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AAC Accepted Manuscript Posted Online 6 September 2016 Antimicrob. Agents Chemother. doi:10.1128/AAC.01545-16 Copyright © 2016, American Society for Microbiology. All Rights Reserved. FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ

1 Antileishmanial activity of ezetimibe: inhibition of sterol biosynthesis, in vitro synergy with azoles

2 and efficacious in experimental cutaneous leishmaniasis

3

4 Running title: Antileishmanial activity of ezetimibe

5

6 Valter Viana Andrade-Netoa, Edézio Ferreira Cunha-Júniora, Marilene Marcuzzo do Canto-

7 Cavalheiroa, Geórgia Correa Atellab, Talita de Almeida Fernandesc, Paulo Roberto Ribeiro Costac, Downloaded from

8 Eduardo Caio Torres-Santosa*

9

10 aLaboratório de Bioquímica de Tripanosomatídeos, Instituto Oswaldo Cruz, FIOCRUZ, Rio de

11 Janeiro, Brazil. http://aac.asm.org/

12 bInstituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

13 cLaboratório de Química Bioorgânica, Instituto de Pesquisas de Produtos Naturais, Universidade

14 Federal do Rio de Janeiro, Brazil.

15 on February 16, 2017 by

16 * Corresponding author. Tel: +55-21-3865-8247; E-mail: [email protected]

17

18

19

20

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21 ABSTRACT

22 Leishmaniasis affects mainly low-income populations in tropical regions. Radical innovation in

23 drug discovery is time- and money-consuming, causing severe restrictions to launch new chemical

24 entities to treat neglected diseases. Drug repositioning is an attractive strategy to attend a specific

25 demand more easily. In this project, we have evaluated the antileishmanial activity of 30 drugs

26 currently in clinical usage for different morbidities. Ezetimibe, clinically used to reduce intestinal

27 cholesterol absorption in dyslipidemic patients, killed promastigotes of L. amazonensis, with an Downloaded from

28 IC50 of 30 μM. Morphological analysis revealed that ezetimibe caused the parasites to become

29 rounded with multiple nuclei and flagellae. Analysis by GC/MS showed that promastigotes treated

30 with ezetimibe had a lower amount of C14-demethylated sterols and accumulated cholesterol and

31 lanosterol. Then, we evaluated the combination of ezetimibe with well-known antileishmanial http://aac.asm.org/

32 azoles. The Fractional Inhibitory Concentration Index (FICI) indicated synergy when ezetimibe is

33 associated with ketoconazole or miconazole. Ezetimibe activity was confirmed against intracellular

34 amastigotes, with an IC50 of 20 μM, and reduced the IC90 of ketoconazole and miconazole from

35 11.3 and 11.5 μM to 4.14 and 8.25 μM, respectively. Following, ezetimibe confirmed its activity in on February 16, 2017 by

36 vivo, decreasing the lesion development and parasite load in murine cutaneous leishmaniasis. We

37 concluded that ezetimibe has promising antileishmanial activity and should be considered in

38 association with azoles in further preclinical and clinical studies.

39

40 Keywords: Sterol biosynthesis, Leishmania amazonensis, azoles, ezetimibe, drug repositioning.

41

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42 INTRODUCTION

43 Leishmaniasis is a non-contagious infectious disease caused by parasites of the genus Leishmania

44 and is usually transmitted by sandflies belonging to the genera Phlebotomus and Lutzomyia.

45 According to the species of Leishmania involved, the infection can affect the skin and mucous

46 membranes (cutaneous leishmaniasis - CL) or the internal organs (visceral leishmaniasis - VL) (1,

47 2). Official estimates point an annual incidence of approximately 300.000 VL cases and 1.0 million

48 CL cases worldwide (3). The basis of chemotherapy of leishmaniasis has its origin in the work of Downloaded from

49 Vianna (1912), whom successfully treated a patient with emetic tartar (trivalent antimonial), a

50 formulation broadly used at that time to treat infectious diseases (4). From this empirical approach,

51 pentavalent antimonials were developed in the 1940´s and have saved thousands of lives for several

52 decades. Other drugs have been repositioned to treat leishmaniasis, such as , http://aac.asm.org/

53 and more recently, . Unfortunately, the therapeutic arsenal for leishmaniasis

54 has become quite limited and outdated. Antimonials have many toxic effects including cardiac,

55 hepatic, pancreatic and renal toxicity and should be used with caution and with clinical and

56 laboratory monitoring in patients with heart disease and liver disease (5). Miltefosine, the only oral on February 16, 2017 by

57 drug licensed, was the most important advance for the treatment of leishmaniasis in recent years.

