---
title: "Simvastatin and Primaquine Show Promise for Endometriosis in Human Epithelial–Stromal Assembloid S"
id: "biorxiv-0-simvastatin-and-primaquine-identified-as-potential-endometriosis-therapeutics"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-simvastatin-and-primaquine-identified-as-potential-endometriosis-therapeutics"
content_type: "clinical_feed_article"
specialty: "General"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1?rss=1"
published_at: "2026-09-27T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Simvastatin and Primaquine Show Promise for Endometriosis in Human Epithelial–Stromal Assembloid S
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-simvastatin-and-primaquine-identified-as-potential-endometriosis-therapeutics
- **Specialty:** [General](https://medichelpline.com/clinical-feed/general.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1?rss=1)
- **Published At:** 2026-09-27T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study used a novel human endometrial **epithelial–stromal assembloid** model to test candidate therapeutics for **endometriosis** identified by prior drug-repositioning analyses. - Assembloids combined immortalized epithelial (12Z) and stromal fibroblast (iEc) cell lines, and were also generated from primary patient tissue in 96-well agarose molds to better recapitulate tissue interactions. - Four compounds were tested: **simvastatin**, **primaquine**, fenoprofen, and ibuprofen, each applied for a 24-hour exposure period; monolayer cultures were included for comparison. - RNA was profiled using stranded mRNA sequencing on an Illumina NovaSeqX Plus System, and gene set enrichment analyses evaluated pathway-level reversals associated with endometriosis. - Key pathway findings: primaquine reversed a chemical carcinogenesis–ROS pathway in assembloids; simvastatin reversed **cytokine–cytokine receptor interaction** pathways in both epithelial and stromal cell lines and affected a cytoskeleton-in-muscle pathway in stromal lines; fenoprofen reversed calcium signaling in stromal lines. - **Simvastatin** produced the largest gene expression changes and specifically reversed inflammatory cytokine-related pathways, consistent with prior behavioral pain reduction observed in a rat model referenced by the authors. - The authors highlight assembloid models as a promising intermediate platform for testing therapeutic candidates but note the study’s small sample size as a limitation. - The report is a preprint (not peer reviewed); competing interests include patent holdings by some authors and declared advisory/consultancy roles for one author. Funding sources were reported.
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Giudice doi: https://doi.org/10.64898/2026.09.27.754752 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Ferheen Abbasi 1 Department of Obstetrics, Gynecology & Reproductive Sciences, UCSF, San Francisco, CA, USA; School of Medicine, UC Davis, Sacramento, CA, USA; Mass General Brigham Hospital, Harvard University, Boston, MA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ferheen%2BAbbasi%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Abbasi%20F&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AFerheen%2BAbbasi%2B) Xinyu Tang 2 Bakar Computational Health Sciences Institute, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Xinyu%2BTang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Tang%20X&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AXinyu%2BTang%2B) * [ORCID record for Xinyu Tang](http://orcid.org/0000-0002-4567-4012 "Open in new tab") Juan C Irwin 3 Department of Obstetrics, Gynecology & Reproductive Sciences, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Juan%2BC%2BIrwin%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Irwin%20JC&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJuan%2BC%2BIrwin%2B) Binya Liu 3 Department of Obstetrics, Gynecology & Reproductive Sciences, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Binya%2BLiu%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Liu%20B&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ABinya%2BLiu%2B) Tomiko T Oskotsky 4 Bakar Computational Health Sciences Institute, UCSF, San Francisco, CA, USA; Division of Clinical Informatics and Digital Transformation, Department of Medicine, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Tomiko%2BT%2BOskotsky%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Oskotsky%20TT&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ATomiko%2BT%2BOskotsky%2B) * [ORCID record for Tomiko T Oskotsky](http://orcid.org/0000-0001-7393-5120 "Open in new tab") Marina Sirota 5 Bakar Computational Health Sciences Institute, UCSF, San Francisco, CA, USA; Department of Pediatrics, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Marina%2BSirota%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Sirota%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMarina%2BSirota%2B) * [ORCID record for Marina Sirota](http://orcid.org/0000-0002-7246-6083 "Open in new tab") Frederick J Meyers 6 Department of Internal Medicine, Division of Hematology and Oncology, UC Davis Health, Sacramento, CA, USA * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Frederick%2BJ%2BMeyers%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Meyers%20FJ&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AFrederick%2BJ%2BMeyers%2B) Linda C. Giudice 3 Department of Obstetrics, Gynecology & Reproductive Sciences, UCSF, San Francisco, CA, USA; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Linda%2BC.