L-Sulforaphane

DL-Sulforaphane N-acetyl-L-cysteine (SFN-NAC), a metabolite of sulforaphane, induces apoptosis through down-regulation of α-microtubulin and phosphorylation of ERK1/2-mediated Stathmin-1, and up-regulation of Hsp70 through phosphorylation of ERK1/2 in non-small-cell lung cancer (NSCLC).

(R)-Sulforaphane (L-Sulforaphane) is a potent inducer of the Keap1/Nrf2/ARE pathway.

S-(N-Methylsulfinylbutylthiocarbamoyl)-L-cysteine (SFN-Cys) is an isothiocyanate derivative, functioning as an active metabolite of sulforaphane, a class I and II histone deacetylase (HDAC) inhibitor, and anticancer agent. This compound is generated from sulforaphane through intermediates - DL-sulforaphane glutathione and sulforaphane cysteinylglycine - via the mercapturic acid pathway enzymes. At a concentration of 20 µM, SFN-Cys diminishes invasion and migration of U87MG and U373 MG glioblastoma cells as observed in wound healing and chamber assays. Furthermore, at 45 µM, it significantly lowers the expression of α-tubulin, βIII-tubulin, stathmin 1, and X-linked inhibitor of apoptosis (XIAP), and also reduces cell density in paclitaxel-resistant A549 lung cancer cells (A549/T). Additionally, when used at 30 µM, SFN-Cys prompts apoptosis and cell cycle arrest at the G2/M phase in U87MG and U373 MG cells.