Neopterin

Neopterin is an immune system activator metabolized by GTP and can be produced by activated macrophages. Neopterin has the potential to resist vascular inflammation and atherosclerosis. Neopterin inhibits the phosphorylation of NF-κB and promotes the expression of PPAR-γ, thereby suppressing the inflammatory response of vascular endothelial cells, reducing the formation of macrophage foam cells, and regulating the migration and proliferation of vascular smooth muscle cells. Neopterin can be used in research fields such as cardiovascular diseases (such as atherosclerosis), inflammation-related diseases and tumor immunomonitoring^{[1][2][3][4][5]}. In Vitro:Neopterin (200 nM; 4-48 h) inhibits cell proliferation, reduces the mRNA and protein expression of inflammatory factors such as MCP-1, ICAM-1, and VCAM-1 induced by TNF-α, and reduces monocyte adhesion in human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs)^[1].
Neopterin (200 nM; 7 d+19 h) inhibits oxidized low-density lipoprotein (oxLDL)-induced foam cell formation in human monocyte-derived macrophages (HMDMs), downregulates CD36 expression, upregulates ABCA1, ABCG1, and LXR-α protein levels, and promotes cholesterol efflux^[1].
Neopterin (200 nM; 24-48 h) inhibits angiotensin II-induced cell migration and proliferation, downregulates the c-Src/Raf-1/ERK1/2 signaling pathway, and upregulates the expression of fibronectin, MMP-2, and TIMP-2 proteins in human aortic smooth muscle cells (HASMCs)^[1].
In Vivo:Neopterin (1.2 μmol/kg; ip; once a day; 4 weeks) significantly slows the progression of aortic atherosclerotic lesions, reduces plaque area and monocyte/macrophage and CD8+ T cell infiltration, and reduces the content of vascular smooth muscle cells and plasma PTX-3 levels in apolipoprotein E-deficient (Apoe-) mice[1].
Neopterin (0.4-4.0 mg/kg; iv; single dose, tested for 21 days) causes a decrease in the number of bone marrow erythroid progenitors (BFU-E, CFU-E) and an increase in the number of myeloid progenitors (CFU-GM) in young mice in the aging-associated stromal cell damage model of male senescence-accelerated mice, while the number of erythroid progenitors decreases in aged mice, but serum erythropoietin (Epo) concentrations did not decrease.^[2].