marrow-derived macrophages

NDMC101 是有效的破骨细胞形成抑制剂，通过下调 NFATc1 调控基因表达抑制破骨细胞分化。它与 DPP4底物相似，通过抑制DPP4抑制早期 T 细胞激活。它能够用于骨疾病的研究，如类风湿关节炎、滑膜炎等。

NLRP3-IN-NBC6 是一种有效的选择性 NLRP3炎性小体抑制剂 ，IC50为574 nM，其作用独立于 Ca2+。NLRP3-IN-NBC6 抑制 Nigericin 诱导的 THP-1 细胞炎症反应和 Imiquimod 诱导的 LPS-primed 的骨髓源性巨噬细胞 (BMDMs) 释放 IL-1β。

NLRP3-IN-49（又名compound Z48）是一种高效且选择性极强的NLRP3抑制剂，其在THP-1 细胞中的IC50值为0.26 μM，在小鼠骨髓巨噬细胞中为0.21 μM。该化合物能直接与NLRP3蛋白结合（Kd=1.05 μM），有效阻断NLRP3炎性小体的组装及其激活，显示出显著的抗炎效果。NLRP3-IN-49适用于炎症性肠病的研究领域。

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.

11R-VIVIT TFA (592517-80-1 Free base) 是一种 NFAT 抑制剂。 11R-VIVIT TFA 抑制 LPS 或 LPS 加 IFN-γ 诱导的骨髓源性巨噬细胞 (BMDM) 分泌 IL-12 p40、IL-12 p70、IL-23 和 TNF。 11R-VIVIT TFA 减弱 LPS 刺激的 BMDM 中 NO 的产生和 Nos2 mRNA 的表达。 11R-VIVIT TFA 改善结肠炎小鼠模型的症状。 11R-VIVIT TFA 表现出免疫抑制作用并提高小鼠移植物的存活率。 11R-VIVIT TFA 具有细胞渗透性。

NFAT inhibitor. Inhibits LPS or LPS plus IFN-γ-induced IL-12 p40, IL-12 p70, IL-23 and TNF secretion from bone marrow-derived macrophages (BMDMs). Also attenuates NO production and Nos2 mRNA expression in LPS-stimulated BMDMs. Improves symptoms in a mouse

YHS-12是一种电离性阳离子脂质（pKa = 6.506），可在脂质纳米粒子（LNPs）中封装并传递siRNA和mRNA，用于体外及体内应用。这些LNPs由YHS-12与靶向巨噬细胞的肽CRVLRSGSC组成，主要用于封装针对甲氧西林抗性金黄色葡萄球菌（MRSA）的嵌合抗原受体mRNA以及针对caspase-11的siRNA。此外，这些LNPs能够增强RAW 264.7巨噬细胞及原代小鼠骨髓来源巨噬细胞（BMDMs）清除MRSA的效能。通过静脉注射这些LNPs于环磷酰胺诱导的免疫抑制小鼠的脓毒症模型中，可以显著降低血液中的细菌数量并提高生存率。

Potent and selective p38α and p38β degrader (DC50 < 50 nM). Displays no significant degradation of p38γ, p38δ, JNK1/2 or ERK1/2. Inhibits phosphorylation of MK2 in UV-treated cancer cells and LPS-stimulated bone marrow-derived macrophages (BMDM). Exhibits similar effect to p38α gene knockout in BBL358 cells. Active in vivo.

Potent and selective GPR84 biased agonist (EC50 = 33 nM). Exhibits no significant activity in a panel of 168 other GPCRs. Exhibits bias for G protein signaling pathways. Induces morphological changes in primary murine bone marrow-derived macrophages (BMDMs) in a cellular impedance assay, and promotes phagocytosis by M1 polarized U937 cells. Induces migration of primary human monocytes, but has no effect on macrophage chemotaxis.

Cheilanthifoline has anti-osteoclastogenic property, it gives significant inhibitions on receptor activator of nuclear factor-κB ligand-induced differentiation of mouse bone marrow-derived macrophages into multinucleated osteoclasts.

SPA0355 是硫脲衍生物，展现抗氧化和抗炎特性。它抑制RANKL(核因子 κB 受体活化因子配体)在初级骨髓来源巨噬细胞中的诱导破骨细胞生成，影响MAPKs、Akt和NF-κB通路的激活。同时，SPA0355 促成成骨细胞分化，提高碱性磷酸酶活性和矿化结节形成。通过刺激成骨细胞分化并抑制破骨细胞吸收，SPA0355 可以保护去卵巢小鼠免受骨丢失，适用于绝经后骨质疏松症的研究。

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。

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。

LL-37 is a cationic and α-helical antimicrobial peptide expressed in human bone marrow, testis, granulocytes, and gingival epithelium and is upregulated in psoriatic lesions. It inhibits growth of Gram-positive E. coli D21 and Gram-negative B. megatarium in a concentration-dependent manner and LL-37 expression is induced in A549 epithelial cells, alveolar macrophages, neutrophils, and monocyte-derived macrophages following M. tuberculosis infection. LL-37 binds sheep erythrocytes coated with S. minnesota Re-LPS and induces agglutination with a minimal agglutinating concentration (MAC) of 12.1 μg/ml. It is a chemoattractant for, and can induce calcium mobilization in, human monocytes, neutrophils, and T cells that naturally express formyl peptide receptor-like 1 (FPRL1) and FPRL1-transfected HEK293 cells. LL-37 (10-15 μM) pretreatment of dengue virus type 2 (DENV-2) reduces its infectivity as well as levels of viral genomic RNA and NS1 antigen. In vivo, LL-37 inhibits cecal ligation and puncture-induced caspase-1 activation and pyroptosis of peritoneal macrophages, reduces levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α, and improves survival in polybacterial septic mice.

Resolvin conjugate in tissue regeneration 1 (RCTR1) is a specialized pro-resolving mediator (SPM) biosynthesized from docosahexaenoic acid by isolated human macrophages and apoptotic polymorphonuclear (PMN) neutrophils.1It has been found in human spleen and bone marrow.2RCTR1 is produced via lipoxygenase-mediated oxidation of DHA to 7(S)-8-epoxy-17(S)-HDHA, which is conjugated to glutathione.1,2,3RCTR1 (10 nM) increases phagocytosis ofE. colior apoptotic neutrophils in isolated human monocyte-derived macrophages.2It decreases chemotaxis induced by leukotriene B4in isolated human neutrophils when used at a concentration of 10 nM. RCTR1 (1 and 10 nM) accelerates tissue regeneration in planaria. Intraperitoneal administration of RCTR1 (100 ng/animal) shortens the inflammatory resolution period and decreases inflammatory exudate neutrophil infiltration in a mouse model ofE. coli-induced peritonitis. 1.Dalli, J., Ramon, S., Norris, P.C., et al.Novel proresolving and tissue-regenerative resolvin and protectin sulfido-conjugated pathwaysFASEB J.29(5)2120-2136(2015) 2.de la Rosa, X., Norris, P.C., Chiang, N., et al.Identification and complete stereochemical assignments of the new resolvin conjugates in tissue regeneration in human tissues that stimulate proresolving phagocyte functions and tissue regenerationAm. J. Pathol.188(4)950-966(2018) 3.Rodriguez, A.R., and Spur, B.W.First total synthesis of pro-resolving and tissue-regenerative resolvin sulfido-conjugatesTetrahedron Lett.58(16)1662-1668(2017)

3',4',7-Trihydroxyflavone 是分离自蚕豆荚的黄酮苷元化合物。