Iridin

Iridin is an orally active natural isoflavone. Iridin inhibits the PI3K/AKT and PKM2 signaling pathways, and downregulates the JAK/STAT and NF-κB pathways. Iridin induces Fas-mediated extrinsic apoptosis, G2/M cell cycle arrest, and inhibits cell proliferation. Iridin reduces inflammation, inhibits ROS production, suppresses glycolysis, and also exhibits antioxidant and antidiabetic activities. Iridin can be used in research related to gastric cancer and acute lung injury^[1][2][3]. In Vitro:Iridin (12.5-200 μM) induces apoptosis via the extrinsic pathway and regulates the PI3K/AKT signaling pathway in AGS gastric cancer cells, HaCaT cells, and TRAIL-resistant gastric cancer cells^[1].
Iridin (12.5-50 μM; 18 h) inhibits the production of proinflammatory mediators in LPS (HY-D1056)-stimulated RAW 264.7 cells in a dose-dependent manner^[1].
Iridin (10 nM-100 μM) exerts no anticancer effects on MCF-7 and T-47D breast cancer cells^[1].
Iridin (12.5-200 μM; 48 h) inhibits the proliferation and induces the death of human gastric cancer AGS cells, with an IC₅₀ of 161.3 μM; whereas it exerts no significant effect on the cell viability of human keratinocyte HaCaT cells after 48 h of treatment^[2].
Iridin (50-200 μM; 48 h) induces G2/M cell cycle arrest in human gastric cancer AGS cells after 48 h of treatment by downregulating the expression of cell cycle regulatory proteins Cdc25C, CDK1, and Cyclin B1^[2].
Iridin (50-200 μM; 48 h) induces apoptotic cell death in human gastric cancer AGS cells via the extrinsic apoptotic pathway^[2].
Iridin (50-200 μM; 48 h) inhibits the PI3K/AKT signaling pathway in human gastric cancer AGS cells by downregulating the phosphorylated (active) forms of PI3K and AKT, without affecting the expression of total PI3K or AKT^[2].
Iridin (6.25-200 μM; 24 h) shows no cytotoxicity against RAW264.7 cells even at concentrations up to 100 μM. Based on its anti-inflammatory efficacy, concentrations of 12.5, 25 and 50 μM are selected for subsequent studies^[3].
Iridin (12.5-50 μM; 18 h) reverses LPS-induced Warburg effect in RAW264.7 cells in a dose-dependent manner by enhancing oxidative phosphorylation and reducing glycolytic activity^[3].
Iridin (12.5-50 μM; 18 h) dose-dependently inhibits LPS-induced production of NO, TNF-α, IL-1β and MCP-1 in RAW264.7 cells^[3].
Iridin (12.5-50 μM; 18 h) dose-dependently abrogates LPS-induced accumulation of ROS and NO in RAW264.7 cells^[3].
Iridin (12.5-50 μM; 18 h) dose-dependently inhibits LPS-induced excessive phagocytic activity in RAW264.7 cells^[3].
Iridin (12.5-50 μM; 18 h) dose-dependently downregulates the expression of PKM2 and its downstream JAK/STAT and NF-κB pathway proteins in LPS-stimulated RAW264.7 cells, and this effect is reversed by PKM2 activation or ROS scavenging^[3]. In Vivo:Iridin (20-80 mg/kg; p.o.; once daily; 5 days) dose-dependently ameliorates LPS-induced acute lung injury in male ICR mice by reducing inflammatory cell infiltration, modulating macrophage polarization to an anti-inflammatory M2 phenotype, and inhibiting the PKM2-mediated JAK/STAT and NF-κB signaling pathways^[3].