Inflammatory Drug Targets
Many signaling pathways have been shown to be critical in the inflammatory response. Within these pathways, key signaling molecules have emerged as attractive drug targets. SB Drug Discovery has established an extensive panel of assays relevant to key inflammatory drug targets, enabling screening and rapid progression of candidate compounds.
Cyclic nucleotides (cAMP and cGMP) are key effector molecules known to regulate many stages on the inflammatory response. Given that phosphodiesterases remain the sole means of degradation of cyclic nucleotides within the cell, this family of enzymes has received considerable interest as a therapeutic target for inflammation. SB Drug Discovery offers the most comprehensive panel of human phosphodiesterases for screening and cell-based assays. Learn more about our PDE screening services here.
Nuclear Hormone Receptors
Glucocorticoids remain a primary therapeutic intervention for the treatment of many inflammatory disorders. In addition to Glucocorticoid receptor assays, SB also offers a broad panel of nuclear hormone receptors for HTS and selectivity profiling. Learn more about our nuclear receptor screening services here.
G Protein-Coupled Receptors
GPCRs play an important role in inflammation and modulation of associated pathways is core to discovery of new anti-inflammatory therapies. SB Drug Discovery's GPCR assays enable the evaluation of binding and downstream effects of small molecules against a wide variety of GPCR targets. Our assays employ radioligand binding and whole-cell functional assays in order to investigate affinity and nature of binding. Learn more here.
Many ion channels play a role in inflammatory processes including TRP, potassium, chloride and purinergic channels. SB has generated an extensive range of stable cell lines expressing voltage and ligand-gated channels which are available for screening and selectivity profiling using fluorescence and electrophysiology platforms. Details of our ion channel capabilities can be found here.