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Poster Presentation at ELRIG Advances in Cell Based Screening Conference

May 15th 2017

The ELRIG conference focuses on the latest advances in cellular screening methods applied in drug discovery and this was an ideal opportunity to present 'A Humanized Screening Platform for Chronic Pain', our poster in association with Cellectricon.

The poster was presented by Dr Daniel Tams, Neuroscience Lead in Drug Discovery Services at Censo Biotechnologies, who is based at our facilities in Cambridge at the Babraham Research Campus.

Daniel described the development of sensory neurons derived from induced pluripotent stem cells (iPSCs) with a relevant phenotype and how these cells can be applied in screening to identify compounds that change a disease phenotype rather than the activity of specific targets.

Physiologically relevant human models of chronic pain are essential to developing new therapeutics and overcome poor translation between animal studies and the clinical setting.

A key issue in understanding neuropathic pain is identification of mechanisms involved in hyper-excitability and pain maintenance and to distinguish molecules that modulate the excitability of pain-conducting sensory neurons.

Differences in sensory processing between human and model organisms may, however, lead to poor translation between animal studies and the clinical setting. One solution is to use cultured human DRG neurons and manual patch clamp. While the patch clamp technique provides unparalleled insight into the excitability of native tissue, it is extremely low-throughput and costly.

We aimed to identify an alternative in vitro approach with similar translational predictability by utilising human iPSC-derived sensory neurons and a physiological stimulus in a high capacity format to detect changes in neuronal excitability.

The results strongly suggest that the humanised phenotypic screening platform applying high quality human iPSC-derived sensory neurons provides a dramatically higher-throughput means of quantifying the excitability of human neurons while maintaining the translational validity. This enables identification and prioritisation of molecules that are likely to also modulate chronic pain earlier on in the drug development process.

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