Table 1.

In vitro and in vivo studies investigating the effects of LiAcAc on cell proliferation, tumor growth, and cancer metabolism.

Effect of LiAcAc	Equimolar Controls	Ref.
LiAcAc or LiCl (1.5 mM) did not affect proliferation in breast cancer cells.	LiCl	[6]
LiAcAc but not LiCl increased BRAF positive melanoma tumor growth and increased MEK1 and ERK1/2 phosphorylation in the same cells. No effects is shown in BRAF negative melanomas.	LiCl	[7]
Both LiAcAc and LiCl (10 mM) inhibited bovine lymphocytes proliferation; the 3.125 mM concentration showed a trend to enhance the proliferation.	LiCl, NaCl	[8]
LiAcAc but not LiCl (3.6 mM) enhanced development of bovine embryos. Higher concentrations of both compounds were inhibitory.	LiCl	[9]
LiAcAc and LiCl (5 mM) neither affected glioma cells growth in normoxia nor in hypoxia conditions.	LiCl	[10]
LiAcAc (10 mM) significantly reduced cell growth and ATP and UCP2 production in several colon and breast cancer cell lines.	n.r.	[11]
LiAcAc (0.5–5 mM) reduced viability in dermal endothelium cells. A solution of 4 mM 3-HB and 1 mM LiAcAc induced moderate oxidative stress and reduced Nrf2 expression.	n.r.	[12]
LiAcAc (10–50 mM) reduced mouse hippocampal neuronal cell growth. LiAcAc (1–5 mM) protected the cells from glutamate induced toxicity.	n.r.	[13]
LiAcAc (5–20 mM) reduced pancreatic cancer cell growth. LiAcAc (10 and/or 20 mM) increased caspase 3/7 activity and reduced glucose and glutamine uptake, lactate release, ATP and ROS levels, and the expression of glycolytic enzymes. LiAcAc (20 mM) prevented cachexia.	n.r.	[14]
LiAcAc (13.9 mM) did not prevent the decrease in cell viability in neuroblastoma cells deprived of glucose but increased apoptosis. Normal fibroblasts were not affected.	n.r.	[15]

ATP, adenosine 3-phosphate; BRAF, proto-oncogene B-Raf; ERK, extracellular-signal regulated kinases; MEK, Mitogen-activated protein kinase kinase; Nrf2, Nuclear factor (erythroid-derived 2)-like 2; n.r., not reported; Ref., reference; UCP, mitochondrial uncoupling protein.