58 Currently, it is the treatment of choice of program elimination of visceral leishmaniasis in India and

59 recently was approved by FDA for all forms of this disease, but cases of resistance have been

60 reported with increased failure of treatment (6-9). This scenario is a reflex of the difficulty of

61 launching new chemical entities as drugs for this disease. Radical innovation in drug discovery is a

62 time- and money-consuming process. Drug repositioning is an approach very used in the past and

63 that can be useful nowadays to address specific demands in areas of public health, such as neglected

64 and orphan diseases (10-12). This strategy offers the advantage of working with compounds that

65 have already been proved to be safe and to have a favorable pharmacokinetic profile in humans.

66 Thereby, we selected a small set of drugs currently in clinical usage for several morbidities for

67 testing against Leishmania amazonensis, the causal agent of cutaneous diffuse leishmaniasis.

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68 Ezetimibe, the most active in the initial screening, was then evaluated about its mode of action and

69 its effectiveness in association with well-known leishmanicidal azoles in vitro and in vivo.

70 MATERIALS AND METHODS

71 Drugs. Ezetimibe was extracted from sixty Ezetrol® 10 mg tablets (Merck Sharp & Dohme Corp.,

72 Kenilworth, NJ, USA), using dichloromethane in the proportion of 1:0.3 (wt/v). The mixture was

73 incubated for 30 min under agitation and filtrated afterwards. The solvent was evaporated, yielding

74 200 mg. The extracted product was dissolved in deuterated chloroform and analyzed in a 400 MHz Downloaded from

75 1H-NMR (Fig. S1). All other drugs were provided by the Sigma–Aldrich Corp. (St Louis, MO,

76 USA). The drugs were dissolved in a 10 mM stock of dimethylsulfoxide (DMSO) or PBS and

77 stored at -20 C.

78 Maintenance and cultivation of parasites. Leishmania amazonensis promastigotes (strain http://aac.asm.org/

79 MHOM/BR/77/LTB 0016) were maintained at 26°C in RPMI medium (Sigma- Aldrich Corp., St.

80 Louis, MO, US) supplemented with 10% fetal bovine serum (FBS), 100 μg/ml streptomycin, 100

81 U/ml penicillin and 5 mg/ml hemine. Subcultures were performed twice a week until the tenth

82 passage. Afterwards, old cultures were discarded and fresh parasites were obtained from infected on February 16, 2017 by

83 BALB/c mice.

84 Promastigote morphology. L. amazonensis promastigotes (1.0 x 106/mL) were grown at 10, 20

85 and 40 μM ezetimibe. After 72 hours, the parasites were washed twice with PBS, fixed, and stained

86 using the Instant Prov hematological dye system (Newprov, Curitiba, Brazil).

87 Antipromastigote activity. Assays were performed with promastigotes of L. amazonensis at 26°C

88 in RPMI medium without phenol red (Sigma- Aldrich Corp., St. Louis, MO, USA) supplemented as

89 described above. The tests were performed in 96-well plates, with an initial inoculum of 1.0 x 106

90 cells/ml and compound concentrations ranging to 24 μM for ketoconazole and miconazole, and to

91 100 μM for all other drugs. In association experiments, ezetimibe concentrations were 2.5, 5 and 10

92 μM. Plates were incubated at 26°C for 72 hours. After this period, parasite growth was evaluated by

93 adding 10% tetrazolium salt (MTT) (5 mg/ml) per well. The plates were incubated at 26°C for a

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94 further 1 hour, and formazan crystals were dissolved by adding 80 μl DMSO each well. The

95 reaction was analyzed in a spectrophotometer at a 570 nm wavelength. IC50 values were obtained by

96 non-linear regression using Graphpad Prism 6 software (GraphPad Software, Inc., La Jolla, USA).

