cd86

G-744 is a selective and orally active inhibitor of Btk (IC50: 2 nM). G-744 is well-tolerated, metabolically stable. It also has an efficacious to treat arthritis.

Anti-Mouse CD86/B7-2 Antibody (GL-1) 是一种源自大鼠的 IgG2a, κ 型抗体，可以抑制小鼠 CD86/B7-2。

Calcium influx inducer compound 634 是一种钙内流诱导剂。Calcium influx inducer compound 634 (10 µM) 增加小鼠骨髓来源树突状细胞 (mBMDCs) 外泌体 (EVs) 的释放，并提升 mBMDCs 表面CD86和CD80的水平，这种效应可被钙释放激活钙通道抑制剂YM-58483 阻断。

LSD1-IN-38 (Compound 23e) 是一种具有口服活性的可逆性赖氨酸特异性脱甲基酶 1 (LSD1) 抑制剂，IC50为 1.2 nM。该化合物能有效抑制癌细胞MV4-11、Kasumi-1和NCI-H526的增殖，其IC50分别为5 nM、4 nM和11 nM。LSD1-IN-38 还能够激活CD86的表达，EC50为0.034 μM，促进MV4-11细胞分化。在小鼠模型中，LSD1-IN-38 展示了明显的抗肿瘤活性。

TLR7 agonist 29 (Compound 1) 是一种TLR7激动剂，人TLR7的EC50为5.2 nM（小鼠TLR7的EC50为48.2 nM）。它可以激活骨髓来源的巨噬细胞 (BMDM)，刺激肿瘤微环境中的髓系细胞，并促进PD-L1、CD86和IFN-α的表达。TLR7 agonist 29 还可用作合成ADC的有效载荷。

Cyclic di-IMP (sodium salt) (c-di-IMP) is a synthetic second messenger structurally related to the bacterial second messengers cyclic di-GMP and cyclic di-AMP . C-di-IMP has adjuvant properties when co-administered with antigens in vitro and by mucosal routes in vivo. C-di-IMP enriches the population of MHC class I and II, CD80, CD86, CD40, and CD54 positive dendritic cells derived from murine bone marrow. It also stimulates macrophages at 500 ng ml. Mice immunized with β-galactosidase (β-gal) plus c-di-IMP through the intranasal route show a humoral immune response, evidenced by an increase in IgG titers up to 2-fold compared to mice immunized with β-gal alone. Mice immunized with β-gal plus c-di-IMP also exhibit a Th1 Th2 response, indicating that the adjuvant activity of c-di-IMP leads to a cellular immune response as well.

Anti-inflammatory agent 16 (compound 14) is a highly effective peptidomimetic with potent anti-inflammatory properties. It effectively reduces the expression levels of TNFα, NO, CD40, and CD86 [1].

LSD1-IN-13 (compound 7e) 是一种口服具有活力的 LSD1 抑制剂 (IC50: 24.43 nM)，也能够激活 CD86 表达 (EC50: 470 nM)。LSD1-IN-13 可以诱导 AML (急性髓系白血病) 细胞系分化。

LSD1-IN-13 hydrochloride (compound 7e) 是一种口服具有活力的 LSD1 抑制剂 (IC50: 24.43 nM)。LSD1-IN-13 hydrochloride 能够激活 CD86 表达 (EC50: 470 nM)。LSD1-IN-13 hydrochloride 可以诱导 AML (急性髓系白血病) 细胞系分化。

BTK-IN-18 是一种有效的、可逆的 BTK 抑制剂，IC50为 0.002 µM。BTK-IN-18 在体内抑制 CD69和 CD86。

ODN D-SL03是C类CpG寡核苷酸，能诱导PBMCs产生高水平IFN-α，激活人B细胞、NK细胞和单个核细胞，同时上调PBMCs亚群表面CD80、CD86和HLA-DR的表达，还能抑制肿瘤生长。ODN D-SL03序列：5'-tcgcgaacgttcgccgcgttcgaacgcgg-3'。

M04 acts as a stimulator of interferon genes (STING) agonist, effectively inducing IFN reporter gene expression in HEK293T cells equipped with wild-type human STING. Its activity is specific, not affecting HEK293T cells with the R71H-G230A-R293Q (HAQ) human STING variant or mouse RAW 264.7 cells, showcasing allelic- and species-dependent effects at a concentration of 75 µM. This compound also stimulates the production of TNF-α, IL-10, IL-1β, and IL-12p70 in human peripheral blood mononuclear cells (PBMCs). At 50 µM, M04 enhances human monocyte-derived dendritic cells' expression of HLA-DR (MHC class II receptor) and co-stimulatory molecules CD40, CD80, and CD86, improving T cell cross-priming in an ex vivo assay.

HSP90-IN-31（compound Be01）能够显著降低树突状细胞（DC）表面CD80与CD86的表达。在LPS激活的BMDC和腹膜巨噬细胞中，该化合物有效减少了促炎细胞因子（IL-6、TNF-α和IL-1β）的产量。此外，在迟发型超敏反应（DTH）的小鼠模型中，HSP90-IN-31能减轻耳部的肿胀及脾脏内的促炎细胞因子水平。

Macluraxanthone (3-Hydroxyblancoxanthone) 具有许多生物活性，包括抗胆碱酯酶、抗氧化、抗癌、抗疟疾、抗炎和免疫调节作用。Macluraxanthone 通过增加表达CD86的巨噬细胞的百分比，同时减少其CD14、CD11b 和CD80的表达，来促进M1类促炎症巨噬细胞的极化。Macluraxanthone 在促炎症刺激物脂多糖的存在下明显减少了TNF-α和IL-10细胞因子的产生。