%2BGiudice%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Giudice%20LC&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALinda%2BC.%2BGiudice%2B) * [ORCID record for Linda C. Giudice](http://orcid.org/0000-0002-1677-0822 "Open in new tab") * For correspondence: linda.giudice@ucsf.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5816876/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5816876/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5816876/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5816876/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5816876/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Background: Endometriosis is an estrogen-driven, inflammatory disorder affecting ~10% of menstruators, causing severe pain. Current treatments that reduce estrogen or inflammation have inconsistent efficacy and poor tolerability. Therapies identified via drug-repositioning methods, which target patient-specific pathways, offer a promising alternative. Simvastatin and primaquine were identified as potential treatments, strongly reversing endometriosis-associated gene expression pathways, and behavioral testing in an animal model showed that these drugs diminish endometriosis-associated pain. This paper examines their effects in human assembloids to provide proof-of-concept validation and insights into their mechanisms of action relevant to endometriosis. Methods: We established human endometrial assembloids using immortalized epithelial (12Z) and stromal fibroblast (iEc) cell lines, as well as primary tissue from patients. Assembloids were generated in 96-well agarose molds with both cell types. We tested ibuprofen, fenoprofen, primaquine, and simvastatin. Following a 24-hour exposure, assembloids and monolayer cultures were harvested and stranded mRNA-seq libraries were sequenced on an Illumina NovaSeqX Plus System. Results: Gene set enrichment analysis showed key pathway reversals: Primaquine reversed the chemical carcinogenesis ROS pathway in assembloids. Simvastatin reversed cytokine-cytokine receptor interaction in both epithelial and stromal cell lines, and the cytoskeleton in muscle cells pathway in stromal cell lines. Fenoprofen reversed the calcium signaling pathway in stromal cell lines. Conclusion: Simvastatin induced the most significant gene expression changes, notably reversing cytokine-cytokine receptor interactions in both cell lines, mirroring findings from our rat model. Despite the small sample size limitation, these experiments highlight the promise of assembloid models to test therapeutic candidates for endometriosis. ### Competing Interest Statement LCG has received fees and/or travel grant support during the last 3 years as follows; Scientific Advisory Board Chair, Gesynta Pharma; consultant, Chugai Pharmaceuticals; Advisory Board member, Sumitomo Pharma America; Scientific Advisory Board member, Celmatix. She is on the World Endometriosis Research Foundation Board of Directors (unpaid position). TTO, MS, and LCG have a patent related to this work. The remaining authors declare no competing interests. ## Funder Information Declared Eunice Kennedy Shriver National Institute of Child Health and Human Development ASCI, PSSF Fellowship UC Davis, ARC-MD Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY-NC-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. [Donate to openRxiv ](https://www.zeffy.com/en-US/donation-form/donate-to-make-a-difference-10981) [ Back to top](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1?rss=1#page) [ Previous](https://www.biorxiv.org/content/10.64898/2026.09.21.753191v1 "Benchmarking single-cell foundation models for aging biology")[Next ](https://www.biorxiv.org/content/10.64898/2026.09.25.754057v1 "Combining CHARMM36m with OPC water improves accuracy") Posted September 27, 2026. [ Download PDF](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/09/27/2026.09.27.754752.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.09.27.754752v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) Simvastatin and Primaquine Identified as Potential Endometriosis Therapeutics via a Novel Epithelial-Stromal Assembloid Drug Screening Assay Ferheen Abbasi, Xinyu Tang, Juan C Irwin, Binya Liu, Tomiko T Oskotsky, Marina Sirota, Frederick J Meyers, Linda C. Giudice bioRxiv 2026.09.27.754752; doi: https://doi.org/10.64898/2026.09.27.754752 This article is a preprint and has not been certified by pe
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