Sphinganine 1-phosphate, also known as D-erythro-Dihydrosphingosine 1-phosphate, is a polar sphingolipid metabolite. It plays a crucial role in regulating various cellular processes including cell migration, differentiation, survival, and complex physiological processes.

Sphinganine 1-phosphate (S1P) is a critical signaling molecule that plays diverse roles in cellular processes including stress responses, cancer progression, angiogenesis, lymphocyte trafficking, and the regulation of cell metabolism. It achieves its functions by activating specific members of the endothelial differentiation gene (EDG) family of G-protein coupled receptors located on cell surfaces. Interestingly, S1P exhibits dual functions in metabolic regulation. It is essential for the differentiation and regeneration of skeletal muscle[1], and plays a significant role in cancer by mediating processes like inflammation, which promotes tumor development, neovascularization—supplying cancer cells with necessary nutrients and oxygen—and the proliferation and survival of cells[1]. In experimental studies, S1P at a concentration of 1μM has been shown to phosphorylate ERK MAPK, Akt, and HSP27, as well as induce HSP27 expression in human renal endothelial cells, highlighting its role in cell signaling pathways[2]. When evaluated using a Cell Viability Assay, this compound at 1μM concentration triggered the expression of HSP27 mRNA and phosphorylated ERK MAPK and AKT in a time-dependent manner within these cells[2], demonstrating its potent impact on cellular functions.

Sphinganine 1-phosphate can enhance wound healing in diabetic mice[1].

Sphinganine 1-phosphate provides renal and hepatic protection after liver ischemia and reperfusion (IR) injury in mice through selective activation of S1P1 receptors and pertussis toxin-sensitive G-proteins with subsequent activation of ERK and Akt. Sphinganine 1-phosphate (administered 0.1?mg/kg i.v. immediately before reperfusion and 0.2?mg/kg s.c. 2?h after reperfusion) protects against hepatic and renal injury after liver IR[2]. Animal Model: Male C57BL/6 mice (20-25?g)[2]Dosage: 0.1?mg/kg Administration: Administered i.v. immediately before reperfusion and 0.2?mg/kg s.c. 2 h after reperfusion Result: The plasma level of alanine aminotransferase (ALT) and Creatinine (Cr) was 80±6 U/L and 0.46±0.05 mg/dL, respectively. The increases in ALT (7474±557?U/L) and Cr (0.55±0.05?mg/dL) were significantly suppressed at 24?h after reperfusion in mice treated with 0.1?mg/kg i.v. before reperfusion and 0.2?mg/kg s.c. 2?h after reperfusion.