Pain is a leading health problem in the U.S. with 20% of Americans suffering from chronic pain. Currently, only half of pain suffers receive adequate pain relief, often through the use of drugs with adverse side effects.

Painful stimuli are detected by sensory peripheral nerves which have endings at bodily surfaces such as skin. These sensory neurons fire action potentials in response to peripheral stimuli and then release neurotransmitters in the spinal cord. This, in turn, activates other neurons that are connected to the brain. The altered processing of these stimuli associated with chronic pain is maintained dynamically by ongoing peripheral input.

It is likely that pain resulting from a variety of causes becomes chronic as a result of the initial reaction to damaged primary afferent fibers and neurons, recruitment of non-involved peripheral nerves, and engagement of central nervous system mechanisms; together, resulting in altered pain processing by neurons in the brain. Abnormal hyperactivity of damaged primary afferent fibers of the peripheral nervous system induces and maintains abnormal hypersensitivity to pain or to normally non-painful stimuli in neuropathic pain caused by cancer treatment, diabetes, and nerve injury.

Chronic pain management remains an unmet clinical need with only half of patients receiving adequate pain relief using drugs with adverse central nervous system side effects.

DermaXon has identified a novel class of compounds that modulate an undisclosed relevant target to treat chemotherapy-induced peripheral neuropathy.