DOPE (GMP)

DOPE GMP is DOPE (HY-112005) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. DOPE (Dioleoylphosphatidylethanolamine; 1,2-Dioleoyl-sn-glycero-3-phosphoethanolamine) is an orally active inhibitor of ferroptosis with anti-inflammatory and intestinal barrier maintenance activities. DOPE regulates the expression of ACSL4, SLC7A11 and GPX4 to restore the redox system balance, thereby reducing the levels of lipid peroxides, iron ions and intestinal inflammatory factors (IL-1β and IL-6). DOPE promotes the migration and proliferation of intestinal epithelial cells and increases the level of tight junction proteins; it also destabilizes endosomal membranes, mediates the conjugation of RVG peptides with mesenchymal stem cell-derived exosomes to enhance brain targeting. DOPE can be applied to research related to neonatal necrotizing enterocolitis and Alzheimer's disease^[1][2][3][4]. In Vitro: FITC-labeled DOPE GMP (2 h) is internalized by IEC-6 rat intestinal epithelial cells within 2 hours, and fluorescence is detectable in both the cytoplasm and nucleus^[1].
DOPE GMP (5 μg/mL; 1 h) restores the migratory capacity of IEC-6 rat intestinal epithelial cells inhibited by LPS^[1].
DOPE GMP (5 μg/mL; 1 h) restores the migration and proliferation capacities, as well as the expression of tight junction proteins (ZO-1, occludin), in RSL3-induced ferroptotic rat intestinal epithelial cells IEC-6^[1].
DOPE GMP enhances the uptake efficiency of mesenchymal stem cells for AMSC-MP, improves the cell adhesion ability to scaffolds, upregulates the expression of osteogenesis-related gene RUNX2, and enhances in vitro osteogenic differentiation capacity. Moreover, this formulation exhibits excellent biocompatibility and does not exert adverse effects on cell viability^[2]. In Vivo: DOPE GMP (1 mg/kg; p.o.; 3 times daily; 4 days) reduces mortality, lowers NEC pathological injury scores, inhibits intestinal inflammation, restores intestinal barrier and proliferative function, and upregulates anti-ferroptosis marker GPX4 in neonatal SD rats with experimentally induced NEC^[1].