XMU-MP-10 is a selective NEDD4 inhibitor with a K D of 43.92 nM. XMU-MP-10 selectively inhibits NEDD4 auto-ubiquitination without affecting other ubiquitination activity, upregulates of β-TrCP and results YAP degradation without affecting NEDD4 protein expression. XMU-MP-10 exhibits significant in vivo efficacy in inhibiting TNBC tumor growth by enhancing CD8 + T cell infiltration. XMU-MP-10 enhances antitumor immune responses through the β-TrCP / YAP / ECM axis. XMU-MP-10 can be used for Triple-Negative Breast Cancer (TNBC) research [1].
In Vivo, XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) is well tolerated in 4T1 cells induced-BALB/c mice but not in 4T1 cells-induced BALB/c-nu mice[1]. XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) has a crucial role for CD8+ T cells in tumor inhibition and influences the β-TrCP-YAP-ECM axis in EMT6 cells induced-BALB/c mice[1]. XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) enhances antitumor immune response by increasing intratumoral infiltration of CD8 cytotoxic T cells in a humanized immune system mice mode[1].
In Vitro, XMU-MP-10 interacts with the HECT domain of NEDD4 at residues Y604, Y605, and Y634[1]. XMU-MP-10 (0.1-10000 μM) binds specifically to WT NEDD4, but not to NEDD4 mutants at Y604A, Y605A, or Y634A[1]. XMU-MP-10 (0.25-10 μM, 1-12 h) significantly inhibits the polyubiquitination of NEDD4 in a dose-dependent manner, upregulates of β-TrCP and results YAP degradation in a dose and time-dependent manner without affecting NEDD4 protein expression in EMT6, 4T1, MDA-MB-231 and HCC38 cells[1]. XMU-MP-10 (2-10 μM, 4 h) selectively inhibits NEDD4 auto-ubiquitination without affecting the ubiquitination activity of the other tested E3 ligases in HEK-293T cell[1].
References:
[1]. Su N, et al,. Inhibiting NEDD4 in triple-negative breast cancer cells reprograms tumor immune microenvironment via the β-TrCP/YAP/ECM axis. Cell Rep Med. 2025 Oct 21;6(10):102420.
In Vivo, XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) is well tolerated in 4T1 cells induced-BALB/c mice but not in 4T1 cells-induced BALB/c-nu mice[1]. XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) has a crucial role for CD8+ T cells in tumor inhibition and influences the β-TrCP-YAP-ECM axis in EMT6 cells induced-BALB/c mice[1]. XMU-MP-10 (25 mg/kg, i.v., daily for 14 days) enhances antitumor immune response by increasing intratumoral infiltration of CD8 cytotoxic T cells in a humanized immune system mice mode[1].
In Vitro, XMU-MP-10 interacts with the HECT domain of NEDD4 at residues Y604, Y605, and Y634[1]. XMU-MP-10 (0.1-10000 μM) binds specifically to WT NEDD4, but not to NEDD4 mutants at Y604A, Y605A, or Y634A[1]. XMU-MP-10 (0.25-10 μM, 1-12 h) significantly inhibits the polyubiquitination of NEDD4 in a dose-dependent manner, upregulates of β-TrCP and results YAP degradation in a dose and time-dependent manner without affecting NEDD4 protein expression in EMT6, 4T1, MDA-MB-231 and HCC38 cells[1]. XMU-MP-10 (2-10 μM, 4 h) selectively inhibits NEDD4 auto-ubiquitination without affecting the ubiquitination activity of the other tested E3 ligases in HEK-293T cell[1].
References:
[1]. Su N, et al,. Inhibiting NEDD4 in triple-negative breast cancer cells reprograms tumor immune microenvironment via the β-TrCP/YAP/ECM axis. Cell Rep Med. 2025 Oct 21;6(10):102420.
















