Nous quick chain monocarboxylates, MCTs also play a part in the transport of drugs for instance valproic acid, salicylate, bumetanide, nateglinide, simvastatin and atorvastatin [8, 46]. The presence of those transporters in important organs for instance kidney, liver, brain and intestine suggests that they might possess a potential effect on the pharmacokinetics of substrate drug molecules. This might be as a result of influence of those transporters on intestinal absorption, blood-brain and tissue transport, and the renal reabsorption of those drugs. Moreover, due to the widespread distribution of MCT1 in numerous tissues, it might be targeted for drug delivery into precise tissues. Presence of MCTs in the BBB implies that they could serve as potential targets to be able to obtain optimum delivery of their substrates into the brain. Earlier studies in rats have shown that acidic drugs such as valproic acid, benzoic acid, nicotinic acid or beta-lactam antibiotics which includes benzylpenicillin, propicillin and cefazolin may very well be transported into the brain using a carrier mediated transport technique inside the BBB in a pH dependent manner with transport being considerably reduced within the presence of their respective unlabeled compounds [89]. The uptake of acetic acid was studied in major cultured MT1 Agonist Accession bovine brain capillary endothelial cells and was discovered to become drastically inhibited by many monocarboxylates such as nicotinic acid further suggesting a function of MCTs in the transport of those monocarboxylates into the brain [90]. The uptake of nicotinate was also studied in major cultures of astrocytes from rat cerebral cortex [91]. The nicotinate uptake was found to be saturable and pH dependent with uptake becoming drastically inhibited by CHC, suggesting that nicotinate uptake by rat astrocytes is mediated by protondependent monocarboxylate transport program. Recent studies in SMCT1 expressing Xenopus laevis oocytes, suggest the involvement of this transporter in nicotinic acid uptake [92], in addition to proton dependent MCTs. SMCT1-mediated uptake of nicotinate was found to become saturable and sodium dependent and drastically inhibited by lactate and pyruvate. As SMCT1 is expressed in PDE3 Modulator list neurons [88], it might play a function in neuronal uptake of this vitamin in the brain. A deficiency of nicotinic acid may cause serious neurological complications such as dementia, psychosis and ataxia which may be resolved through nicotinic acid supplementation. Dietary nicotinic acid has also been shown to have a protective effect around the development of Alzheimer disease and cognitive decline in a huge prospective clinical study [93]. This suggests that the role of MCTs in mediating the entry of nicotinic acid into the brain might have clinical relevance in the treatment of neurological issues.Curr Pharm Des. Author manuscript; readily available in PMC 2015 January 01.Vijay and MorrisPageHMG-CoA inhibitors like simvastatin and lovastatin exhibit sleep disturbances as their side impact which suggests that they might cross the BBB. Also, such CNS side effects have already been correlated with BBB permeability of these drugs applying an in vivo brain perfusion strategy [94]. In vitro studies utilizing primary cultures of bovine capillary endothelial cells showed that HMG-CoA inhibitors such as simvastatin in their acidic type are transported across the BBB via MCTs [95]. The lipophilic statins for instance simvastatin acid, atorvastatin and lovastatin also have the prospective to inhibit MCT4 in cell lines.