LCC-12 formate

LCC-12 (10 μM) formate reduces the levels of mitochondrial NAD⁺ and NADH pools in primary activated monocyte-derived macrophages (aMDM)^[1].
LCC-12 formate selectively forms a stable monometallic complex with copper (II) in a cell-free system, while it shows no significant binding to most other divalent metal ions or copper (I)^[2].
LCC-12 formate inhibits copper (II)-catalyzed redox cycling of NADH to NAD⁺ in a dose-dependent manner in a cell-free system mimicking the mitochondrial matrix^[2].
LCC-12 formate induces epigenetic reprogramming in activated monocyte-derived macrophages, increases histone methylation levels, decreases histone acetylation levels, and downregulates pro-inflammatory gene expression and cytokine secretion^[2].
LCC-12 formate inhibits the activation of immune cells with upregulated CD44, and exerts effects on CD44-related copper-dependent cellular plasticity^[2].
LCC-12 formate potently interferes with the activation of monocyte-derived macrophages and inhibits CD44-associated epithelial-mesenchymal transition in cancer cells^[4].

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