This technology is a strategy to enhance the efficacy of immunotherapeutics by quantifying and increasing the levels of progenitor T cells within tumors and peripheral blood prior to treatment.
Immune checkpoint inhibitors, such as anti-PD-1 therapies, have transformed therapeutic outcomes in cancers such as melanoma and lung cancer. Despite its success, cancer immunotherapy is often unable to elicit a lasting therapeutic response in many patients. It has become apparent that the amount of progenitor T cells available to respond to checkpoint inhibitors may limit its success. Therapeutic interventions involving metabolic modulation upstream of the T cell activation pathway may expand responses to existing immunotherapeutics in a greater share of patients and in a broad range of cancer types and autoimmune disorders by expanding the amount of critical progenitor T cells. Additionally, measurement of progenitor T cells may help elucidate patient responsiveness to treatment.
This technology identifies a T cell biomarker that can be used to determine and modulate patient response to immune checkpoint inhibitors. By measuring the number of TCF-1+ T cells in the tumor, it can help to identify therapeutic strategy for non-responsive patients and improve immunotherapy efficacy, specifically anti-PD-1 therapy. Further, this technology offers a strategy for modulating metabolic pathways to encourage the repopulation of relevant T cells prior to treatment. As such, this technology has the potential to increase the therapeutic effectiveness of immunotherapies and personalized treatments.
This technology has been validated in mouse models of cancer and corroborated by clinical findings in melanoma patient populations. In melanoma patients, relative levels of the self-renewing progenitor T cells were measured prior to treatment with immunotherapy and predicted clinical benefit.
IR CU20336
Licensing Contact: Kristin Neuman