively) and decreased nerve growth factor (NGF), vascular endothelial growth factor (VEGF), Ki67, and IL-6 and TNF-α mRNA expression within lesions. Unlike elagolix, pexacerfont did not alter peritoneal leptin-to-weight or serum FSH-to-LH ratios, indicating minimal disruption of gonadal endocrine signaling. Notably, pexacerfont reduced macroscopic adhesion scores by half, a therapeutic effect not observed with either vehicle or elagolix. CRHR1 antagonism, therefore, suppressed neuro-inflammatory and proliferative pathways while limiting lesion-associated angiogenesis and postoperative adhesion development. These findings position CRHR1 as a mechanistically distinct, non-hormonal therapeutic target for endometriosis and highlight pexacerfont’s potential to reduce both pain and adhesions.
| Reference Key |
openalex_W7162147340
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Annelyn Torres-Reverón, Jaydie M Valles Ortiz, Myrella L. Cruz, Omar Velez-Lopez, Idhaliz Flores, Caroline B. Appleyard |
| Journal | biology of reproduction |
| Year | 2026 |
| DOI |
10.1093/biolre/ioag107
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.