Webinar (Preview): Dynamic Quantification of Cancer Cell Metabolism Using Live-Cell Analysis

Rewiring core metabolic pathways is fundamental for the survival and dysregulated proliferation of cancer cells within the hostile tumor microenvironment. Given the role of metabolism in drug resistance, there is a growing need to better understand vulnerabilities to drive more targeted treatment strategies. Live-cell analysis speaks to the need for a practical, consistent, and physiologically relevant method for assessing dynamic cell changes in translational models.

Find out more:
 Empowering drug discovery research through imaging and analysis of intracellular ATP levels of cells in mono- and co-culture models
 Advantages of direct ATP analysis in live-cell screens for evaluating metabolic exchanges between cancer cells and their tumor environment
 The value of tracking changes in mitochondrial activity using live-cell analysis to elucidate mechanisms of action and screen for mitochondrial toxicity of potential therapeutic strategies

00:22 Given its positioning at the heart of cell line metabolism, we take a deeper dive into mitochondria and how kinetic measurements of ATP are valuable for early-stage toxicity screening. We will see how kinetic measures of mitochondrial membrane potential are valuable for gathering additional insight into the metabolic effects of chemotherapeutic agents

01:00 With cancer cells employing this and many other metabolic adaptions it is therefore unsurprising that this is a very attractive area for therapeutic intervention. And one such example which I’ll be covering in today’s webinar is the glutaminase 1 inhibitor Telaglenastat (CB-839) which has shown efficacy in several glutamine dependent pre-clinical cancer cell models including triple negative breast cancer.

01:46 I hope this data set has been able to demonstrate how kinetic measurements of ATP on the Incucyte as well as kinetic measurements of proliferation are able to provide greater mechanistic insight into drugs like CB-839 as well as the metabolic plasticity of cancer cells.

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