On November 10, 2022 Myeloid Therapeutics, Inc. ("Myeloid"), a clinical stage mRNA-immunotherapy company, reported that multiple posters on its therapeutics platforms, ATAK CAR receptors and in vivo mRNA programming, at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 37th Annual Meeting, being held in Boston, MA, November 8-12, 2022 (Press release, Myeloid Therapeutics, NOV 10, 2022, View Source [SID1234623868]).
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"The data presented at SITC (Free SITC Whitepaper) further highlight the power of Myeloid’s platform to enable broad immune responses and attack cancer cells, supporting the accelerated development of our deep clinical and preclinical pipeline," said Daniel Getts, Ph.D., CEO of Myeloid. "In particular, we are really excited about the progress we’ve made with in vivo programming with MT-302, our TROP2-FcA-LNP, that has shown confirmed tumor killing activity and strong expression in myeloid cells in non-human primates. We are planning to advance this program into the clinic and expect to file an IND in 2023."
Myeloid has combined the power of mRNA with proprietary ATAK CAR receptors, to program myeloid cells to target and kill cancer through direct mechanisms and the elicitation of a broad anti-tumor responses, including the activation of T cells. Myeloid cells are a primary orchestrator of immune response and accumulate naturally within solid tumors, in some cases representing up to seventy-five percent of the tumor mass. Myeloid’s adaptations of mRNA for the myeloid compartment have enabled the evolution to deliver these receptors directly to the patient without any ex-vivo cell engineering.
Myeloid’s novel in vivo engineering platform specifically targets and activates myeloid cells to elicit broader anti-tumor adaptive immunity. Through this approach, Myeloid demonstrates that delivery of lipid-nanoparticles (LNPs) encapsulating mRNA results in selective uptake and expression by myeloid cells in vivo, leading to potent tumor killing in multiple cold tumor models. These data demonstrate the potential for Myeloid’s technology to program cells directly in vivo.
Myeloid’s lead program from this platform, MT-302, is a TROP2-FcA-LNP currently in IND-enabling studies for the treatment of multiple indications including colon, lung and breast cancer. MT-302 has demonstrated strong expression and favorable safety in myeloid cells in two species, rodents and non-human primates. In addition, treatment with MT-302 demonstrates monotherapy activity in a TROP2/TNBC model, confirming the potency of programmed myeloid cells in the absence of T cells. Myeloid believes that MT-302 has significant advantages over TROP2-ADC approaches through its ability to engage the full immune response.
Myeloid’s novel class of CARs, known as ATAK Receptors, combine tumor recognition with multiple proprietary innate-immune signaling domains. Myeloid scientists have screened multiple unexplored combinations of innate-immune signals and uncovered optimal multi-signal pathways. The combination of cancer recognition binders with these novel intracellular signaling domains allows myeloid cells to be reprogrammed with previously unexplored combinations of immune signals, leading to tumor killing and broad systemic anti-tumor responses that support their clinical development in cell therapies.