DISCOVERY
LEAD OPTIMIZATION
IND-ENABLING
PHASE 1
We are advancing our glioblastoma program to clinical stage in partnership with Duke University after showing potent anti-tumor activity in animal cancer models.
MT-201
Glioblastoma
Cell Therapy Programs
Using a harmonized, one-day manufacturing process, we are moving into the clinic with our ATAK monocytes. These myeloid cells are engineered with a novel CAR design that triggers tumor-specific phagocytosis and secretion of pro-inflammatory cytokines, resulting in a hot tumor microenvironment and causing tumor cell death. In addition, ATAK monocytes sustain the ability to cross-present antigens, generating a durable anti-tumor response by cytotoxic T cells.
MT-101 is being developed for the treatment of relapsed and refractory CD5-expressing T cell lymphomas. Refractory PTCL is a lethal disease with limited treatment options, that until now has not benefited from innovations in cell therapy.
In vitro and in vivo studies show MT-101 demonstrated meaningful anti-tumor activity. Treatment in these models has been associated with potent phagocytosis responses, the production of inflammatory mediators and delays in tumor progression.
DISCOVERY
LEAD OPTIMIZATION
IND-ENABLING
PHASE 1
MT-102 is being developed for individuals with HER2 expressing cancers. In vivo studies show MT-102 has eradicated HER2+ tumors.
MT-102
HER2-ATAK Cells
MT-101
CD5-ATAK Cells
DISCOVERY
LEAD OPTIMIZATION
IND-ENABLING
PHASE 1
DISCOVERY
LEAD OPTIMIZATION
IND-ENABLING
PHASE 1
RIGHTS
INDICATION
PROGRAM/PLATFORM + TARGET
PARTNERED
Peripheral T Cell Lymphoma
MT-101
(CD5-ATAK Cells)
HER2+
MT-102
(HER2-ATAK Cells)
Glioblastoma
MT-201
(CMV-PRIMED)
Liver Cancer
MT-301
(GPC3-FcA LNP)
Colon, Lung, Breast Cancer
MT-302
(TROP2-FcA LNP)
Myeloid Cell Engineering
RETROTRANSPOSON
(RetroT™)
Gene Editing
RETROTRANSPOSON
(RetroT™)
Publications
November 10, 2022
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.
ATAK receptors, a new class of chimeric antigen receptors that harness innate immunity in myeloid cells to target cancer
POSTER 1
April 10, 2022
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.
ATAK receptors, a new class of chimeric antigen receptors that harness innate immunity in myeloid cells to target cancer
POSTER 2
November 10, 2022
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.
In vivo programming of myeloid cells by mRNA-mediated delivery of novel Fc alpha fusion receptor activates anti-tumor immunity
POSTER 2
April 10, 2022
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.
In vivo programming of myeloid cells by mRNA-mediated delivery of novel Fc alpha fusion receptor activates anti-tumor immunity
POSTER 1