h-151

H-151 是一种 STING 拮抗剂，具有高效性和选择性。H-151 与 STING 的 Cys91 共价结合，抑制 Cys91 的棕榈酰化，从而抑制 STING 的活性。H-151 可用于体内外自身炎症性疾病的研究。

[Leu144,Arg147]-PLP (139-151)是髓鞘脂蛋白(PLP)的一种突变肽段，包含位于144和147位置的色氨酸到亮氨酸以及组氨酸到精氨酸的替换。使用[Leu144, Arg147]-PLP (139-151)（50 µg）乳化于完全弗氏佐剂(CFA)免疫后，能增加小鼠脾脏中的IL-4水平。它在体外抑制Th1细胞激活，但在体内不抑制，其中它诱导调节性T细胞的产生。用[Leu144, Arg147]-PLP (139-151)预免疫可以延迟由脑炎肽PLP (178-191)、髓磷脂少突细胞蛋白(MOG) (92-106)或髓鞘基础蛋白(MBP)在小鼠中诱导的实验性自身免疫性脑炎(EAE)的发病。

STING agonist 1a is an agonist of stimulator of interferon genes (STING).1It induces expression of an IRF-inducible SEAP reporter gene in a cell-based assay (EC50= 16.77 μM). STING agonist 1a (12.5-100 μM) induces expression of IFN-β, IL-6, and chemokine (C-X-C motif) ligand 10 (CXCL10) in THP-1 cells, an effect that can be reversed by STING knockout or the STING inhibitor H-151 . 1.Hou, H., Yang, R., Liu, X., et al.Discovery of triazoloquinoxaline as novel STING agonists via structure-based virtual screeningBioorg. Chem.100103958(2020)

Trihydroxycholestanoic acid is an intermediate in the biosynthesis of cholic acid .1 Elevated plasma levels of trihydroxycholestanoic acid have been found in patients with Zellweger syndrome, a neurological disorder characterized by mutations in PEX genes which result in defects in peroxisome formation.2,3 |1. Keane, M.H., Overmars, H., Wikander, T.M., et al. Bile acid treatment alters hepatic disease and bile acid transport in peroxisome-deficient PEX2 Zellweger mice. Hepatology 45(4), 982-997 (2007).|2. Ferdinandusse, S., Overmars, H., Denis, S., et al. Plasma analysis of di- and trihydroxycholestanoic acid diastereoisomers in peroxisomal α-methylacyl-CoA racemase deficiency. J. Lipid Res. 42(1), 137-141 (2001).|3. Klouwer, F.C.C., Berendse, K., Ferdinandusse, S., et al. Zellweger spectrum disorders: Clinical overview and management approach. Orphanet J. Rare Dis. 10, 151 (2015).