97 The fractional inhibitory concentration (FICI) for the analysis of synergy was calculated as follows:

98 FICI = IC50 of drug A in combination/IC50 of drug A alone + IC50 of drug B in combination/IC50 of

99 drug B alone. The interpretation of FICI, according to published guidelines are: synergy (FICI ≤

100 0.5), antagonism (FICI > 4.0) and ‘no interaction’ (FICI > 0.5–4.0) (13). Downloaded from

101 Toxicity to macrophages.

102 Mouse peritoneal macrophages in 96-well plates were treated with ezetimibe, ketoconazole and

103 miconazole alone or in combination for 72 hours at 37°C. After this period, the cell viability was

104 evaluated by adding 10% tetrazolium salt (MTT) (5 mg/ml) to each well. The plates were incubated http://aac.asm.org/

105 at 37°C for another four hours, and the resulting formazan crystals were dissolved by adding 80 μl

106 DMSO to each well. The plates were then read at 570 nm. The results were expressed as the

107 percentage of viable cells compared to the untreated control.

108 Antiamastigote activity. Peritoneal macrophages from BALB/c mice were infected with on February 16, 2017 by

109 promastigotes of L. amazonensis (stationary growth phase) at a 3:1 parasite-to-macrophage ratio

110 and incubated for 4 h in Lab-Tek chambers (Nunc, Roskilde, Denmark) and kept at 37°C. After 4

111 hours, the chambers were washed, and the cultures were treated with the azole derivatives alone or

112 combined with ezetimibe in supplemented RPMI medium for 72 hours. For initial screening, the

113 concentration of drugs was fixed in 25 μM and a threshold of at least 50% of inhibition was

114 stablished. A drug-activity curve was done with ezetimibe, the only drug that reached the threshold,

115 with concentration ranging to 40 μM. In the association assays, the concentration of ezetimibe was

116 fixed at 20 μM, while the concentration of ketoconazole and miconazole ranged to 16 and 32 μM,

117 respectively. After incubation, the slides were stained, and the infection rate was determined by

118 counting under a light microscope. The infection rate was calculated using the formula: % infected

119 macrophages x number of amastigotes / number of total macrophages.

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120 Extraction of lipids. Lipids from promastigotes of L. amazonensis were extracted using the method

121 of Bligh and Dyer (1959) (14). Briefly, samples were pelleted, and a solution of methanol,

122 chloroform and water (2:1:0.5 v/v) was added. After stirring the mixture for 1 hour, the samples

123 were centrifuged for 20 min at 3,000 rpm and the supernatant, containing the lipids was separated

124 from the precipitate. The precipitate was subjected to a second extraction under the same

125 conditions. The supernatants were combined, and chloroform/water (1:1 v/v) was added. After 40

126 seconds of stirring, the material was centrifuged (3.000 rpm/30 min) again. The lower layer Downloaded from

127 (organic) containing the lipids was then separated with the aid of a glass syringe and transferred to a

128 1.5 ml tube resistant to organic solvents (Axygen Scientific, Inc., Union City, CA, USA). The

129 solvent was evaporated under N2 flux, and the lipids were analyzed by gas chromatography- mass

130 spectrometry (GC/MS), as described below. http://aac.asm.org/

131 Analysis of the sterol profile by gas chromatography coupled with mass spectrometry

132 (GC/MS). Promastigotes of L. amazonensis were cultured with 10, 20 or 40 μM ezetimibe or in

133 culture medium alone. After 72 hours, 1x108 parasites of each culture were washed 3 times in cold

134 PBS (pH 7.5), and the sterols were extracted as described above. The samples were injected into a on February 16, 2017 by

135 GCMS - QP2010 Ultra Machine (Shimadzu Scientific Instruments, Tokyo, Japan). After injection,

136 the column temperature was maintained at 50°C for 1 minute and then increased to 270°C at a rate

137 of 10°C/min and finally to 300°C at a rate of 1°C/min. The flow of the carrier gas (He) was kept

138 constant at 1.1 ml/min. The temperatures of the injector and detector were 250°C and 280°C,

139 respectively (15).

140 Ethics Statement

141 Studies in L. amazonensis-infected BALB/c mice were performed in accordance with protocols

142 approved by the Ethics Committee for Animal Use of the Instituto Oswaldo Cruz (L026/2015).

