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[Preprint]. 2026 Jul 20:2026.07.17.739092. [Version 1] doi: 10.64898/2026.07.17.739092

Figure 3. SCD-dependent desaturation redirects the metabolic fate of petroselaidic acid to promote ferroptosis.

Figure 3.

(A) GC-FID quantification of trans 18:1, 18:2, and trans 18:2 in H460 cells treated with 100 μM indicated fatty acid at time t = 0 hr.

(B) Structures of native SCD substrate stearoyl-CoA and product oleoyl-CoA compared to structures of petroselaidyl-CoA and putative Δ9-desaturation product linopetroselaidyl-CoA.

(C) GC-FID quantification of trans 18:2 in H460 cells treated for 24 hours with BSA or 100 μM petroselaidic acid in the presence or absence of 1 μM of the SCD inhibitor CAY10566.

(D) Lethal fraction over time following addition of 125 nM RSL3 for H460 cells pre-treated with BSA or 100 μM petroselaidic acid in the presence or absence of 1 μM of SCD inhibitor for 24 hours.

(E) Lethal fraction over time for wildtype or SCD overexpressing (+ dox) H460 cells co-treated with 2 μM RSL3 and BSA or 100 μM petroselaidic acid.