Mavupharma Selects First Immuno-Oncology Clinical Candidate MAVU-104, an Oral STING Pathway Enhancer

On January 3, 2019 Mavupharma (Mavu) reported that it has selected its first immuno-oncology clinical development candidate, MAVU-104, a novel innate immune modulator (Press release, Mavupharma, JAN 3, 2019, View Source [SID1234537639]).

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MAVU-104 is a first-in-class, orally active, small molecule inhibitor of ENPP1, a phosphodiesterase that negatively regulates the STING (Stimulator of Interferon Genes) pathway. STING signaling plays a crucial role in the generation of an immune response directed at the tumor, and enhancing STING signaling has been shown to induce cures in multiple preclinical cancer models. Inhibiting ENPP1 activity with MAVU-104 allows for highly-controlled enhancement of STING signaling in all tumors and lymph nodes without any injections.

"With our approach, which focuses on blocking a key negative regulator of the STING pathway, as opposed to directly stimulating STING itself, the degree and duration of innate immune activation are tunable, which avoids both overstimulation of the pathway and high levels of cytokine release," stated Mike Gallatin, Ph.D., Mavu’s president and co-founder. "Having selected our first immuno-oncology drug candidate, we are now focused on the path to IND for MAVU-104, which we expect to file in the second half of 2019."

Mavu’s approach may have significant advantages over other developmental therapies that stimulate the STING pathway. Published studies on the direct STING agonists in clinical development show that these therapies are administered via direct injection into the tumor(s) and may induce release of pro-inflammatory cytokines into systemic circulation, which has been associated with side effects.

Previously, Mavu presented data at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 2018 meeting showing that ENPP1 inhibition leads to tumor shrinkage and can be combined with other immunotherapies to induce long-term cures and durable immunologic memory in mouse models of cancer.