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Neuropathic Pain

The need to find novel therapeutics to treat neuropathic pain linked to chemotherapy, diabetes and nerve damage is more urgent than ever with a reported 15% of the global population now affected. Neuropathic pain results from damage and sensitization of the neurons in the peripheral and central nervous systems (CNS). In peripheral sensitization, increased stimulation of peripheral nociceptors amplifies pain signals to the CNS. In central sensitization, hyperstimulation/sensitization of dorsal horn nociceptive neurones of the spinal cord (by peripheral tissue damage/inflammation) increases pain signals to the brain and results in increased pain sensation, perceived as allodynia and/or hyperalgesia.

The CCI (chronic constriction injury) model results in peripheral mononeuropathy, simulating chronic nerve compression in humans. This model is used routinely by the pharmaceutical industry to help guide go/no-go decision making around efficacy, mechanism of action (MoA) and compound development for neuropathic pain indications. In addition, Transpharmation has also developed both diabetic-induced neuropathy (STZ) in collaboration with the University of Hertfordshire and chemotheraphy-induced neuropathy (oxaliplatin) rodent models to evaluate NCEs to treat specifically these increasingly-prevalent chronic conditions. Furthermore, we’ve challenged our understanding beyond traditional end-points, such as allodynia, towards investigating non-evoked clinically relevant behaviours, such as EEG/sleep signatures and cognition disruption (‘chemobrain’).

Examples of the models we offer include:

  • CCI (chronic constriction injury) model
  • Oxaliplatin chemotherapy-induced neuropathy model
  • STZ diabetic-induced neuropathy model

Examples of end points:


pain1This list is not exhaustive, we are always developing new areas of discovery within our preclinical field of expertise. If there is something particular that is not listed here please do contact us.

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