143 In vivo assay. To assess the in vivo activity of the combination of ezetimibe and ketoconazole,

144 BALB/c mice (9 animals per group) were infected on the right ear with 2x106 promastigotes of L.

145 amazonensis in stationary phase. The treatment started ten days after infection. The animals were

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146 treated with ezetimibe (10 mg/kg/day), ketoconazole (100 mg/kg/day), miltefosine (20 mg/kg/day)

147 and the combination of ezetimibe + ketoconazole (10 mg/kg/day + 100 mg/kg/day) by oral route.

148 The animals were treated 5 days per week in a total of 20 doses. Negative controls were also

149 similarly treated with PBS. The ear measurement was recorded once a week. After the treatment

150 period, the animals were euthanized for determination of parasite load and toxicological analysis.

151 Serum levels of urea (URE), albumin (ALB), alanine aminotransferase (ALT), aspartate

152 aminotransferase (AST), creatinine (CREA), total bilirubin (BIL), creatine kinase (CK) and Downloaded from

153 cholesterol (CHO) were measured in a Vitros 250 equipment (Ortho Clinical - Johnson & Johnson)

154 using dry chemistry methodology.

155

156 RESULTS http://aac.asm.org/

157 Antileishmanial screening. The complete list of drugs and the IC50 for promastigotes and

158 intracellular amastigotes of L. amazonensis can be found in the Table 1. Among all tested

159 compounds, only glimepiride, domperidone and ezetimibe showed activity against promastigotes,

μ

160 with IC50 of 54, 51 and 30 M, respectively. For intracellular amastigotes, the clinically relevant on February 16, 2017 by

161 stage of the parasite, only ezetimibe showed IC50 lower than the arbitrated threshold of 25 μM,

162 reaching to 20 μM. Ezetimibe also drew attention by provoking striking morphological changes on

163 the promastigotes of L. amazonensis. We observed that, in a concentration dependent manner, the

164 parasites became rounded and displayed multiple nuclei and flagellae, mainly at 40 μM (Fig. 1).

165 Ezetimibe interferes with sterol biosynthesis in L. amazonensis. The morphological alterations

166 seen in ezetimibe-treated promastigotes induced us to investigate whether this drug interferes with

167 sterol biosynthesis of the parasite. Table 2 shows an analysis of the relative amount of each sterol

168 indicated by GC/MS. Promastigotes treated with miconazole, an inhibitor of C14-demethylase,

169 showed a decrease in the ergostane-derived sterols ergosta-5,7,24-trien-3β-ol (dehydroepisterol) (3)

170 and ergosta-7,24-dien-3β-ol (episterol) (4). Miconazole also induced the accumulation of

171 exogenous cholesterol collected from culture medium and an increase in the methylated sterols

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172 14α-methylergosta-8,24(28)-dien-3β-ol (2) and 4α-14α-dimethylergosta-8,24(28)-dien-3β-ol

173 (obtusifoliol) (5). Treatment with ezetimibe also decreased dehydroepisterol and episterol (C14-

174 demethylated sterols) and promoted the accumulation of cholesterol (1) and lanosterol (C14-

175 methylated sterol) (7). We also observed the accumulation of an unknown sterol (6).

176 Ezetimibe potentiates the effect of azoles. Considering the significative alteration in sterol pattern

177 of the parasites after ezetimibe treatment, the antileishmanial activity of this drug was also

178 evaluated in combination with azoles (ketoconazole and miconazole) in promastigotes and Downloaded from

179 amastigotes of L. amazonensis. To graphically evaluate the interaction of ezetimibe with azoles in

180 promastigotes, the IC50 of the drugs alone and in combination was plotted as isobolograms, and to

181 estimate the type of interaction (synergy, antagonism or neutral), the fractional inhibitory

182 concentration index (FICI) was calculated. As expected, miconazole and ketoconazole were active http://aac.asm.org/

183 against the promastigotes, with IC50 of 2.5±0.1 and 2.7±0.1 μM, respectively. The IC50 of the azoles

184 decreased when in combination with ezetimibe, generating fully concave isobolograms (Fig. 2). The

185 calculation of FICI resulted in values of 0.4 for both combinations, confirming the synergism. Due

186 to the experimental difficulty of performing a “checkerboard” approach to draw isobolograms for on February 16, 2017 by

