Ginsenoside Rk3 NLT 98%

Ginsenoside Rk3 is present in the roots Panax notoginseng herbs. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC₅₀ of 14.24±1.30 μM in HepG2 cells. IC50 & Target: IC50: 14.24±1.30 μM (NF-κB, in HepG2 cell), 15.32±0.29 μM (NF-κB, in SK-Hep1 cell)^[1] In Vitro: Ginsenoside Rk3 exerts the strong activity inhibiting NF-κB in a dose-dependent manner. HepG2 cells are pre-treated with different ginsenosides at concentrations ranging from 0.01 to 10 μM for 1 h, and induced with TNF-α for 20 h. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC₅₀ of 14.24±1.30 μM. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC₅₀ of 15.32±0.29 μM in SK-Hep1 cells, consistent with the data from HepG2 cells. Consistent with the inhibition of NF-κB, Ginsenoside Rk3 inhibits the induction of IL8, CXCL1, iNOS, and ICAM1 mRNA significantly in a dose-dependent manner^[1]. In Vivo: The inhibitory effects of Ginsenoside Rk3 (Rk3) on tumor progression are studied in vivo using a H460 xenograft model in nude mice. Compared with the control group, a significant inhibition of tumor growth (volume) is observed in the Ginsenoside Rk3-treated group. Twenty-one days after treatment initiation, tumor growth is significantly inhibited by approximately 62.99% in the mice receiving 20 mg/kg Ginsenoside Rk3, similar to the inhibitory effect observed in the 20 mg/kg Gefitinib-treated group (57.21%). Compared with the control group, tumor growth is moderately inhibited in the mice receiving 10 and 5 mg/kg Ginsenoside Rk3, with inhibition rates of 32.54% and 11.84%, respectively^[2].