lx3

LX-3 is a selective activator of the p38 mitogen-activated protein kinase (MAPK) pathway, which de-represses a subset of endogenous genes repressed by DNA methylation.

BLX3887 is an inhibitor of 15-lipoxygenase type 1 (15-LO-1; IC50 = 32 nM in a cell-free enzyme assay).1 It is selective for 15-LO-1 over 15-LO-2, which it does not inhibit, 5-LO (IC50 = 472 nM), and 12-LO (IC50 = 3,310 nM). BLX3887 inhibits the production of 15-LO metabolites selectively in eosinophils over neutrophils when used at a concentration of 10 μM. It also inhibits endocytosis in, and the migration of, isolated human peripheral blood mononuclear cell-derived dendritic cells in vitro. |1. Archambault, A.-S., Turcotte, C., Martin, C., et al. Comparison of eight 15-lipoxygenase (LO) inhibitors on the biosynthesis of 15-LO metabolites by human neutrophils and eosinophils. PLoS One 13(8), e0202424 (2018).

GLX351322 is NADPH Oxidase 4 Inhibitor with IC50 of 5 μM.

LX-2931(LX-3305) is a sphingosine-1-phosphate cleavage enzyme (S1P) inhibitor for the treatment of rheumatoid arthritis.

Pexidartinib (PLX-3397) is a capsule containing a small-molecule receptor tyrosine kinase (RTK) inhibitor targeting KIT, CSF1R, and FLT3, with potential antineoplastic activity.

Minzasolmin(DLX-313) is an alpha-synuclein misfolding inhibitor for the study of Parkinson's disease.

Pexidartinib hydrochloride (PLX-3397 HCl) is a selective, orally active, ATP-competitive CSF1R/M-CSFR inhibitor and c-Kit inhibitor with IC50 values of 20 and 10 nM, respectively, capable of inducing cancer cell apoptosis.

RLX-33 is a potent and selective antagonist of relaxin family peptide 3 (RXFP3) that crosses the blood-brain barrier and also blocks relaxin 3-induced ERK1/2 phosphorylation. RLX-33 can block the increase in food intake induced by the RXFP3 selective agonist R3/I5 in rats.RLX-33 can be used to study the metabolic syndrome.

PLX-3618 is an effective BRD4 molecular glue degrader (DC50=12.2 nM) that recruits the E3 ligase substrate receptor DCAF11, promoting BRD4 polyubiquitination and proteasomal degradation to induce apoptosis in AML cells.