187 antiamastigote activity, we fixed the concentration of ezetimibe at the IC50 (20 µM) (Fig. 3A) and

188 varied the concentration of the azoles to calculate the IC90 (concentration that inhibits 90% of the

189 parasites) of the combination. When associated with ezetimibe, the IC90 of ketoconazole and

190 miconazole were reduced from 11.3±0.2 μM and 11.5±0.1 μM to 4.14±0.3 μM and 8.25±0.2 μM,

191 respectively (Figs. 3B and C). Furthermore, ezetimibe, miconazole, ketoconazole alone or

192 combined showed no toxic effects to macrophages (Fig. 4A-E). Figure 5 shows representative

193 micrographs of infected macrophages treated with ezetimibe alone and combined with ketoconazole

194 and miconazole that have normal morphology and a reduced parasite load (Fig. 5).

195 For in vivo assays, BALB/c mice were infected with L. amazonensis and treated with

196 ezetimibe (10 mg/kg/day) and ketoconazole (100 mg/kg/day) alone or in combination by oral route.

197 As can be seen in Figure 6A, ketoconazole and ezetimibe were able to individually control the

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198 lesion development. When both drugs were combined, the lesion growth was more effectively

199 controlled. All treatments reduced the parasite load significantly (Fig. 6A – insert). Nonetheless, no

200 significant differences in serum levels of urea, albumin, ALT, AST, creatinine, bilirubin and

201 creatine kinase were observed in treated and untreated animals, demonstrating that the treatment

202 was not toxic to the mammalian host. Furthermore, no significant change in cholesterol level in

203 serum was observed (Figs. 6B-I).

204 DISCUSSION Downloaded from

205 Thirty drugs in clinical usage were included in this study. Instead of focusing in

206 antimicrobial agents, we selected compounds belonging to a wide spectrum of pharmacological

207 classes (Table 1). There is no previous data in literature about antileishmanial activity of

208 glimepiride and ezetimibe but, interestingly, domperidone has been used in clinical trials in http://aac.asm.org/

209 naturally infected dogs, aiming veterinary use (16, 17). However, in those studies, no intrinsic

210 antileishmanial activity was assigned to domperidone. The therapeutic effect of this drug in dogs

211 has been attributed to its immunomodulatory activity (17).

212 Among the active drugs, ezetimibe drew attention due to its property of causing dramatic on February 16, 2017 by

213 morphological alterations in the promastigotes (Fig. 1). These morphological changes are consistent

214 with those previously described as consequence of drug interference in sterol metabolism of

215 trypanosomatids (18-20). In fact, we observed that ezetimibe causes alterations in the sterol

216 composition of the parasites compatible with inhibition of C14-demethylase (21-23). Curiously,

217 ezetimibe is a potent inhibitor of the intestinal cholesterol absorption mediated by the Niemann–

218 Pick C1-like 1 protein (NPC1L1) and it is clinically used to reduce cholesterolemia (24).

219 Nevertheless, no inhibition in the human sterol biosynthesis pathway has been described for

220 ezetimibe. However, the sterol pathway of the trypanosomatids has diverged sufficiently to allow

221 selective pharmacological inhibition. Thereby, besides its effect on transport of cholesterol in

222 humans, it is possible that ezetimibe also could interfere with sterol biosynthesis in Leishmania.

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223 It is assumed that the sterol biosynthetic pathway is essential for Leishmania, because

224 inhibition of diverse enzymes of this pathway such as, HMG-CoA reductase, squalene epoxidase,

225 C-14 demethylase and C-24 methyltransferase, results in parasite death (25-30). Drug combination

226 in the treatment of infectious diseases is an interesting approach. Drugs acting in the same pathway

227 can be associated to improve their activity (31). Thus, we evaluated the activity of ezetimibe in

228 combination with ketoconazole or miconazole. This association showed synergistic effect on

229 promastigotes (Fig. 2) and increased the activity of these azoles on intracellular amastigotes of L. Downloaded from

230 amazonensis (Figs. 3B and C).

