Given DCs’ critical role in bridging innate and adaptive immunity [48, 49] and their capacity to exacerbate inflammation via TLR4‐mediated cytokine production [50], our findings establish that compound 2 mitigates sepsis severity by inhibiting monocyte‐to‐DC maturation, thereby reducing antigen presentation, interferon responses, and DC migratory functions. Here, TLR4 is linked to Sepsis.