Endeavor BioMedicines gains rights to lead ULK1/2 inhibitor molecule
Endeavor BioMedicines, a clinical-stage precision medicine company targeting the core drivers of multiple terminal diseases, including oncology and fibrosis, has concluded an exclusive licensing agreement with the Salk Institute, along with Sanford Burnham Prebys. Under the license agreement, the California-based company Endeavor gains worldwide, exclusive rights to Salk and Sanford Burnham Prebys’ intellectual property of drug candidates, including a lead ULK1/2 inhibitor molecule that has now been through extensive preclinical and toxicity studies, as well as biomarkers that can help clinicians determine which cancer patients are most likely to benefit from drugs targeting ULK1/2. Endeavor plans to complete IND-enabling studies and advance the program into the clinic, initially in colorectal and lung cancers, in the next 18 months.
“This line of anti-cancer research has the potential to have a significant impact for patients,” says Reuben Shaw, director of the Salk NCI-Designated Cancer Center, professor in Salk’s Molecular and Cell Biology Laboratory and the William R. Brody Chair. “We are thrilled that the benefits of our approach are being realized with this clinically important licensing agreement.” In 2015, Shaw and his colleagues at Salk, working with Nicholas Cosford, professor and deputy director of the NCI-Designated Cancer Center at Sanford Burnham Prebys, demonstrated that by chemically blocking ULK1/2, they could shut down the cellular recycling pathway known as autophagy that some cancer cells use to stay alive. Autophagy breaks down unneeded or damaged cellular components into their building blocks to use for new cellular parts, which is critical for cells that are growing rapidly and don’t have enough nutrient supply, as do many cancers. The researchers found small molecule compounds that effectively blocked ULK1/2 and killed cancer cells, including human and mouse lung cancer cells and human pancreatic cancer cells.
“Since we initially discovered how cancer cells starved of nutrients activate ULK1/2, we focused on finding a drug that could block its activity,” says Cosford. “Using medicinal chemistry, chemical biology and rational drug design we have created this compound and are hopeful it will have an impact as an anti-cancer treatment. This agreement with Endeavor BioMedicines moves our efforts closer to helping people living with cancer.” Over the better part of a decade, Salk and Sanford Burnham Prebys scientists collaborated to perform the early-stage research needed to translate their initial findings about ULK1/2 into improved drug candidates and clinically actionable observations to which cancers are most likely to respond. Inhibition of autophagy has emerged from a number of different research labs in the last few years as an excellent way to overcome therapeutic resistance to both chemotherapies and targeted therapies, and more recently in certain cases of immunotherapy resistance, as well.
Endeavor BioMedicines gains rights to lead ULK1/2 inhibitor molecule
Endeavor BioMedicines gains rights to lead ULK1/2 inhibitor molecule
Endeavor BioMedicines, a clinical-stage precision medicine company targeting the core drivers of multiple terminal diseases, including oncology and fibrosis, has concluded an exclusive licensing agreement with the Salk Institute, along with Sanford Burnham Prebys. Under the license agreement, the California-based company Endeavor gains worldwide, exclusive rights to Salk and Sanford Burnham Prebys’ intellectual property of drug candidates, including a lead ULK1/2 inhibitor molecule that has now been through extensive preclinical and toxicity studies, as well as biomarkers that can help clinicians determine which cancer patients are most likely to benefit from drugs targeting ULK1/2. Endeavor plans to complete IND-enabling studies and advance the program into the clinic, initially in colorectal and lung cancers, in the next 18 months.
“This line of anti-cancer research has the potential to have a significant impact for patients,” says Reuben Shaw, director of the Salk NCI-Designated Cancer Center, professor in Salk’s Molecular and Cell Biology Laboratory and the William R. Brody Chair. “We are thrilled that the benefits of our approach are being realized with this clinically important licensing agreement.” In 2015, Shaw and his colleagues at Salk, working with Nicholas Cosford, professor and deputy director of the NCI-Designated Cancer Center at Sanford Burnham Prebys, demonstrated that by chemically blocking ULK1/2, they could shut down the cellular recycling pathway known as autophagy that some cancer cells use to stay alive. Autophagy breaks down unneeded or damaged cellular components into their building blocks to use for new cellular parts, which is critical for cells that are growing rapidly and don’t have enough nutrient supply, as do many cancers. The researchers found small molecule compounds that effectively blocked ULK1/2 and killed cancer cells, including human and mouse lung cancer cells and human pancreatic cancer cells.
“Since we initially discovered how cancer cells starved of nutrients activate ULK1/2, we focused on finding a drug that could block its activity,” says Cosford. “Using medicinal chemistry, chemical biology and rational drug design we have created this compound and are hopeful it will have an impact as an anti-cancer treatment. This agreement with Endeavor BioMedicines moves our efforts closer to helping people living with cancer.” Over the better part of a decade, Salk and Sanford Burnham Prebys scientists collaborated to perform the early-stage research needed to translate their initial findings about ULK1/2 into improved drug candidates and clinically actionable observations to which cancers are most likely to respond. Inhibition of autophagy has emerged from a number of different research labs in the last few years as an excellent way to overcome therapeutic resistance to both chemotherapies and targeted therapies, and more recently in certain cases of immunotherapy resistance, as well.
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