231 The next step was to evaluate the leishmanicidal activity of ezetimibe alone or combined

232 with ketoconazole in vivo (Figs. 6A and B). Ezetimibe and ketoconazole alone reduced the lesion

233 growth and parasite load equally in murine model of cutaneous leishmaniasis. The combination was http://aac.asm.org/

234 more efficacious in controlling the lesion development, but no difference was observed in parasite

235 burden. Ketoconazole was chosen to be evaluated in vivo because it showed better result on

236 intracellular amastigotes, when in combination with ezetimibe (Fig. 3C). Moreover, clinical trials

237 have demonstrated that ketoconazole could be advantageous for patients with New World species of on February 16, 2017 by

238 Leishmania (32). Oral ketoconazole combined with intra-lesional injections of meglumine

239 antimoniate (Glucantime) has been shown to be more effective than Glucantime alone in the

240 treatment of localized cutaneous leishmaniasis (33). Furthermore, ketoconazole (100 mg/kg/day)

241 reduced splenic parasite load in murine model of visceral leishmaniasis caused by L. infantum, and

242 in the lower dose of 50 mg/kg/day, potentiated the effect of (34).

243 In summary, our screening of FDA approved drugs pointed out ezetimibe as a promising

244 antileishmanial agent. It has antileishmanial activity in vitro and in vivo, supposedly by its effect on

245 parasite sterol biosynthesis, and acts synergistically with azoles. These data suggest that ezetimibe

246 could be useful, in association or not with azoles, in further treatments for leishmaniasis.

247

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248 ACKNOWLEDGMENTS The authors thank the Program for Technological Development in

249 Tools for Health-PDTIS, FIOCRUZ for evaluating the serum toxicological markers.

250

251 FOOTNOTE PAGE

252 FUNDING: This work was supported by the Conselho Nacional de Desenvolvimento Científico e

253 Tecnológico (CNPq), the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

254 and the Programa Estratégico de Apoio à Pesquisa em Saúde (PAPES/FIOCRUZ; grant Downloaded from

255 407680/2012-8 to E. C. T. S.).

256

257 CONFLICT OF INTEREST

258 All authors: No reported conflict of interest. http://aac.asm.org/

259

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338 braziliensis successfully treated with fluconazole. Clin Exp Dermatol 39(6): 708-12. on February 16, 2017 by

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347 29. Kulkarni MM, Reddy N, Gude T, McGwire BS. 2013. Voriconazole suppresses the growth

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349 3274-x.

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350 30. Haughan, P.A., Chance, M.L., Goad, L.J. (1992). 1992. Synergism in vitro of lovastatin and

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359 33. Salmanpour R, Handjani F, Nouhpisheh MK. 2001. Comparative study of the efficacy of

360 oral ketoconazole with intra-lesional meglumine antimoniate (Glucantime) for the treatment of http://aac.asm.org/

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Drug Promastigotes Intracellular Indication Chemical Class Mode of Action

IC50 (μM) amastigotes

IC50 (μM) Amoxycillin >100 >25 Antibiotic Aminopenicillin Binds to and inactivates penicillin-binding proteins on the inner bacterial cell wall. Atenolol >100 >25 Antianginal/antihypertens Beta-adrenergic Inhibits stimulation of beta-receptor sites. ive blocker Buflomedil >100 >25 Vasoactive agent/Non- Pyrrolidinyl- Non-selective competitive inhibition of α- selective, competitive α- trimethoxylphenyl adrenoceptors in vascular smooth muscle. adrenoceptor antagonist Cefalexin >100 >25 Antibiotic cephalosporin Binds to and inactivates penicillin-binding proteins on the inner bacterial cell wall.

Cetirizine 100±10.5 >25 Antihistamine Piperazine Potent H1-receptor antagonist. Chlorthalidone >100 >25 Antihypertensive/diuretic Phthalimidine Promotes sodium, chloride, and water derivative of excretion by inhibiting sodium reabsorption benzenesulfonamide in the distal tubules of the kidneys. Clarithromycin >100 >25 Antibiotic Macrolide derivative Inhibits RNA-dependent protein synthesis in many types of aerobic, anaerobic, gram- positive, and gram-negative bacteria. Downloaded from Diclofenac sodium >100 >25 Non-steroidal anti- Phenylacetic acid Inhibitor of cyclooxygenase inflammatory derivate Domperidone 51±0.6 >25 Antiemetic/antimuscarinic Phenothiazine Specific blocker of dopamine receptors. Enalapril >100 >25 Antihypertensive Dicarbocyl- Reduce blood pressure by affecting the containing ACE renin-angiotensin-aldosterone system. inhibitor Ezetimibe 30±1.2 20±1.6 Antihypercholesterolemic Azetidinone Reduces blood cholesterol by inhibiting its absorption through the small intestine.

