Macrophages are remarkably plastic innate immune cells that adopt distinct functional phenotypes in response to environmental cues, a process broadly conceptualized as polarization along an M1 to M2 spectrum. Classically activated M1 macrophages, induced by signals such as interferon-gamma and microbial products, are proinflammatory and microbicidal. A defining M1 effector is inducible nitric oxide synthase (iNOS), which generates nitric oxide for pathogen killing, while the costimulatory molecules CD86 and CD80 are upregulated to license T-cell activation and reinforce a Th1-skewed adaptive response. In contrast, alternatively activated M2 macrophages, driven by IL-4 and IL-13, promote tissue repair, angiogenesis, immunoregulation, and the resolution of inflammation. The enzyme Arginase-1 is a hallmark of M2 cells, competing with iNOS for the substrate arginine and channeling it toward polyamine and proline synthesis that support wound healing and fibrosis. The mannose receptor CD206/MRC1 and the scavenger receptor CD163 are widely used M2 surface markers reflecting endocytic and anti-inflammatory functions. Pan-macrophage and lineage markers such as CD68, an intracellular lysosomal glycoprotein, and F4/80, a classic murine macrophage marker, allow identification of the broader population regardless of polarization state. This polarization framework has profound implications in disease: M1-skewed responses contribute to chronic inflammation and autoimmunity, whereas tumor-associated macrophages frequently adopt M2-like, immunosuppressive phenotypes that foster tumor growth and angiogenesis, making macrophage reprogramming an active therapeutic strategy. Distinguishing polarization states in tissue and culture requires reagents that pair phenotype-specific and pan-macrophage markers. This sampler pack brings together validated antibodies against iNOS, CD86, CD80, Arginase-1, CD206/MRC1, CD163, CD68, and F4/80 for studying macrophage polarization and function.