From:  Targeting the NRF2 pathway to enhance lipid peroxidation: a novel therapeutic strategy in hepatocellular carcinoma

 Pharmacological modulators targeting the NRF2 pathway in HCC and their impact on lipid peroxidation and ferroptosis.

CompoundModelDosesNRF2 pathway targeting strategyEffect on lipid peroxidation/NRF2ConclusionStudy
In vitro studies
CPT + sorafenibHepG2 and Huh7 cellsCPT 1–5 μM + sorafenib 5 μMCPT inhibits NRF2’s expression, synergizing with sorafenib to induce ferroptosis↓ NRF2 intracellular levels, ↑ lipid peroxidationCPT synergizes with sorafenib to induce ferroptosisElkateb et al., 2023 [38]
Metformin + sorafenibHCC cell lines, mouse xenograftPPI 1–4 μMMetformin + sorafenib inhibits p62-KEAP1-NRF2 pathway↓ NRF2’s translocation to the nucleus, ↑ ferroptosis with combo therapyReverses NRF2-driven resistance to sorafenibTang et al., 2022 [41]
Picropodophyllin (PPP)In vitro and in vivo HCC modelsPPP 2.5–10 μMPPP inhibited the PI3K-AKT-NRF2 pathway↓ NRF2 target genes, ↑ lipid ROS; ferroptosis via iron overloadInduces ferroptosis through NRF2 inhibitionZheng et al., 2025 [42]
Arsenic trioxide (ATO)HCC cell linesML385 10 μMATO-induced ferroptosis enhanced by silencing NRF2↑ Lipid ROS, MDA, Fe2+, ↑ NRF2 knockdown ferroptosisFerroptosis enhanced by NRF2 silencingHuang et al., 2025 [43]
TilirosideHCC cell lines and tumor xenografts in nude miceNot applicableTiliroside promotes the ubiquitination of NRF2 and sensitizes cells to ferroptosis inducers↓ NRF2 intracellular levels, ↑ lipid peroxidation, and enhanced ferroptotic cell deathSensitizes HCC cells to ferroptosis inducersYang et al., 2023 [44]
BavachinHuh7 and HepG2 cellsBavachin 20–40 μMBavachin mildly activates NRF2/HO-1 pathway↑ ROS, MDA, exceeding the protective effect of NRF2’s activationPromotes ferroptosis via oxidative stressLi et al., 2024 [45]
BrusatolCell lines and patient tissueBrusatol 100 nM; sulforaphane 5 μMNRF2-driven CYP4F11 expression promotes HCC and resistance↑ NRF2 inhibition sensitizes cells, ↑ lipid peroxidationSuppresses HCC via CYP4F11-NRF2 inhibitionChen et al., 2025 [39]
In vivo studies
DSF/CuHCC cell linesDSF 1 μM + Cu 1 μMDSF/Cu treatment elevates NRF2 as a compensatory response↑ Lipid peroxidation impairs mitochondrial homeostasisPotentiated by NRF2 inhibitionRen et al., 2021 [48]
ArenobufagiHepG2 cells, nude miceArenobufagin 20 μMArenobufagin modulates p62-KEAP1-NRF2 to induce autophagy-dependent ferroptosis↓ NRF2 intracellular levels, ↑ MDA, lipid ROSInduces autophagy-dependent ferroptosisYang et al., 2024 [46]
NSC48160HepG2, SMMC-7721 and BEL-7402 cellsNSC48160 36 μMDisrupts TCA cycle metabolism and indirectly inhibits the NRF2-SLC7A11-GPX4 axis↑ Lipid peroxidation and ferroptosis, ↓ NRF2 expression, and its downstream effectorsPromotes ferroptosis via NRF2 suppressionZhang et al., 2025 [47]

This table is of the author’s own elaboration based on the review literature. This table summarizes in vitro and in vivo studies evaluating compounds that modulate the NRF2 pathway in HCC, including their models, doses, molecular mechanisms, effects on lipid peroxidation, and therapeutic implications in improving ferroptosis or overcoming drug resistance. AKT: protein kinase B; CPT: camptothecin; Cu: copper; DSF: disulfiram; GPX4: glutathione peroxidase 4; GSH: glutathione; HCC: hepatocellular carcinoma; HO-1: heme oxygenase-1; KEAP1: Kelch-like ECH-associated protein 1; MDA: malondialdehyde; NRF2: nuclear factor erythroid 2-related factor 2; p62: sequestosome 1; PI3K: phosphatidylinositol 3-kinase; ROS: reactive oxygen species; SLC7A11: solute carrier family 7 member 11; TCA: tricarboxylic acid.