Enhanced extracellular lactate levels play a central role in the pathophysiology of obesity, cancer, lactic acidosis, and lactate associated genetic disorders. During liver and kidney dysfunction, lactate builds up and leads to lactic acidosis, which could be fatal. Traditionally, dichloroacetate and phenylbutyrate have been used to decrease extracellular lactate levels, which do not change the pH levels or mortality. In some cases, intravenous injection of bicarbonate is also used, which increases the pH and pCO2 levels, but does not clear lactate from the blood. The extracellular lactate levels are a hallmark of several diseases, but have not been targeted because of difficulty in designing small molecules that can bind and eliminate it. It is difficult to eliminate because monocarboxylate transporters (MCTs) require a proton as the counter ion, leading to intracellular acidification, and kidney actively transporting lactate back into the blood. Scientist at UC Berkeley have invented a strategy of passively eliminating extracellular lactate via forced intracellular transport of sodium lactate and enhancement of its metabolism into pyruvate by directly binding lactate to a small molecule. They successfully demonstrated that binding of this molecule converts the lactate log P to 0.6 from -0.6, and makes lactate available for intracellular metabolism. They have utilized the effectiveness of enhanced lactate metabolism in vivo by using a small molecule to normalize the blood pH of metformin treated mice to 7.18±0.13 from 6.67±0.09 and decrease the blood lactate level by 2 to 4 fold. This first generation class of molecule can be utilized to modify lactate metabolism by specifically binding to lactate, and therefore have a large impact in several diseases needing modification of lactate metabolism.