Administered at 10 mg/kg intraperitoneally, Fenretinide specifically counters ceramide buildup in HFD-fed male C57Bl/6 mice, enhancing glucose tolerance and insulin sensitivity as evidenced by glucose and insulin tolerance tests^[2].

The administration of 25 mg/kg ketoconazole with Fenretinide in NOD/SCID mice raises the plasma levels of 4-HPR^[3].

Fenretinide (4-HPR) is a synthetic retinoid deriverative, binding to the retinoic acid receptors (RAR) at concentrations necessary to induce cell death.Fenretinide (4-HPR) demonstrates both immediate and prolonged antitumor effects in specific T-ALL cell lines. It suppresses DES activity in CCRF-CEM leukemia cells dependent on dosage and duration, resulting in increased levels of endogenous cellular dhCer. A rise in dhCer levels is observed in both CCRF-CEM and Jurkat cells with Fenretinide treatment at 3 µM^[1].

Ceramide inhibition with fenretinide protects insulin signaling, which prevents lipid-induced reductions in insulin-stimulated glucose uptake^[2].

When applied at concentrations over 1 µM, Fenretinide impedes OVCAR-5 cell growth and survival, achieving 70-90% growth suppression at 10 µM. Preincubation with Fenretinide at 1 µM notably reduces OVCAR-5 cell invasion over three days. Furthermore, endothelial cells exposed to 1 µM of 4-HPR do not form tubular structures, instead forming small cell clusters^[4].