The commercially available compounds used were
erastin (Selleckchem S7242),
nutlin-3a (Sigma-Aldrich 444152), MDMX inhibitor NSC207895 (Calbiochem 444158),
staurosporine (Selleckchem S1421), deferoxamine (Calbiochem 252750), MEL23 (InterBioscreen) (Herman et al. 2011 (
link)), PPARα agonist (
Pirinixic acid; Selleckchem S8029), PPARα antagonist (
GW6471; Santa Cruz Biotechnology CAS 436159-64-7), PPARγ antagonist (
GW9662; Santa Cruz Biotechnology CAS 22978-25-2), and
DGAT1 inhibitor (Cayman Chemicals A-922500).
The following compounds were synthesized: IKE as in Larraufie et al. (2015) (
link), fer-1 and RSL3 as in Dixon et al. (2012) (
link), and FIN56 as in Shimada et al. (2016) (
link).
All compounds were dissolved in DMSO (Sigma-Aldrich
D8418). The fixed concentrations of compounds used was as follows (unless otherwise mentioned): 10 µM nutlin, 14 µM MEL23, 20 µM ferrostatin-1 (Fer-1), 90 µM deferoxamine (DFO), and 5 µM MDMX inhibitor.
Venkatesh D., O'Brien N.A., Zandkarimi F., Tong D.R., Stokes M.E., Dunn D.E., Kengmana E.S., Aron A.T., Klein A.M., Csuka J.M., Moon S.H., Conrad M., Chang C.J., Lo D.C., D'Alessandro A., Prives C, & Stockwell B.R. (2020). MDM2 and MDMX promote ferroptosis by PPARα-mediated lipid remodeling. Genes & Development, 34(7-8), 526-543.