Targretin oral (bexarotene oral)

The low-risk group exhibited improved survival outcomes and increased sensitivity to immunotherapy, whereas the high-risk group showed heightened sensitivity to to bexarotene, bicalutamide, embelin, FH535, and pazopanib. Quantitative PCR results indicated that ILF3-DT and PPP1R14B-AS1 were downregulated in CC tissues, whereas RUSC1-AS1 was upregulated. In conclusion, we developed a novel prognostic risk signature based on 9 disulfidptosis-related lncRNAs, which may serve as an independent predictor of immunotherapy response and chemotherapy sensitivity in CC.

GSTK1 was shown to be a tumor suppressor via its role in MQC and L-carnitine metabolism. Bexarotene and L-carnitine supplementation may serve as potential therapeutic strategies for HCC treatment.

This case highlights bexarotene as a promising therapeutic option for refractory pcALCL. Our experience reinforces the potential of bexarotene as a viable treatment for pcALCL, particularly in recurrent or refractory cases where conventional therapies are contraindicated or ineffective.

Bexarotene alleviates BCP in rats by suppressing the aberrant overexpression of SLC38A3, thereby blocking the PI3K/AKT signaling pathway-mediated upregulation of TRPV1. These findings indicate that SLC38A3, through its downstream PI3K/AKT-TRPV1 axis, may serve as a potential molecular mechanism for analgesia in BCP.

Under BXR treatment, a reduced frequency of cells with these gut-homing receptors was observed in the blood of CTCL patients regarding memory T cells (mean off: 1.9%; on: 0.6%) and B cells (mean off: 5.7%, on: 4%). BXR via RXRs directly targets B and T lymphocytes, inducing retinoid target gene expression, including gut-homing receptors.

P1, N=12, Completed, National Cancer Centre, Singapore | Recruiting --> Completed | Trial primary completion date: Sep 2024 --> Aug 2025

These findings suggest a novel extracellular activity of bexarotene and validate the combined use of TRIC and TR-FRET as a scalable screening strategy for SLIT2-targeted small molecules. This platform lays the groundwork for future high-throughput discovery efforts against SLIT2 and its signaling axis.

An axially substituted polypyridyl Re(CO)3 complex bearing bexarotene triggered caspase-3/7-mediated apoptosis in cancer cells through ROS generation and NADH photo-oxidation.

These findings clarify the cell-specific complexity of RXR-mediated regulation and underscore APOE as a central mediator of bexarotene's neuroprotective effects. This study provides mechanistic insights into RXR-targeted interventions, and supports APOE-associated pathways as promising therapeutic targets in AD.

They were also more sensitive to Dasatinib, Bexarotene, and Bicalutamide. APOBEC1 was overexpressed across multiple cancer types and promoted proliferation and migration in LUSC cell lines. This study presents a robust CR-based survival model and highlights APOBEC1 as a potential therapeutic target in LUSC.

Screening a lipid metabolism-focused compound library (653 molecules) yielded bexarotene, as the most potent small molecule SLIT2 binder reported to date, with a dissociation constant ( K D ) of 2.62 µM...This platform lays the groundwork for future high-throughput discovery efforts against SLIT2 and its signaling axis. TRIC-based small molecule screening platform protocol steps with implementation of TR-FRET for the identification of SLIT2 inhibitors.

Furthermore, we observed that the integrin αvβ3 inhibitor, cilengitide, not only reverts these effects but also enhances the anti-lymphoma activity to a greater extent than the JAK1/2 inhibitor, ruxolitinib, when combined with bexarotene, a synthetic rexinoid clinically used for cutaneous TCL treatment. Additionally, we observed that high integrin αvβ3 mRNA levels are enriched in pathways associated with lymphoma progression and reduce overall survival in TCL patient samples. Our findings support the therapeutic potential of targeting THs signaling through integrin αvβ3 inhibition in combination with bexarotene as a less toxic therapeutic strategy to mitigate aberrant JAK/STAT activation and limit lymphoma dissemination.