52:4200-4209

52:4200-4209. virulence, indicating that the enzyme is an ideal drug target. We developed a phosphate sensor-based high-throughput screening assay to quantify the activity of GDP-MP and screened a library containing 80,000 lead-like compounds for GDP-MP inhibitors. On the basis of their GDP-MP inhibitory properties and chemical structures, the activities of 20 compounds which were not Levobunolol hydrochloride toxic to mammalian cells were tested against ex vivo amastigotes and in macrophage amastigote assays. The most potent compound identified in the primary screen (compound 3), a quinoline derivative, demonstrated dose-dependent activity in both assays TEL1 (50% inhibitory concentration = 21.9 M in the macrophage assay) and was shown to be nontoxic to human fibroblasts. In order Levobunolol hydrochloride to elucidate signs of an early structure-activity relationship (SAR) for this class of compounds, we obtained and tested analogues of compound 3 and undertook limited medicinal chemistry optimization, which included the use of a number of SAR probes of the piperazinyl aryl substituent of compound 3. We have identified novel candidate compounds for the design and synthesis of antileishmanial therapeutics. is a protozoan parasite that shuttles between sand fly vectors and mammalian hosts, causing a spectrum of diseases known as leishmaniases (13). Leishmaniasis is prevalent in Africa, Latin America, Asia, the Mediterranean basin, and the Middle East, with an estimated 12 million people currently being infected and a further 350 million people in 88 countries being threatened by the disease. For many years, the public health impact of leishmaniasis has been underestimated, as a substantial number of cases were never recorded. The expansion of leishmaniasis and the sharp rise in its prevalence are related to both environmental changes and the migration of nonimmune people to regions of endemicity (33). Moreover, there is an increase in the overlap between HIV infection and visceral leishmaniasis, especially in intravenous drug users in both southwestern Europe and Brazil (6, 27). The situation may be much worse in Africa and Asia, where the prevalence and rates of detection of HIV and coinfections are still largely underestimated. Current treatment is based on chemotherapy, which relies on a handful of drugs with serious limitations, such as high cost and toxicity, the difficult route of administration, and a lack of efficacy in areas of endemicity (7). Extensive evidence from studies with animal models indicates that solid protection can be achieved by immunization; however, to date no vaccine is available in clinical practice. Therefore, there is an urgent need to develop new, effective, and affordable antileishmanial therapeutics in order to control different forms of the disease. synthesizes a range of mannose-rich glycoconjugates, which are considered essential for both parasite virulence and survival. A prerequisite for glycoconjugate biosynthesis in have indicated that PMM and GDP-MP constitute attractive targets for the development of novel therapeutics. Both PMM and GDP-MP mutants are unable to establish infection in mice or survive in macrophages GDP-MP forms a hexamer in solution, whose stability might be compromised at both low ionic strength and high pH (8). We have also reported Levobunolol hydrochloride that leishmanial PMM shows a high degree of similarity to its human isoforms, PMM1 and PMM2, suggesting that the development of parasite-selective inhibitors would not be an easy task (21). Here, we report on the development of a highly sensitive, 384-well plate-based enzyme activity assay that uses phosphate detection technology and the high-throughput screening (HTS) of 80,000 small, lead-like molecules to identify inhibitors of leishmanial GDP-MP. Although some of these compounds demonstrated antileishmanial activity on both parasite life stagespromastigotes and amastigotesand may therefore be considered generally cytotoxic, one class of quinoline derivatives showed promising and selective activity for the amastigote stage. This class is exemplified by compound 3, which inhibited mouse macrophage infection in a dose-dependent manner (50% inhibitory concentration [IC50] = 21.9 M) and was nontoxic to human fibroblasts at concentrations up to 100 M. MATERIALS AND METHODS Chemical library. Our lead discovery chemical library is a collection of 80,000 compounds purchased from commercial vendors and stored in neat dimethyl sulfoxide (DMSO) at a final compound concentration of 10 mM. The Levobunolol hydrochloride compounds represent a diverse set of molecules, as judged by Tanimoto dissimilarity analysis (Tanimoto dissimilarity value 0.85), and although simple filters based on the Lipinski criteria were not used in the selection process, 89% of the compounds in the library are Lipinski compliant (24) and 81% conform with Oprea’s criteria for lead.