HS-2 shows strong potential as an oral anticancer agent by dual inhibiting HDAC1 and SPOP. It effectively suppresses cancer cell proliferation, outperforming reference drugs with IC50 values of 7.6 nM (HDAC1) and 9.1 μM (SPOP). MD confirms stable binding, and in vivo studies demonstrate significant tumor suppression with minimal toxicity. This evidence concerns the gene HDAC1 and neoplasm.