Cridanimod (10-carboxymethyl-9-acridanone, CMA) is a potent STING agonist that directly binds to STING and triggers a strong antiviral response through the TBK1/IRF3 route.

STING (mouse):3.5 μM (Kd)

CMA诱导了强烈的IRF3磷酸化，随后引发了Ifnb mRNA的大量诱导和翻译。CMA介导的IFNβ产量在刺激后已于4小时内达到高峰，甚至超过了LPS在触发IFNβ合成的准备度[1]。rSTING和hSTING对CMA的反应不明显或仅弱反应，而mSTING则被强烈激活。在小鼠巨噬细胞中，CMA处理后Ifnb、Cxcl10和Il6的内源性mRNA水平显著增加，但在大鼠巨噬细胞和人THP-1细胞中则未见明显增加[2]。

For transfection experiments, primary macrophages were seeded with a density of 1 × 10^5?per?ml. Cells were transfected with poly(I:C) (2?μg/ml), pppRNA (1.33?μg/ml), ISD (2?μg/ml) and c-diGMP (8.66?μg/ml) using Lipofectamine 2000, according to the manufacturer's instructions. LPS (200?ng/ml) and CMA were directly added to the medium. Human PBMCs were transfected as described above, at a density of 4 × 10^6?per?ml, human fibroblasts at a density of 1.5 × 105?per?ml. For western blot experiments, cells were lysed after 2?h, if not indicated otherwise. For cytokine assays, supernatants were collected after 18–20?h. For RNA isolation, cells were lysed after 4?h [1].