Table 1.

List of studies evaluating the effects of compounds inducing FAO and the standard therapy combination in tumor treatment.

Drug	Tumor	Effect	References
Oleanolic acid	Hepatocellular carcinoma	Oleanolic acid enhances lipolysis stimulating ROS production, which is responsible for mitochondrial apoptosis.	[125]
Arachidonic acid	Rat hepatoma cells	Arachidonic acid-induced ROS leading cells to apoptosis.	[127]
Trolox	Rat hepatoma cells	Trolox prevents arachidonic acid-induced apoptosis buffering ROS	[127]
Palmitate	Rat hepatoma cells Human hepatoblastoma	Palmitate stimulates mitochondrial metabolism and ROS production, leading cells to apoptotic death	[128,129]
N-acetyl cysteine (NAC)	Rat hepatoma cells Breast cancer	NAC limits ROS accumulation in palmitate treatment reducing apoptotic and enhancing cell viability.	[128,138]
SU6656	Lung cancer	SU6656, an Src inhibitor, results in FABP4 induction. The consequent activation of β-oxidation generates ROS that induces apoptosis	[92]
Docosahexaenoic acid (DHA)	Prostate cancer Breast cancer Leukaemia	DHA generates ROS, consequently activating apoptosis. The co-treatment of DHA with other drugs increases the responsiveness to these.	[130]
SkQ1	Cancer stem cell	SkQ1 is a mitochondrial-specific antioxidant in combination with the pharmacological inhibition of FAO has been proposed as a promising therapeutic approach	[133,135]
Cytarabine (AraC)	Leukaemia	AraC treatment causes an increase of the OXPHOS with higher ROS content. This aspect is useful to increase the sensitivity to other drugs, including etomoxir.	[136,137]
Vitamin C/E	Breast cancer	The introduction of vitamins C and E in the diet confers a protective effect from tumor recurrence and survival of patients.	[138]
BMS309403	Ovarian cancer	BMS309403 is an inhibitor of FABP4 that impacts cell proliferation affecting β-oxidation and ROS production.	[139]
Etomoxir	Glioblastoma Leukaemia	Etomoxir is a CPT1a inhibitor that affects the redox homeostasis causing the decrease of NADPH level and thus the GSH content leading cells to death. An off-taget effect of Etomoxir is due to the oxidative stress caused by inhibiting the mitochondrial adenine nucleotide transporter and complex Ι of the electron transport chain.	[143,144,147]
Buthionine sulfoxamine (BSO)	Lung cancer Pancreatic cancer	BSO is an inhibitor of the GSH synthesis that leads to an overproduction of ROS by removing glutathione-based redox buffering capacity.	[120]