Famotidine >100 >25 Antiulcer agent/gastric derivative H2-receptor antagonist. acid secretion inhibitor Gabapentin >100 >25 Anticonvulsant Cyclohexane-acetic Structural analog of gamma-aminobutyric

acid derivative acid (GABA). http://aac.asm.org/ Gemfibrozil >100 >25 Antihyperlipidemic Fibric Acid Reduces triglycerides and increases derivative cholesterol carried in high-density lipoprotein (HDL) in the blood. Glimepiride 54±1.5 >25 Antidiabetic Sulfonylurea Stimulates insulin release from beta cells in pancreas. Hydrochlorothiazide >100 >25 Diuretic Benzothiadiazide Promotes movement of sodium, chloride and water from blood in peritubular capillaries into nephron’s distal convolutes tubule. Ibuprofen >100 >25 Analgesic, anti- Propioninc acid Inhibitor of cyclooxygenase. inflammatory, antipyretic derivative Lisinopril >100 >25 Antihypertensive/vasodila Lysine ester of Reduce blood pressure by affecting the on February 16, 2017 by tor enalapril renin-angiotensin-aldosterone system. Losartan >100 >25 Antihypertensive Angiotensin II Blocks binding of angiotensin II to receptor receptor antagonist sites. Meloxicam >100 >25 Anti-inflammatory Oxicam derivative Inhibitor of cyclooxygenase. Mesalazine >100 >25 Anti-inflammatory Aminosalicylic acid Their mode of action is unclear but a local effect on epithelial cells by a variety of mechanisms to moderate the release of lipid mediators, cytokines and reactive oxygen species is proposed. Metoprolol >100 >25 Antianginal/antihypertens Beta-adrenergic Inhibits stimulation of beta-receptors. ive antagonist Nimesulide >100 >25 non-steroidal anti- Phenoxymethanesulf Inhibitor of cyclooxygenase. inflammatory onamilide Oxacillin >100 >25 Antibiotic Penicillin Inhibits bacterial cell wall synthesis. Pantoprazole >100 >25 Antiulcer Substituted Inhibiting proton pump in gastric parietal cells. Prednisolone >100 >25 Anti- Glicocorticoid Binds to intracellular glucocorticoid inflammatory/immunosup receptors. pressant Ranitidine >100 >25 Antiulcer agent, gastric Aminoalkyl- Competitive blockade of histaminergic H2 acid secretion inhibitor substituted furan receptors derivative Scopolamine >100 >25 Anticholinergic Belladonna alkaloid, Competitively inhibits acetylcholine at tertiary amine autonomic postganglionic cholinergic receptors Secnidazole >100 >25 Antimicrobial DNA damage Tenoxicam >100 >25 Non-steroidal anti- Thienothiazine Inhibitor of cyclooxygenase inflammatory 367

368

16 FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ

369

370 371 Table 2: Sterol composition of L. amazonensis promastigotes under effect of ezetimibe.

Compound MW Relative amount (%) Control Miconazole Ezetimibe 8 μM 10 μM 20 μM 40 μM (1) Cholesterol 386 1.58 31.15 16.91 19.30 43.28 (2)14α-methylergosta- 412 - 41.18 4.44 6.21 2.43 8,24(28)-dien-3β-ol (3) Ergosta-5,7,24-trien-3β-ol 396 93.32 - 62.18 23.70 4.58 (dehydroepisterol) (4) Ergosta-7,24-dien-3β-ol 398 5.10 - 12.20 9.83 1.72 (Episterol) Downloaded from (5) 4α-14α-dimethylergosta- 426 - 33.60 - - - 8,24(28)-dien-3β-ol, (obtusifoliol) (6) Unknown 424 - - - 3.71 8.75 (7) Lanosterol 426 - - 3.34 37.88 39.24 372 MW - Molecular Weight; Relative Amount (%) – Relative to total lipid content from each sample. 373 http://aac.asm.org/ 374

375 on February 16, 2017 by

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376 Legends to Figures

377 Fig. 1. Micrographs of promastigotes of L. amazonensis treated with ezetimibe. L. amazonensis

378 promastigotes were grown at 10, 20 and 40 μM of ezetimibe to 72 hours. A control, B ezetimibe 10

379 μM, C ezetimibe 20 μM, D ezetimibe 40 μM. The slides were stained using Instant Prov

380 hematological dye system.

