Sunitinib (marketed as Sutent by Pfizer, and previously known as SU11248) is an oral, small-molecule, multi-targeted receptor tyrosine kinase inhibitor that was approved by the FDA for the treatment of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor. Sunitinib was evaluated for its inhibitory activity against a variety of kinases and was identified as an inhibitor of platelet-derived growth factor receptors (PDGFRa and PDGFRb), vascular endothelial growth factor receptors (VEGFR1, VEGFR2, and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony-stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor receptor (RET). Sunitinib adverse events are considered somewhat manageable and the incidence of serious adverse events low. The most common adverse events associated with sunitinib therapy are fatigue, diarrhea, nausea, anorexia, hypertension, yellow skin discoloration, hand-foot skin reaction, and stomatitis. In the placebo-controlled Phase III GIST study, adverse events which occurred more often with sunitinib than placebo included diarrhea, anorexia, skin discoloration, mucositis/stomatitis, asthenia, altered taste, and constipation. Dose reductions were required in 50% of the patients studied in RCC in order to manage the significant toxicities of this agent.

N-Desethyl Sunitinib is a major and pharmacologically active metabolite of sunitinib, which is potent, ATP-competitive VEGFR, PDGFRβ, and KIT inhibitor.

L-Malic acid is a tart-tasting organic dicarboxylic acid that plays a role in many sour or tart foods. L-Malic acid is the naturally occurring form, whereas a mixture of L- and D-malic acid is produced synthetically. In humans, L-malic acid is both derived from food sources and synthesized in the body through the citric acid cycle or Krebs cycle which takes place in the mitochondria. L-Malate's importance to the production of energy in the body during both aerobic and anaerobic conditions is well established. Under aerobic conditions, the oxidation of L-malate to oxaloacetate provides reducing equivalents to the mitochondria through the malate-aspartate redox shuttle. During anaerobic conditions, where a buildup of excess of reducing equivalents inhibits glycolysis, L-malic acid's simultaneous reduction to succinate and oxidation to oxaloacetate is capable of removing the accumulating reducing equivalents. This allows L-malic acid to reverse hypoxia's inhibition of glycolysis and energy production. In studies on rats it has been found that only tissue malate is depleted following exhaustive physical activity. Notably, the administration of malic acid to rats has been shown to elevate mitochondrial malate and increase mitochondrial respiration and energy production. L-Malic acid is the source of extreme tartness in United States-produced confectionery, the so-called extreme candy. It is also used with or in place of the less sour citric acid in sour sweets. These sweets are sometimes labeled with a warning stating that excessive consumption can cause irritation of the mouth. The quantitative determination of L-malic acid is especially important in the manufacture of wine, beer, bread, fruit and vegetable products, as well as in cosmetics and pharmaceuticals. It is one of the most important fruit acids, and has the highest concentration of all acids in wine. In the wine industry, the level of L-malic acid is monitored, along with L-lactic acid, during malolactic fermentation. Malic acid is approved for use as a food additive in the EU, US and Australia and New Zealand. Malic acid, when added to food products, is denoted by E number E296.