Tubeimoside II

Tubeimoside II is an orally active triterpenoid saponin and antiviral agent that binds to PACT/PRKRA with K_d values of 5.37 μM and 133.1 μM, respectively. Tubeimoside II inhibits oxidase-dependent EGFR activation and reduces TGF-β1-induced oxidative stress. Tubeimoside II activates the RIG-I signaling pathway and increases IFN-β secretion. Tubeimoside II suppresses TPA-induced ear edema, mouse sarcoma 180 growth, and TPA-induced skin tumor formation. Tubeimoside II exerts broad-spectrum antiviral activity against SARS-CoV-2, HCoV-OC43, and IAV-H1N1/FM1. Tubeimoside II can be used in research related to retinoblastoma, respiratory viral infections, skin tumors, and sarcoma 180^[1][2][3]. In Vitro:Tubeimoside II (1-5 μM; 24 h) dose-dependently reverses TGF-β1-induced epithelial-mesenchymal transition in retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 24 h) dose-dependently inhibits TGF-β1-induced phosphorylation of SRC and Vav2 in retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 48 h) dose-dependently inhibits TGF-β1-induced extracellular matrix adhesion of retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 48 h) inhibits TGF-β1-induced migration of retinoblastoma Y-79 and WERI-Rb-1 cells in a dose-dependent manner^[1].
Tubeimoside II (1-5 μM; 48 h) dose-dependently inhibits TGF-β1-induced invasion of retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 6 h) dose-dependently reduces TGF-β1-induced ROS production in retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 6 h) dose-dependently reduces TGF-β1-induced intracellular H₂O₂ production in retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 12 h) dose-dependently reduces TGF-β1-induced active Rac1-GTP expression in retinoblastoma Y-79 and WERI-Rb-1 cells^[1].
Tubeimoside II (1-5 μM; 12 h) inhibits TGF-β1-induced phosphorylation, oxidation and nuclear translocation of EGFR in retinoblastoma Y-79 and WERI-Rb-1 cells, while co-treatment with H₂O₂ or the EGFR activator NSC228155 reverses this effect^[1].
Tubeimoside II (0.25-1 μmol/L) exerts broad-spectrum antiviral activity against SARS-CoV-2, HCoV-OC43 and IAV-H1N1/FM1 in Caco-2-N, RAW264.7, A549 and Calu-3 cells, reduces viral load and alleviates cytopathic effects in a dose-dependent manner^[2].
Tubeimoside II exhibits broad-spectrum antiviral activity in A549 cells infected with IAV-H1N1/FM1, and this activity depends on the functional RIG-I signaling pathway, as knockout of RIG-I, MAVS or IFN-β abolishes its ability to reduce viral load and upregulate IFN-β expression^[2]. In Vivo:Tubeimoside II (0.65-2.6 mg/kg; i.g.; daily; 5 days) dose-dependently reduces pulmonary viral load, restores CD4⁺/CD8⁺ T-lymphocyte levels, alleviates pulmonary inflammation, and upregulates key RIG-I signaling pathway proteins to enhance innate antiviral immunity in ICR mice infected with IAV-H1N1/FM1^[2].
Tubeimoside II (0.65-2.6 mg/kg; i.g.; daily; 5 days) dose-dependently reduces pulmonary and brain viral load, restores CD4⁺/CD8⁺ T-lymphocyte levels, alleviates pulmonary and cerebral inflammation, and upregulates key RIG-I signaling pathway proteins to enhance innate antiviral immunity in BALB/c mice infected with HCoV-OC43^[2].
Tubeimoside II (0.0075-0.11 μmol per ear; topical; single dose) inhibits TPA-induced ear edema in male ICR mice in vivo in a dose-dependent manner, achieving 100% inhibition at the highest tested dose of 0.11 μmol per ear^[3].
Tubeimoside II (12 mg/kg; i.m.; single dose, daily for 2 days, daily for 3 days) inhibits the growth of transplantable mouse S₁₈₀ tumors in BALB/c mice in a dose-dependent manner, achieving 60.1% inhibition at 12 mg/kg administered intramuscularly for 3 days^[3].
Topical Tubeimoside II (0.5 mg per painting; topical; twice weekly; 17 weeks) completely inhibits DMBA-initiated, TPA-promoted skin tumor formation in female ICR mice, while oral Tubeimoside II (0.1 g/L; p.o.; ad libitum; 17 weeks) reduces tumor number but not tumor incidence^[3].