ArticleEndocrinology2025
Androgen Receptor PROTAC ARV-110 Ameliorates Metabolic Complications in a Mouse Model of Polycystic Ovary Syndrome.
Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Ubiquitination and NOncology letters · 2026Review
- AR PROTACs for PCOS: A Long-awaited Breakthrough?Endocrinology · 2025Article
- Androgen Receptor PROTAC ARV-110 Ameliorates Metabolic Complications in a Mouse Model of Polycystic Ovary Syndrome.Endocrinology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive-age women. Hyperandrogenemia (HA) is a hallmark of PCOS and is positively associated with metabolic complications. Androgens exert their biological actions through the androgen receptor (AR), which regulates transcriptional activity. Antiandrogens are not recommended for managing metabolic complications in PCOS due to their hepatotoxicity, despite being a viable therapy to treat HA. We hypothesized that the novel AR Proteolysis Targeting Chimera (PROTAC) degrader ARV-110 would downregulate AR protein levels and actions to abolish or mitigate HA-mediated metabolic complications using a well-established HA mouse model of PCOS. Three-week-old female mice were implanted with dihydrotestosterone (DHT) or control pellets. Four weeks later, mice were treated with low- (ARV-110-L, 1 mg/kg.day) or high-dose (ARV-110-H, 10 mg/kg.day) ARV-110 for an additional 8 weeks. ARV-110 dose-dependently reduced AR protein levels in white adipose tissue (WAT), kidney, liver, and ovary. ARV-110 attenuated DHT-induced increases in body weight, fat mass, kidney mass, WAT mass, circulating leptin and antimüllerian hormone, and altered glucose homeostasis. ARV-110-H increased kidney (UACR, KIM-1, NGAL) and liver (ALT, AST, LDH) injury markers and caused severe hepatomegaly, while ARV-110-L mostly spared those deleterious effects. Unbiased proteomics analysis revealed that ARV-110-H treatment severely affected the liver proteome and dysregulated multiple signaling and metabolic canonical pathways, while only minimal effects were observed with ARV-110-L treatment. In summary, our findings underscore the potential of AR PROTACs as a novel therapeutic approach for managing metabolic complications in PCOS, provided the dosing is carefully optimized to avoid adverse effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.