Ginsenoside F3

Ginsenoside F3 is a saponin extracted from the leaves of Panax ginseng with immunoenhancing and antitumor immunostimulatory activities. Ginsenoside F3 upregulates RIPOR2 with a K_d value of 3.77 μM. Ginsenoside F3 enhances NF‑κB activation, upregulates T‑bet and downregulates GATA‑3, increases the production of IL‑2 and IFN‑γ, decreases the production of IL‑4 and IL‑10, reverses CD8⁺ T‑cell exhaustion, restores cytokine secretion, and enhances antitumor immunity in a mouse non‑small cell lung cancer model. Ginsenoside F3 can be used for the research of non-small cell lung cancer^[1][2]. In Vitro:Ginsenoside F3 (0.1-100 μmol/L; 72 h) significantly enhances Concanavalin A (HY-P2149)-induced murine spleen cell proliferation, with the maximal 87.2% increase occurring at 10 μmol/L^[1].
Ginsenoside F3 (0.1-100 μmol/L; 48 or 72 h) increases Concanavalin A-induced IL-2 and IFN-γ production and decreases ConA-induced IL-4 and IL-10 production in murine spleen cells, with maximal effects at 10 μmol/L^[1].
Ginsenoside F3 (0.1-100 μmol/L; 10 h) upregulates Concanavalin A-induced IFN-γ and T-bet mRNA expression and downregulates ConA-induced IL-4 and GATA-3 mRNA expression in murine spleen cells^[1].
Ginsenoside F3 (10 μmol/L; 1 h) enhances Concanavalin A-induced NF-κB DNA binding activity in murine spleen cells^[1].
Ginsenoside F3 directly binds to RIPOR2 with a binding affinity of 3.77 μM^[2].
Ginsenoside F3 (0.1-10 μM; day 4 and day 6 of chronic stimulation) dose-dependently reduces the frequency of PD-1⁺ TIM-3⁺ exhausted primary mouse CD8⁺ T cells under chronic anti-CD3 stimulation, and restores RIPOR2 expression in these cells^[2].
Ginsenoside F3 (0.1-10 μM; 6 days) dose-dependently restores TNF-α and IFN-γ cytokine production in exhausted primary mouse CD8⁺ T cells cultured under chronic anti-CD3 stimulation for 6 days^[2].
Ginsenoside F3 (1-10 μM; 48 h) significantly promotes the proliferation of Jurkat T cells^[2]. In Vivo:Ginsenoside F3 (5 mg/kg; i.p.; daily; 28 days) alone reduces NSCLC tumor burden and increases intratumoral CD4⁺ T cell infiltration, and synergizes with anti-PD-1 therapy to further reduce tumor burden and enhance CD8⁺ T cell infiltration in the tumor microenvironment^[2].