LG100268 is a potent, selective, and orally active retinoid X receptor (RXR) agonist that agonizes RXR-α, RXR-β, and RXR-γ at the nanomolar level, selectively exceeding the RAR by three orders of magnitude.LG100268 is capable of inducing transcriptional activation in adipocytes; affecting the RXRs and their chaperone receptor, Foxl2/Dmrt1, to induce flounder masculinization in juvenile flounder; inhibits keratin 17 expression in nigrostriatal epithelial cells; and increases PD-L1 expression in HER2 or triple-negative breast cancer.

Methods: RAW264.7 cells were treated with LG100268 (100 nM-1 μM, 24 hours) and protein level changes were detected by WB. Results: LG100268 can downregulate CSF3 in RAW264.7 cells and reduce CXCL2 and IL-1β mRNA expression by 2.5 times. [6]

Methods: To prevent invasive breast cancer, MMTV-erbB2 mice were treated chronically with vehicle, LG100268 (10 mg/kg), or LG100268 (100 mg/kg) by gavage starting at 3 months of age. For pre-invasive lesion studies, mice were treated with vehicle or LG100268 (100 mg/kg) by daily gavage for 4 months.
Results: Chronic LG100268 treatment significantly prevented the development of invasive breast tumors. The median time to tumor development (age) was delayed from 217 days in the vehicle group to 357 days in the low-dose group. In the high-dose group, only 2 of 20 mice developed tumors after 430 days of treatment. [5]