Spliceostatin A is an anticancer agent and splicing inhibitor that inhibits the splicing mechanism of the spliceosome and inhibits mitotic clonal expansion and adipogenesis.Spliceostatin A induces cell cycle arrest in the G1 and G2/M phases, and induces apoptosis.

SF3B1 (WT):5.5 nM, SF3B1 (mutant):4.9 nM

Spliceostatin A (0, 2.5 nM, 5 nM, 10 nM, and 20 nM; 0, 6 h, 12 h, and 24 h) increases apoptosis in chronic lymphocytic leukemia (CLL) cells[1].

BTA-EG4 (30 mg/kg; injections; daily; 2 weeks) improved dendritic spine density and cognitive function of 3xTg AD mice in an age-dependent manner. BTA-EG4 injected 3xTg AD mice at 6-10 months of age showed improved learning and memory; however, only minimal improvement was observed at 13-16 months of age. This behavioral improvement corresponds to a decrease in soluble Aβ 40 levels. These findings suggest that BTA-EG4 may be beneficial in ameliorating the synaptic loss seen in early AD.[2]