tcsc3839 Ginsenoside Rd

Ginsenoside Rd inhibits TNFα-induced NF-κB transcriptional activity with an IC₅₀ of 12.05±0.82 μM in HepG2 cells. Ginsenoside Rd inhibits expression of COX-2 and iNOS mRNA. Ginsenoside Rd also inhibits Ca²⁺ influx. Ginsenoside Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9, with IC₅₀s of 58.0±4.5 μM, 78.4±5.3 μM, 81.7±2.6 μM, and 85.1±9.1 μM, respectively.

IC50 & Target: IC50: 12.05±0.82 μM (NF-κB, in HepG2 cells)^[1]


COX-2, iNOS^[1]


Ca²⁺ influx (L-type calcium channel)^[2]


IC50: 58.0±4.5 μM (CYP2D6), 78.4±5.3 μM (CYP1A2), 81.7±2.6 μM (CYP3A4), 85.1±9.1 μM (CYP2C9), >100 μM (CYP2A6)^[4]

In Vitro: Ginsenoside Rd is one of the most abundant ingredients of Panax ginseng. Ginsenoside Rd significantly inhibits TNF-α-induced NF-κB transcriptional activity with an IC₅₀ of 12.05±0.82 in HepG2 cells. Ginsenoside Rd also inhibits expression of COX-2 and iNOS mRNA and iNOS promoter activity in a dose-dependent manner. To determine nontoxic concentrations, HepG2 cells are treated with various concentrations (0.1, 1, and 10 μM) of compounds (e.g., Ginsenoside Rd) and cell viability is measured using an MTS assay. No compounds are significantly cytotoxic at up to 10 μM, indicating that NF-κB inhibition is not due to cell toxicity^[1]. Ginsenoside Rd is one of the most abundant ingredients of Panax ginseng, protects the heart via multiple mechanisms including the inhibition of Ca²⁺ influx. Ginsenoside Rd reduces I_Ca,L peak amplitude in a concentration-dependent manner (IC₅₀=32.4±7.1 μM)^[2]. Ginsenoside Rd exhibits an inhibition against the activity of CYP2D6 in human liver microsomes with an IC₅₀ of 58.0±4.5 μM, a weak inhibition against the activity of CYP1A2, CYP3A4, and CYP2C9 in human liver microsomes with IC₅₀s of 78.4±5.3, 81.7±2.6, and 85.1±9.1, respectively, and an even weaker inhibition against the activity of CYP2A6 in human liver microsomes with an IC₅₀ value of more than 100 μM^[4].

In Vivo: Ginsenosides Rd is a major compound isolated from Gynostemma pentaphyllum that holistically improves gut microenvironment and induces anti-polyposis in Apc^Min/+ mice. Six-weeks-old mice are subjected to Ginsenoside Rd treatment, before the appearance of the intestinal polyps. All the mice are monitored for food intake, water consumption, and weight changes. Throughout the experiment, no Rb3/ Ginsenoside Rd-associated weight loss in mice is observed. In addition, none of the treated mice show variations in food and water consumption. Whereas, the number and size of the polyps are effectively reduced by Ginsenoside Rd treatments^[3].