Myeloid cells are a key immune population in the tumor microenvironment (TME) and represent a tractable target. Precursors can differentiate into multiple cell types, including macrophage (Mɸ), which are heterogeneous. Tumor-associated macrophage (TAM) and myeloid-derived suppressor cells (MDSC) can be found in the TME and may promote tumor progression. We have developed a range of in vitro assays to assess whether immunosuppressive mechanisms can be overcome by immuno-modulators. Monocytes were differentiated into TAM following exposure to tumor cell supernatants alongside classical M1, M2(a) or M2(b) Mɸ. Mɸ phenotype and cytokine/chemokine production were determined and function assessed via phagocytosis and antigen-presentation assays. TAM exhibited a resting phenotype whereas M1 were CD25hi, CD127+, CD80hi, CD68hi and MHCIIhi. M2a were CD25lo, CD80lo, CD163lo, CD68lo and MHCIIint whereas M2b expressed high levels of CD184, CD80 and little CD163 or CD68. TAM produced little IL-12p70 and raised IL-10 and VEGF. M1 produced IL-6, IL-12p70, TNFα and IL-23 whereas M2a produced little detectable cytokine. M2b produced IL-6, IL-10 and TNFα. Mɸ expressed checkpoint inhibitors such as PD1 and Tim-3. Phagocytosis assays were performed using tumor targets and inhibition of the CD47-SIRPα pathway drove enhanced uptake. T cell co-cultures were also performed to assess effects on antigen-presentation. Gene expression analysis was performed using an nCounter® Myeloid Innate Immunity Panel (Nanostring). Our myeloid/macrophage assay platform can be used to test novel myeloid-targeted therapies, and help elucidate the MOA. This has potential for use in immune oncology screening programs and may accelerate progress into the clinic.