The complement system is an evolutionarily ancient network of plasma and membrane proteins that provides rapid, antibody-independent and antibody-dependent defense against pathogens, links innate and adaptive immunity, and clears immune complexes and apoptotic debris. It can be triggered through three converging routes: the classical pathway, initiated when C1q recognizes antibody-antigen complexes; the lectin pathway, activated by carbohydrate-recognition molecules; and the alternative pathway, which is continuously primed by spontaneous hydrolysis and amplified by Factor B. All three pathways converge on the central component C3, whose cleavage generates the opsonin C3b that tags surfaces for phagocytosis and the anaphylatoxin C3a, and which feeds into cleavage of C5 to release the potent inflammatory mediator C5/C5a and initiate assembly of the membrane attack complex that lyses target cells. The early classical component C2 contributes to formation of the C3 convertase. Because complement activation is potentially destructive to host tissue, it is restrained by regulators acting at multiple steps. The fluid-phase regulator Factor H controls the alternative pathway by accelerating decay of the convertase and serving as a cofactor for C3b inactivation, while the membrane-bound regulators CD55 (decay-accelerating factor) and CD59 protect host cells by destabilizing convertases and blocking terminal membrane attack complex formation, respectively. Dysregulated complement, whether through deficiency or excessive activation, underlies diverse diseases including age-related macular degeneration, atypical hemolytic uremic syndrome, paroxysmal nocturnal hemoglobinuria, and various inflammatory and autoimmune conditions, and complement-directed therapeutics are now in clinical use. Investigating activation and regulation demands reagents across effectors and inhibitors. This sampler pack brings together validated antibodies against C3, C1q, C5/C5a, Factor B, Factor H, CD55, CD59, and C2 for studying complement activation and its regulation.