Making sense of sensors

Targeting nucleic acid sensors makes sense for cancer

Two new pathways are emerging as viable options for harnessing nucleic acid sensors in immuno-oncology, offering an alternative to the toll-like receptors (TLRs) that paved the way. By activating STING or RIG-I, researchers are expanding the possibilities for tapping into the innate immune system to create stand-alone treatments or combination therapies with checkpoint inhibitors.

With one compound targeting STING in Phase I and another targeting RIG-I scheduled to enter the clinic in 2017, companies are looking at the pathways as sources of new targets that could help establish or boost their immuno-oncology portfolios.

Aduro Biotech Inc. announced the start of a Phase I trial last month on its lead STING activator ADU-S100 for metastatic lymphomas or solid tumors. The compound is partnered with Novartis AG. Rigontec GmbH has its first compound, the RIG-I agonist ImOI100 in IND-enabling studies and expects to initiate a Phase I trial in cancer early next year.

According to Aduro CSO Thomas Dubensky, the targets are attracting attention across the industry because the biology is relevant to so many immune mechanisms.

"I think just about every pharma company is working on STING. If you look at the publications around STING in the last two or three years, almost every top tier journal has an article every month," he said. "STING has evolved to recognize host cell damage, which is a very central pathway that exists in all immune cell subsets."

STING, RIG-1 and TLRs belong to a class

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