Darapladib (SB-480848) is a lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor with an IC50 value of 0.25 nM, which can exert cardiovascular protective effects [1,3].

Lp-PLA2:0.25 nM

METHODS: Bone marrow-derived macrophages (BMDM) were primed with LPS (100 ng/mL) for 3 h, then treated with 100 nM Darapladib (SB-480848) for 1 h, followed by Ang II (100 nmol/L) treatment for the indicated times.
RESULTS Darapladib (SB-480848) attenuated Ang II-induced NLRP3 inflammasome activation and IL-1β production in cardiac macrophages. [3]

METHODS: Atherosclerotic Sprague-Dawley rats were fed a high-cholesterol diet for 10 weeks, followed by oral administration of low-dose Darapladib (SB-480848) (25 mg·kg-1·d-1) and high-dose Darapladib ( SB-480848) (50 mg·kg-1·d-1) intervention.
RESULTS Serum triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP) in the atherosclerosis model group ) and Lp-PLA2 levels were significantly increased, Rho kinase activity and cardiomyocyte apoptosis were also significantly increased (p<0.05 vs. sham operation group), while nitric oxide (NO) production was decreased; Darapladib (SB-480848 ) TC, LDL-C, CRP, Lp-PLA2, and Rho kinase activities were reduced in each group, and NO production was increased; compared with the low-dose Darapladib (SB-480848) group, TC, LDL -C, CRP, and Lp-PLA2 decreased more significantly (p<0.05), and NO production increased more significantly (p<0.05). Compared with the low-dose Darapladib (SB-480848) group, cardiomyocyte apoptosis in the high-dose Darapladib (SB-480848) group was also significantly reduced (p<0.05). However, there was no significant difference in Rho kinase activity between the low-dose Darapladib (SB-480848) group and the high-dose Darapladib (SB-480848) group (p>0.05). [2]