Neuropathic Pain Overview

Neuropathic pain, also known as neuralgia or neurogenic pain, is a chronic pain syndrome directly caused by damage or disease of the somatosensory nervous system, with a global prevalence of approximately 7–10%. It occurs at higher rates in diabetic patients, cancer chemotherapy recipients, spinal cord injury, and multiple sclerosis populations. Typical etiologies include diabetic peripheral neuropathy, postherpetic neuralgia, chemotherapy-induced peripheral neuropathy, spinal cord injury-related pain, and trigeminal neuralgia. Patients often describe burning, electric-shock-like, stabbing, or lancinating pain, frequently accompanied by spontaneous pain, allodynia (pain from light touch), and hyperalgesia.

Unlike inflammatory or nociceptive pain, the essence of neuropathic pain lies in pathological remodeling of the nervous system itself: persistent changes in ion channel expression and firing patterns in peripheral nociceptors and dorsal root ganglion (DRG) neurons (e.g., upregulation of Nav1.7/1.8/1.9 voltage-gated sodium channels leading to ectopic discharges), sustained amplification of excitatory input in the spinal dorsal horn and higher centers (thalamus, cortex), combined with reduced inhibitory modulation (GABAergic and glycinergic neurons), resulting in disinhibition. Activated microglia and astrocytes form vicious positive feedback loops with neurons via P2X4/P2X7 receptors, inflammatory cytokines, and neurotrophins (e.g., BDNF), transforming acute nociceptive signals into an independent “neural network disease.” At the peripheral level, TRPV1 and TRPA1 are highly sensitized to thermal, mechanical, and chemical stimuli; centrally, NMDA receptor-mediated excitotoxicity and mTOR pathway-driven plasticity further consolidate abnormal pain memory.

Because its pathogenesis is no longer simple inflammation or tissue damage, traditional NSAIDs and opioids have limited efficacy in neuropathic pain and are constrained by tolerance, adverse effects, and addiction risk. Current guidelines emphasize calcium channel modulators (gabapentin, pregabalin), serotonin–norepinephrine reuptake inhibitors, and local anesthetic patches. However, a significant proportion of patients remain inadequately controlled, underscoring the urgent need for precision-targeted therapies around Nav channels, TRPV1/P2X4/P2X7, NGF–TrkA axis, and central inhibitory circuits—the focus of recent small-molecule, monoclonal antibody, and gene therapy development.

Five Core Target Classes in Neuropathic Pain

For related targets in other neurological disorders (Alzheimer’s, ALS, Parkinson’s, Huntington’s, etc.), see abinScience Neuroscience Hub.

Latest Research & Clinical Progress 

The table below summarizes key clinical and basic research breakthroughs in neuropathic pain, sourced from top journals, clinical trial registries, and authoritative institutions.

abinScience Neuropathic Pain Research Tool kit

All 102 abinScience products targeting neuropathic pain core pathways are listed below, grouped and collapsible for readability.

For partners & distributors: A complete portfolio covering Nav1.7, TRPV1, P2X7, NGF-TrkA, α2δ-1, opioid, and cannabinoid receptors supports full workflow from in vitro screening to in vivo models. Consistent batch quality and detailed technical documentation enable rapid customer recommendation.