IO-108

IO-108 selectively binds to LILRB2⁺ reporter cells, shows no cross-reactivity with other tested LILR family members or LAIR1, and binds to LILRB2 with high affinity^[1].
IO-108 (0.0001-100 nM) blocks the binding of HLA-G to LILRB2 on the surface of HEK293 cells in a dose-dependent manner, while potently inhibiting the activation of LILRB2 reporter cells induced by plate-immobilized ANGPTL2 and SEMA4A^[1].
IO-108 (100 nM; 3 days) enhances the production of pro-inflammatory cytokines (TNF-α, GM-CSF) and reduces the level of the anti-inflammatory cytokine IL-10 in lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMCs)^[1].
IO-108 (100 nM; 3 days) enhances the production of proinflammatory cytokines and chemokines (IFN-γ, TNF-α, IL-1β, IL-6, CXCL8) in anti-CD3-stimulated peripheral blood mononuclear cells (PBMCs)^[1].
IO-108 (100 nM) enhances TNF-α production in monocyte-derived macrophages stimulated with 2’3’-cGAMP^[1].
IO-108 (100 nM; 2 days) reduces the expression of tolerogenic CD209 and enhances the production of proinflammatory TNF-α in LPS-stimulated immature monocyte-derived dendritic cells^[1].
IO-108 (100 nM; 6 days) enhances the pro-inflammatory effect of anti-PD-1 antibody in a co-culture system of monocyte-derived macrophages and CD4⁺ T cells, and increases the production level of IFN-γ^[1].
IO-108 (100 nM; 6 days) promotes the differentiation of classical monocytes into CD86⁺ pro-inflammatory dendritic cells when co-cultured with GM-CSF and IL-4^[1].
IO-108 (100 nM; 2 days) modulates the phenotype of immature monocyte-derived dendritic cells, reduces the expression of the tolerogenic CD209, and increases the expression level of the proinflammatory CD86^[1].
IO-108 reverses the PMN-MDSC-mediated suppression of autologous CD8⁺ T cell proliferation in a cancer-derived cell co-culture system^[1].
IO-108 antagonizes the tolerogenic polarization of CD33+ PBMCs induced by SK-MEL-5 melanoma cells, reduces the expression of anti-inflammatory markers, and restores the expression of pro-inflammatory markers^[1].
IO-108 specifically binds to LILRB2 on the surface of human primary myeloid cells and patient-derived tumor-infiltrating myeloid cells, blocks the interactions between LILRB2 and its ligands HLA-G, SEMA4A, and ANGPTL2, enhances the inflammatory response of primary human macrophages to natural agonists, induces primary human monocyte-derived dendritic cells to develop a pro-inflammatory phenotype, and promotes T cell activation in an in vitro co-culture system with patient-derived myeloid cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.