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Fermented and aged mountain‐cultivated ginseng sprouts (FAMCGS) exhibit superior antioxidant and anti‐inflammatory properties compared to mountain‐cultivated ginseng sprouts (MCGS). However, the mechanisms behind these properties of FAMCGSE remain unclear. This study explores the anti‐inflammatory effects of FAMCGS extract (FAMCGSE) on LPS‐stimulated RAW 264.7 macrophages and the underlying mechanisms. The MTT assay confirmed that FAMCGSE (0 to 0.1%) maintained cell viability without inducing morphological changes. Pretreatment with FAMCGSE significantly mitigated LPS‐induced morphological alterations dose‐dependently. RT‐PCR and Western blot analyses showed that FAMCGSE significantly reduced the mRNA and protein levels of proinflammatory mediators such as TNF‐α, IL‐1β, IL‐6, iNOS, and COX‐2. Additionally, FAMCGSE decreased the production of TNF‐α, IL‐1β, IL‐6, nitric oxide, and PGE2 in LPS‐activated RAW264.7 cells. Mechanistically, FAMCGSE inhibited the phosphorylation of mitogen‐activated protein kinases (MAPKs; ERK, p38, and JNK) and prevented the LPS‐induced nuclear translocation of NF‐κB, with effects comparable to compound K (CK) or dexamethasone. Notably, FAMCGSE was particularly effective in inhibiting ERK and JNK activation, with less impact on p38, suggesting a specific inhibitory action on certain MAPK pathways. These findings highlight FAMCGSE's potential as an inhibitor of MAPK and NF‐κB pathways, indicating that FAMCGSE, including its main component CK, may be a promising therapeutic agent for inflammation‐related conditions. [ABSTRACT FROM AUTHOR]