Thursday 19th May @ 4pm CET (10am EST)
Don’t miss our upcoming webinar on phenotypic screening approaches in pain research and how iPSC-derived neurons can be used in a drug discovery setting. Attendees can gain knowledge of compound profiling to advance research in the CNS and pain therapeutic fields and get an understanding of the principles of operation of Cellectricon’s phenotypic screening platform.
Darren Cawkill, Associate Research Fellow, Neusentis (A Pfizer Research Unit), UK
Paul Karila, VP Discovery Services, Cellectricon AB, Sweden
In this webinar, we will describe how screening against a disease-relevant phenotype can be used to identify compounds that change the outcome of biological pathways rather than just the activity of specific targets. However, in the area of Pain research, use of phenotypic screens has historically been impeded by the challenge of sourcing relevant neuronal cell types in sufficient quantity and developing key functional endpoint measurements that have a direct link with disease.
Recent work at Pfizer’s UK-based Neusentis research site has resulted in the successful generation of stem cell (hiPSC)-derived sensory neurons at a robust production scale; a process that has been used to supply neurons for assay development from both normal donors and pain (erythromelalgia) patients. This progress, together with development of functional assays as a measure of neuronal excitability, has enabled pain-relevant high throughput-compatible phenotypic screening.
In this presentation we will provide an overview of the phenotypic assay development and validation together with a summary of ongoing screening initiatives. As well as addressing the main goal of identifying new targets/pathways/MOA for modulating neuronal excitability, we have also investigated how the nature of the stimulus (chemical vs electrical excitation) impacts the molecules and mechanisms identified by the functional assays. Lastly, we propose a screening strategy including the use of pain patient-derived hiPSC-sensory neurons to identify compounds acting on a disease-relevant phenotype rather than having more general effects on neuronal excitability.