Vancouver’s Quark Venture has inked a research sponsorship agreement with Harvard University’s Office of Technology Development.
The $4.5 million agreement supports the joint research of principal investigators Arlene Sharpe, MD, PhD, and Dennis Kasper, MD, who are trailblazers in their fields of cancer immunology and microbiome science, respectively.
The premise of the research is that the missing ingredients for cancer immunotherapy may be found in the gut. Combining cutting-edge insights, the scientists will deploy a new “immune-oncology-microbiome” platform to identify new bacterial strains, molecules, or drug targets that address the problem of resistance to immunotherapy and create new treatment strategies in immune-oncology.
Under the terms of the agreement, Quark will have the option to negotiate a license for the intellectual property that arises from the project, and to enable a startup company to develop that IP toward commercial applications and therapies that ultimately benefit patients.
“As a new venture model, we’ve said from the outset that Quark Venture will seek out the best science and scientists the world has to offer,” said Karimah Es Sabar, Chief Executive Officer, Quark Venture. “We look forward to ongoing collaboration with Harvard Medical School to identify and support additional innovative technologies that will lead to breakthrough therapies and start-up companies.”
Drawing on the expertise, advanced research tools, and skills of their two labs, Sharpe and Kasper hope to delve further into the mechanisms of interaction between the microbiome and the immune system to create a library of new knowledge and define possible therapeutic strategies in immune-oncology.
“It has become clear through clinical experience with checkpoint inhibitors that the composition of the microbiome has a strong effect on patients’ response to the drugs,” said Michal Preminger, Executive Director of Harvard OTD’s HMS branch. “These two pioneering Harvard scientists are now coming together to tackle the riddle of what, in the microbiome, is causing this differential response.”