Introduction

Pain sensation is mediated by io channels in nerve endings (such as TRPA1, TRPV1, TRPM3 and P2X receptors ) that trigger pain input to the central nervous system (CNS) via the dorsal root ganglia (DRG) neuron. TRPA1, TRPV1, TRPM3 channel could detect noxious stimuli, triggering pain signals in peripheral nerve endings.TRPV4: Plays a role in mechanical hypersensitivity in inflammation; ASIC1a, ASIC2a, ASIC3 are Involved in pain perception during acidosis caused by inflammation or injury. Nav1.1, Nav1.7, Nav1.8, Nav1.9 could mediate action potentials in dorsal root ganglia neurons, key to conducting pain signals to the spinal cord; Cav2.2 is critical in neurotransmitter release at synaptic junctions in the spinal cord, modulating pain signal transmission; Kv1.3, Kv1.4, Kv4.2, IK, BK regulate neuronal excitability and inflammation, offering potential for targeting immune-related pain while KCNQ2/3 is  Important for dampening excitatory pain signals in neurons;P2X3, P2X4, P2X7: are involved in sensory signaling and inflammation, making them key targets for neuropathic and inflammatory pain; nAChRα7, NMDA receptors could modulate synaptic plasticity and pain hypersensitivity, particularly in chronic and inflammatory pain; HCN1: Modulates neuronal excitability, contributing to chronic pain states.

Pain-Inflammation ion channel Portfolio

Our Pain-Inflammation Ion Channel Portfolio is designed to identify and validate ion channel targets involved in the regulation of pain and inflammatory pathways. This panel includes ion channels implicated in central and peripheral pain signaling, hypersensitivity in neuropathic and inflammatory conditions, and immune regulation, offering a comprehensive tool for drug discovery.