Atomwise, the leader in using artificial intelligence (AI) for small molecule discovery, and Bridge Biotherapeutics (KOSDAQ: 288330), a clinical stage biotech company, announced today a research collaboration to launch up to 13 small molecule programs across multiple therapeutic areas using structure-based AI technology for drug discovery.
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Under the agreement, Atomwise will use its AI technology and homology modeling capabilities to evaluate Pellino E3 ubiquitin ligases and their interactions with target protein substrates. Atomwise and Bridge will rapidly cycle through the design and testing of potent small molecule compounds, evaluating billions of possibilities that will selectively inhibit Pellino proteins.
Bridge is a pioneer in Pellino therapies and leads the development of BBT-401, the first-in-class Pellino-1 peptide inhibitor, currently in Phase 2 for ulcerative colitis (UC) treatments. BBT-401 targets Pellino-1, the protein mediating the myeloid differentiation primary-response protein 88 (MYD88), which activates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathways triggering inflammation.1,2,3 Pellino-1 engages with multiple inflammatory signaling pathways.
“Atomwise’s leading AI technology and the expert team will help us unlock opportunities to discover new drug candidates with exciting targets,” said James Lee, Founder and CEO of Bridge Biotherapeutics. “Our partnership with Atomwise will give us a competitive edge to build and expand an innovative first-in-class portfolio, upon our rich experience in Pellino-1 inhibitor development.”
“We are excited to partner with James and seasoned industry leaders on the Bridge team,” said Abraham Heifets, Ph.D., Co-founder and CEO of Atomwise. “Our team has been impressed by their ability to consistently bring new therapies to the clinic and develop partnerships worldwide. We are looking forward to a productive and long-term relationship.”
Under the research collaboration agreement, Atomwise will receive upfront, milestone and royalty payments upon success for each research program.
About Bridge Biotherapeutics
Bridge Biotherapeutics Inc. (KOSDAQ: 288330), based in South Korea, US and China is a clinical stage biotech company founded in 2015. Bridge Biotherapeutics is engaged in the discovery and development of novel therapeutics, focusing on therapeutic areas with high-unmet needs, such as ulcerative colitis, fibrotic diseases, and cancers. BBT-401, the first-in-class, GI-restricted Pellino-1 inhibitor for treatment of ulcerative colitis, is currently in Phase II in the US, and BBT-877, an autotaxin inhibitor to treat various fibrosing interstitial lung diseases including idiopathic pulmonary fibrosis (IPF), was licensed to Boehringer-Ingelheim for further development in July 2019 with potential license value more than 1.1 billion euro. BBT-176, a potent targeted cancer therapy for non–small cell lung cancer (NSCLC) is also in development. Bridge Biotherapeutics is a resident company of JLABS @ Shanghai.
Atomwise Inc. invented the first deep learning AI technology for structure-based small molecule drug discovery. Created in 2012, today Atomwise performs hundreds of projects per year in partnership with some of the world’s largest pharmaceutical and agrochemical companies, as well as more than 200 universities and hospitals in 40 countries. Atomwise has raised over $50 million from leading venture capital firms to support the development and application of its AI technology. Learn more at atomwise.com or follow @AtomwiseInc.
1 Choi, K. et al. Smad6 negatively regulates interleukin 1-receptor–Toll-like receptor signaling through direct interaction with the adaptor Pellino-1. Nat Immunol 7, 1057–1065 (2006)
2 Chang, M.et al. Peli1 facilitates TRIF-dependent Toll-like receptor signaling and proinflammatory cytokine production. Nat Immunol 10, 1089–1095 (2009)
3 Lee,Y. et al. Inhibition of lethal inflammatory responses through the targeting of membrane-associated Toll-like receptor 4 signaling complexes with a Smad6-derived peptide EMBO Mol Med 7, 577–592 (2015)