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ASCO 2025 | Targeting GSK-3ß with elraglusib in pancreatic cancer
Devalingam Mahalingam, MD, PhD, Northwestern University, Evanston, IL, discusses the rationale for targeting GSK-3ß with elraglusib in pancreatic cancer. Because GSK-3ß plays a multi-regulatory role, targeting through elraglusib affects key tumor pathways like epithelial-mesenchymal transition, fibrosis, and immune response. Elraglusib has shown efficacy across multiple tumor types, including a complete response in melanoma, and may resensitize chemo-refractory patients when combined with gemcitabine and nab-paclitaxel. This interview took place during the 2025 American Society of Clinical Oncology (ASCO) Meeting in Chicago, IL.
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Transcript
So GSK-3ß is kind of known to target multiple pathways in oncology. In fact, when it was first developed, it was felt to be a good target for neurodegenerative diseases. And then in 2010, based on a lot of preclinical data, we saw that GSK-3ß, at least in the cancer space, regulated a multifaceted kind of targets in oncology from the EMT modulating fibrosis, NF-kappa B, apoptosis, and also immunomodulatory functions from increasing NKT cells into tumors...
So GSK-3ß is kind of known to target multiple pathways in oncology. In fact, when it was first developed, it was felt to be a good target for neurodegenerative diseases. And then in 2010, based on a lot of preclinical data, we saw that GSK-3ß, at least in the cancer space, regulated a multifaceted kind of targets in oncology from the EMT modulating fibrosis, NF-kappa B, apoptosis, and also immunomodulatory functions from increasing NKT cells into tumors. So when we saw this, and especially in pancreatic cancer because of the EMT, the NF-kappa B, we felt it could be a target, especially because pancreatic cancers are also very fibrotic tumors. So that’s really some of the rationale based on the preclinical work that we would kind of look at it in pancreatic cancer alongside other tumor types as well. And obviously as we developed the program across multiple tumor types, we started seeing signals. For example, we had a complete response in a patient with melanoma in a phase one trial, we’d already progressed on immunotherapy. And so we said maybe it’s kind of continuing an immunomodulatory effect as well. And then as we kind of went on and combined it with chemo, we were seeing kind of effects of kind of clinical benefit, especially in patients who are already refractory to chemo, and it was able to resensitize them to gemcitabine and paclitaxel, which is what kind of brought us to our kind of first-line study in combination with gemcitabine and paclitaxel, initiated as a single arm, and then subsequently now is kind of a larger randomized study.
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