LACTB2 Inhibitors

Chemical inhibitors of LACTB2 can inhibit the protein through various mechanisms that target the mitochondrial environment where LACTB2 is operative. Benzethonium chloride disrupts membrane integrity; this disruption can compromise mitochondrial membrane potential, an environment critical for LACTB2's function in mitochondrial lipid metabolism. Chlorpromazine, by accumulating in mitochondria, alters mitochondrial functions, thus impairing the mitochondrial milieu necessary for LACTB2's activity. Trifluoperazine, acting as a calmodulin antagonist, inhibits LACTB2 by interfering with calcium signaling pathways, essential for mitochondrial processes that LACTB2 participates in. Propranolol, a beta-blocker, concentrates within mitochondria and can alter their function, thereby disrupting the context in which LACTB2 operates.

Additionally, Tamoxifen, known for its mitochondrial effects, can inhibit LACTB2 by causing mitochondrial dysfunction. Oligomycin A and Antimycin A target mitochondrial ATP synthase and complex III, respectively, reducing mitochondrial membrane potential, essential for LACTB2's role. This leads to an energy supply depletion and an altered mitochondrial environment, indirectly inhibiting LACTB2's activity. Rotenone, by inhibiting mitochondrial complex I, disrupts overall mitochondrial function, affecting LACTB2. Zinc pyrithione induces oxidative stress, disrupting mitochondrial function and inhibiting LACTB2's role in mitochondrial lipid metabolism. Allicin's interference with thiol-containing enzymes in mitochondria can inhibit LACTB2 by affecting its structural integrity. Betulinic acid induces mitochondrial membrane permeabilization, affecting the environment where LACTB2 functions. Lastly, Cerulenin inhibits fatty acid synthase, an enzyme crucial for lipid metabolism, thereby indirectly inhibiting LACTB2's activity within the same metabolic pathway. Each of these chemicals, by targeting specific mitochondrial processes or environments, can inhibit LACTB2's functionality within mitochondrial lipid metabolism.