The colon length is markedly extended, and the colon weight is significantly reduced in mice treated with EMD638683 compared to those treated with a placebo, suggesting an impact of EMD638683 on tumor growth subsequent to chemical carcinogenesis. Furthermore, the stomach weight is significantly lower in the EMD-treated group. Notably, EMD638683 treatment significantly suppresses the development of tumors following carcinogenic treatment ^[2].

EMD638683 administration (20 mg/kg, intragastrically) prevents the progression of monocrotaline (MCT)-induced pulmonary vascular remodeling in rats. Hemodynamic parameters indicate that EMD638683 treatment reduces right ventricular systolic pressure (RVSP) (15.8±2.5 vs. 28.2±3.1 mmHg; P<0.05; n=6) and right ventricular hypertrophy index (RVHI) (0.27±0.02 vs. 0.41±0.06; P<0.05; n=6) compared to vehicle-treated controls ^[3].

EMD638683 is a selective SGK1 inhibitor. EMD638683 suppresses the phosphorylation of NDRG1 (N-Myc downstream-regulated gene 1), with an IC50 value of 3.35±0.32 μM in the cell culture medium. Additionally, EMD638683 exhibits inhibitory activity against cAMP-dependent protein kinase (PKA), mitogen- and stress-activated protein kinase 1 (MSK1), protein kinase C-related kinase 2 (PKR2), as well as the SGK isoforms SGK2 and SGK3 ^[1].

In both control and EMD638683 (50 μM)-treated CaCo-2 cells, radiation significantly elevates the proportion of cells undergoing late apoptosis. Treatment with EMD638683 alone tends to increase the percentage of apoptotic CaCo-2 cells. Post-radiation, the proportion of apoptotic EMD638683-treated CaCo-2 cells is notably higher than that of apoptotic control cells. Therefore, EMD638683 treatment substantially enhances apoptosis following radiation ^[2].