381 Fig. 2. Isobolographic analysis of the antileishmanial activity of association of ezetimibe and azoles. Downloaded from

382 L. amazonensis promastigotes were incubated with ezetimibe and the indicated azoles in different

383 concentrations for 72 hours at 26°C. Each plotted point in the isobolograms is the IC50 of the drugs

384 alone or in combination. The straight lines connecting the individual IC50s represent the theoretical

385 line of additivity for each combination. The experiments were performed in triplicate, n = 3. The http://aac.asm.org/

386 graphics are representative of a single experiment, with the standard deviation value. The graphics

387 and IC50 values were produced with GraphPad Prism 4 software.

388 Fig. 3 Antiamastigote activity of ezetimibe combined with azoles. Peritoneal macrophages infected

389 with L. amazonensis treated with ezetimibe and the indicated azoles were incubated for 72 hours at on February 16, 2017 by

390 37°C. After incubation, the cells were fixed and stained. The infection rate was calculated as

391 indicated in the methodology. The experiments were performed in triplicate, n = 3. The graphics are

392 representative of a single experiment, with the standard deviation value. * p < 0.05, ** p < 0.01,

393 *** p < 0.001.

394 Fig. 4 Toxicity to macrophages. Uninfected macrophages were incubated with ezetimibe,

395 miconazole, ketoconazole alone or in combination for 72 hours at 37 °C. After this period, the cells

396 were incubated with MTT for 1 hour at 37 °C. The absorbance was read in a spectrophotometer at

397 570 nm. (A) ezetimibe, (B), ketoconazole (C), miconazole (D) + Eze20 ketoconazole (E) Eze20 +

398 miconazole. The experiments were performed in triplicate, n = 3. *** p <0.001 compared to the

399 control.

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400 Fig. 5. Micrographs of L. amazonensis-infected macrophages treated with ezetimibe and azoles.

401 Peritoneal macrophages infected with L. amazonensis treated with ezetimibe and the indicated

402 azoles were incubated for 72 hours at 37°C. After incubation, the cells were fixed and stained. (A)

403 control, (B) ezetimibe 20 μM, (C) ketoconazole 8 μM, (D) ketoconazole 8 μM + ezetimibe 20 μM,

404 (E) miconazole 4 μM, (F) miconazole 4μM + ezetimibe 20 μM.

405 Fig. 6. In vivo activity of ezetimibe in combination with ketoconazole. BALB/c mice (9/group) Downloaded from 406 were infected on the right ear with 2 x 106 promastigotes of L. amazonensis stationary phase and

407 orally treated with ezetimibe (10 mg/kg/day) (Eze10), ketoconazole (100mg/ kg/day) (Keto100),

408 miltefosine (20 mg/kg/day) and ezetimibe + ketoconazole (10 mg/kg/day + 100 mg/kg/ day) (Eze10

409 + keto100). The treatment started ten days after infection. The animals were treated 5 days per http://aac.asm.org/ 410 week, in a total of 20 doses. The euthanasia was proceeded after 35 days of infection. Negative

411 controls were also similarly treated with PBS. A - Lesion growth and parasite load. B-I -

412 Biochemical evaluation of toxicity of the treatment, according to the indicated parameters. Urea

413 (URE), albumin (ALB), alanine aminotransferase (ALT), aspartate aminotransferase (AST),

414 creatinine (CREA), total bilirubin (BIL), creatine kinase (CK) and cholesterol (CHO). 2way on February 16, 2017 by

415 ANOVA, * p <0.05, ** p <0.01 *** p <0.001 compared to the control group. # # p <0.01 compared

416 to the Eze10 group. π p <0.05, π π p <0.01 π π π p <0.001 compared to the Keto100 group.

19 Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ Downloaded from http://aac.asm.org/ on February 16, 2017 by FUNDA??????????????????????????????????????????????????????????????????????????????O OSWALDO CRUZ