Renal fibrosis is a key pathological hallmark of chronic kidney disease (CKD), contributing to the irreversible decline of renal function and representing a major global health concern. Despite its clinical importance, no therapies have been approved to specifically target renal fibrosis. Current treatments, including RAAS inhibitors and SGLT2 inhibitors, may slow CKD progression but do not directly modulate fibrotic remodeling. In this study, we identified a novel small-molecule compound with significant anti-fibrotic activity, initially discovered as an inhibitor of the Wnt signaling pathway—an axis increasingly recognized for its role in tissue fibrosis. Using a folic acid-induced mouse model of renal fibrosis, we demonstrated that administration of this compound markedly reduced renal injury and fibrotic responses. Specifically, it suppressed the upregulation of kidney injury markers Kim1 and Lcn2, attenuated the expression of extracellular matrix components including Collagen I, Vimentin, and α-SMA. These findings highlight the therapeutic potential of this compound in renal fibrosis, although the precise mechanisms remain to be elucidated.