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Lack of persistence and sensitivity to apoptosis and activation induced cell death are key contributors to cellular immunotherapy failure. The protein Bcl-Xl functions as an anti-apoptotic protein that resides in mitochondria. Moffitt researchers found that certain amino acid utations help Bcl-Xl maintain this crucial antiapoptotic function. A mutated Bcl-Xl variant was created, and was found to produce a more potent and durable immune response by reducing exhaustion, maintaining function, and increasing the viability of T-cells. Our novel egradation-resistant Bcl-Xl variant increased efficacy of cellular immunotherapies.

PUBLICATION/PATENT

Provisional Patent filed for Drs. Locke and Atkins

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