Recently, the heterocyclic compound 8-oxo-3-thiomorpholino-8H-acenaphtho[1,2-b]pyrrole-9-carboni-trile (S1) was synthesized and shown to induce apoptosis in both (H22) hematoma and (MCF-7) ade-nocarcinoma cells. The IC50 values of S1 against the two cell lines were 0.17 and 0.09 μmol/L, respec-tively. Furthermore, the apoptosis-inducing activity of this compound was highlighted both in vivo and in vitro. Subsequent experiments identified Bcl-2 as the primary target of S1, as a significant reduc-tion in Bcl-2 protein levels was observed in H22 cells following a two-hour treatment with 10 μmol/L S1. While rapid depolarization of mitochondrial membranes led immediately to caspase 9 activation, no changes were identified in either caspase 8 levels or levels in Bcl-2 mRNA. These data were consistent with the results of circular dichroism (CD) spectra analysis, revealing that S1 inactivated the Bcl-2 protein by destroying its critical alpha helices. Taken together, these results suggest the potential of S1 in the development of new therapeutic agents. Recently, the heterocyclic compound 8-oxo-3-thiomorpholino-8H-acenaphtho [1,2-b] pyrrole- 9-carboni-trile (S1) was synthesized and shown to induce apoptosis in both (H22) 7) ade-nocarcinoma cells. The IC50 values ​​of S1 against the two cell lines were 0.17 and 0.09 μmol / L, respecively-tively. Furthermore, the apoptosis-inducing activity of this compound was highlighted both in vivo and in vitro. Subsequent experiments identified Bcl-2 as the primary target of S1, as a significant reduction in Bcl-2 protein levels was observed in H22 cells following a two-hour treatment with 10 μmol / L S1. While rapid depolarization of mitochondrial membranes led immediately to These data were consistent with the results of circular dichroism (CD) spectra analysis, revealing that S1 inactivated the Bcl-2 protein by destroying its critical alpha helices. Taken together, these results suggest th e potential of S1 in the development of new therapeutic agents.