5-nitro-furan-2-carboxylic acid-(4-chloro-anilide)

LCS3 inhibits glutathione disulfide reductase (GSR) and thioredoxin reductase 1 (TXNRD1) (IC50=3.3 µM and 3.8 µM, respectively) synergistically. LCS3 shows anti-tumor activity, and induces apoptosis. LCS3 can be used in lung adenocarcinoma (LUAD) research[1].

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

LCS3 (5 nM-10 µM; 96 h) inhibits lung cancer cell lines, but not non-transformed lung cells[1]. LCS3 (3 µM; 96 h) selectively kills lung adenocarcinoma (LUAD) cell lines, in part through the induction of apoptosis[1]. LCS3 induces ROS and NRF2 pathway activation in sensitive lung adenocarcinoma (LUAD) cells[1]. Cell Viability Assay[1] Cell Line: Non-small cell lung cancer (NSCLC) cells and non-transformed lung cells Concentration: 5 nM-10 µM Incubation Time: 96 hours Result: Inhibited the growth of 24/25 NSCLC cell lines at low micromolar concentrations (IC50<5 µM), both of the non-transformed lung cell lines were relatively insensitive (IC50>10 µM). Apoptosis Analysis[1] Cell Line: lung adenocarcinoma (LUAD) cells Concentration: 3 µM Incubation Time: 96 hours Result: Increased cleavage of caspase 3, caspase 7 and/or PARP1 in all LCS3-sensitive LUAD cell lines. Cell Viability Assay[1] Cell Line: H23 and H1650 cells Concentration: 3 µM Incubation Time: 3, 6, and 12 hours Result: Responded to LCS3 by accumulating ROS and activating the NRF2 transcription program.

[1]. Fraser D Johnson, et al. Characterization of a small molecule inhibitor of disulfide reductases that induces oxidative stress and lethality in lung cancer cells. Cell Rep. 2022 Feb 8;38(6):110343.