Acute pain signaling has a key protective role and is highly evolutionarily conserved.
Chronic pain, however, is maladaptive, occurring as a consequence of injury and disease …

The voltage-gated sodium channel NaV1. 9 is preferentially expressed in nociceptors and
has been shown in rodent models to have a major role in inflammatory and neuropathic …

Pathogenic variants in the voltage-gated sodium channel gene family lead to early onset
epilepsies, neurodevelopmental disorders, skeletal muscle channelopathies, peripheral …

Osteoarthritis (OA) is the most common joint disease. Currently there are no effective
methods that simultaneously prevent joint degeneration and reduce pain. Although limited …

In common with other chronic pain conditions, there is an unmet clinical need in the
treatment of inherited erythromelalgia (IEM). The SCN9A gene encoding the sodium …

Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1. 7) is a key
molecular determinant of pain sensation. However, defining the Nav1. 7 contribution to …

Loss-of-function mutations in Na V 1.7 cause congenital insensitivity to pain (CIP); this
voltage-gated sodium channel is therefore a key target for analgesic drug development …

Human genetic studies have implicated the voltage-gated sodium channel NaV1. 7 as a
therapeutic target for the treatment of pain. A novel peptide, μ-theraphotoxin-Pn3a, isolated …

Acute pain is adaptive, but chronic pain is a global challenge. Many chronic pain syndromes
are peripheral in origin and reflect hyperactivity of peripheral pain-signaling neurons …

Pain places a devastating burden on patients and society and current pain therapeutics
exhibit limitations in efficacy, unwanted side effects and the potential for drug abuse and …