in cell culture and in monkey infections. antimalarial compounds against novel

in cell culture and in monkey infections. antimalarial compounds against novel targets. lacks the enzymatic machinery to synthesize purines (Reyes et al., 1982). Additionally, the parasite lacks adenosine kinase or adenine phosphoribosyltransferase activity and relies on the conversion of hypoxanthine to inosine 5-monophosphate by hypoxanthine-guanine-xanthine phosphoribosyltransferase (in monkeys (Cassera et al., 2011). The transition states of N-ribosyl transferases are usually characterized by ribocation character and low bond order to the purine ring and the attacking nucleophile. For example, orotate phosphoribosyltransferases (Tao et al., 1996; Zhang et al., 2009) and purine nucleoside phosphorylases (Kline and Schramm, 1993, 1995) share these properties. HGXPRTs have resisted transition state analysis because of kinetic commitment factors. We proposed a transition state structure for (1999) proposed this transition state for HG(X)PRT with a protonated N7 and oxocarbenium ion formation at C1. (b) Immucillin-H 5-phosphate was designed as a mimic of this proposed transition state. The acyclic Immucillin phosphonates (AIPs) 2 and 3 are powerful and selective inhibitors of and inhibit hypoxanthine incorporation. The mechanism of inhibition has been revealed with crystal structures of in the presence of hypoxanthine (data not shown). We synthesized a prodrug of ImmHP to overcome the cell permeability barrier created by the negative charges of the 5-phosphate group (1 in Figure 2a). Compound 1 demonstrated a 5.8 1.2 M half maximal inhibitory concentration (IC50) in assays with parasites (Fig. 2b). However, metabolic labeling studies of erythrocytes with 1 showed inhibition of inosine conversion to hypoxanthine resulting from the dephosphorylation of 1 1 to Immucillin-H, a powerful inhibitor of PNP (Fig. 2c and d). Treatment of infected erythrocytes with 1 and analysis by UPLC/MS/MS revealed that 1 MGC79399 is permeable to cells, but that cellular metabolism rapidly removes the 5-phosphate to form Immucillin-H (Table S1), a potent inhibitor of and human PNPs (Kicska et al., 2002a). Open in a separate window Figure 2 A prodrug of Immucillin-H 5-phosphate (ImmHP) is converted to Immucillin-H by intracellular activities(a) The structure of ImmHP bis-pivalate prodrug AEG 3482 1. (b) Inhibition of cultured parasite growth by 1. (c) Extracellular purine analysis of metabolic labeling with [3H]hypoxanthine in uninfected erythrocytes treated with 25 M 1. (d) The AEG 3482 same experiment as in (c) but labeling with [3H]inosine. See also Table AEG 3482 S1. Acyclic Immucillin phosphonates are selective and potent inhibitors of in culture by inhibiting hypoxanthine metabolism The free phosphonate inhibitors showed no activity against cultured parasites, consistent with a lack of membrane permeability. Prodrug 4 (Fig. 3a), the bis-pivalate of 2, inhibited the growth of cultured parasites with an IC50 of 45 6 M (Fig. 3b). Metabolic labeling of erythrocytes with [3H]hypoxanthine in the presence of 100 M 4 revealed incorporation of radiolabel into extracellular inosine and other intermediates and labeling with [3H]inosine showed inhibition of inosine conversion to hypoxanthine (Fig. 3c). UPLC/MS/MS analysis of infected erythrocytes treated with 100 and 200 M of 4 for 30 minutes confirmed that 4 is processed to 2 in infected erythrocytes, causing an increase in inosine concentration (Table S1). Hypoxanthine was not found in treated or control samples, suggesting that HG(X)PRT activity was unaffected. 2 inhibits human PNP with AEG 3482 submicromolar affinity (Table S2). The accumulation of extracellular inosine from labeled erythrocytes indicates that 4 is permeable, but is converted to 2 before crossing the parasite membranes. In the erythrocyte, compound 2 inhibits PNP causing accumulation of inosine. At higher concentrations, 4 also crosses the parasite membranes, is activated and inhibits strain 3D7 (Fig. 4b). Compounds 5, 6 and 7 inhibited parasite growth with IC50 values of 2.5 0.2 AEG 3482 M, 1.9 0.1 M, and 7.0 0.1 M, respectively. The IC50 values for compounds 5 and.