On October 5, 2021 Aulos Bioscience, an immuno-oncology company working to revolutionize cancer care through a potentially best-in-class, computationally evolved IL-2 human antibody, reported the planned presentation of preclinical data on its lead investigational therapy, AU-007, at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 36th Annual Meeting (Press release, Aulos Bioscience, OCT 5, 2021, View Source [SID1234590845]). The SITC (Free SITC Whitepaper) meeting will run Nov. 10-14, 2021, in Washington D.C., as well as virtually.
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"We believe in the potential of our initial clinical candidate, AU-007, as a novel cancer treatment that could meaningfully impact the lives of patients with its highly differentiated approach to harnessing the power of IL-2 to eradicate solid tumors," said Aron Knickerbocker, Aulos Bioscience’s chief executive officer. "We look forward to presenting preclinical data at the SITC (Free SITC Whitepaper) Annual Meeting and to initiating clinical testing in patients with cancer by year end."
Abstract ID
Poster Number and Title
Presenting Author
14867
704: The computationally designed human antibody, AU-007, mediates human immune activation by endogenous IL-2, while uniquely breaking the IL-2 auto-inhibitory loop and preventing Treg expansion
Yanay Ofran, Ph.D.
Biolojic Design and Aulos Bioscience
The poster will be presented in the Poster Hall at the Walter E. Washington Convention Center in Washington, D.C. Saturday, Nov. 13, 2021. It will also be available as an ePoster on display on the SITC (Free SITC Whitepaper) 2021 virtual meeting platform from 7 a.m. EST on Friday, Nov. 12, 2021, until the virtual meeting platform is closed on Jan. 9, 2022.
About AU-007
AU-007 is a computationally evolved, human IgG1 monoclonal antibody that is highly selective to the CD25-binding portion of IL-2. With a mechanism of action unlike any other IL-2 therapeutic in development, AU-007 leverages the body’s own IL-2 to reinforce anti-tumor immune effects. This is achieved by preventing IL-2 secreted by T effector cells from binding to trimeric receptors on T regulatory cells while still allowing IL-2 to bind and expand effector cells. This prevents the negative feedback loop caused by other IL-2 based treatments and biases the immune system towards activation over suppression. AU-007 also prevents IL-2 from binding to trimeric receptors on vasculature and pulmonary endothelium, which may significantly reduce the vascular leak syndrome and pulmonary edema associated with high-dose IL-2 therapy.