S-(N-Methylsulfinylbutylthiocarbamoyl)-L-cysteine

S-(N-Methylsulfinylbutylthiocarbamoyl)-L-cysteine (SFN-Cys) is a isothiocyanate derivative and an active metabolite of the class I and II histone deacetylase (HDAC) inhibitor and anticancer agent sulforaphane.^[1] It is formed from sulforaphane via DL-sulforaphane glutathione and sulforaphane cysteinylglycine intermediates by mercapturic acid pathway enzymes. SFN-Cys (20 µM) reduces invasion and migration by U87MG and U373 MG glioblastoma cells in wound healing and chamber assays, respectively.^[2] It decreases levels of α-tubulin, βIII-tubulin, stathmin 1, and X-linked inhibitor of apoptosis (XIAP) in, as well as reduces cell density of, paclitaxel-resistant A549 lung cancer cells (A549/T) when used at a concentration of 45 µM.^[3] SFN-Cys (30 µM) induces apoptosis and cell cycle arrest at the G2/M phase in U87MG and U373 MG cells.^[4]

References:
[1]. Al Janobi, A.A., Mithen, R.F., Gasper, A.V., et al. Quantitative measurement of sulforaphane, iberin and their mercapturic acid pathway metabolites in human plasma and urine using liquid chromatography-tandem electrospray ionisation mass spectrometry. J. Chromatogr. B. Analyt. Technol. Biomed. Life Sci. 844(2), 223-234 (2006).
[2]. Zhou, Y., Wang, Y., Wu, S., et al. Sulforaphane-cysteine inhibited migration and invasion via enhancing mitophagosome fusion to lysosome in human glioblastoma cells. Cell. Death. Dis. 11(9), 819 (2020).
[3]. Wang, Y., Zhou, Y., Zheng, Z., et al. Sulforaphane metabolites reduce resistance to paclitaxel via microtubule disruption. Cell Death Dis. 9(11), 1134 (2018).
[4]. Li, J., Zhou, Y., Yan, Y., et al. Sulforaphane-cysteine downregulates CDK4 /CDK6 and inhibits tubulin polymerization contributing to cell cycle arrest and apoptosis in human glioblastoma cells. Aging (Albany N.Y.) 12(17), 16837-16851 (2020).