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1  standard of care treatment with pentavalent antimonials.
2 QP1 that prevents the transport of trivalent antimonials.
3 is) and favors accumulation of surrogates of antimonials.
4 responsible for resistance to arsenicals and antimonials.
5 therapy and/or intralesional injections with antimonials.
6 ized the 2 independent resistant isolates to antimonials.
7                                              Antimonial agents are a mainstay for the treatment of le
8 roducts of this operon catalyze extrusion of antimonials and arsenicals from cells.
9  this compound was equally effective against antimonials and miltefosine-resistant clinical isolates
10                              The pentavalent antimonials are considered the first-choice drugs for tr
11                               Arsenicals and antimonials are first line drugs for the treatment of tr
12 cause current treatments such as pentavalent antimonials are toxic and require prolonged administrati
13 h KD Sb(R)LD enhanced the sensitivity toward antimonials compared with infection with Sb(R)LD, and in
14      In Bihar state, India, the cure rate of antimonial compounds (eg, sodium stibogluconate) in the
15                                        While antimonial compounds are the standard of care worldwide,
16                                              Antimonial compounds are used as first-line treatment dr
17 tor R773 confers resistance to arsenical and antimonial compounds in Escherichia coli, where resistan
18 ovide the knowledge base for optimization of antimonial drug treatments, guiding the selection and/or
19 trains with different inherent resistance to antimonial drugs (antimony sensitive strain Sb-S; and an
20 eby the initial anti-leishmanial activity of antimonial drugs alleviates checkpoint inhibition on T c
21       Children have a lower response rate to antimonial drugs and higher elimination rate of antimony
22                           Resistance against antimonial drugs has probably been a contributing factor
23                                              Antimonial drugs have long been the mainstay to treat vi
24 nonhealing forms of human leishmaniasis with antimonial drugs in combination with gamma interferon (I
25 ptake systems, but the uptake system for the antimonial drugs in Leishmania is unknown.
26 e in Bihar because inadequate treatment with antimonial drugs is not exclusive to India, whereas wide
27 water coexists with widespread resistance to antimonial drugs that are used to treat the parasitic di
28 ttributed to long-term, widespread misuse of antimonial drugs within the Indian private health-care s
29 atients produces a common mode of action for antimonial drugs, which define a novel compound class th
30  choice for the treatment of this disease is antimonial drugs.
31 f Leishmania donovani parasites resistant to antimonial drugs.
32 ain the development of PKDL: (i) the role of antimonial drugs; (ii) UV-induced skin damage; (iii) rei
33                                  Pentavalent antimonials (e.g., sodium stibogluconate [SSG]) remain f
34       Leishmania resistant to arsenicals and antimonials extrude arsenite.
35  distinct population frequently resistant to antimonials has a two base-pair insertion in the aquagly
36 -dependent extrusion pump for arsenicals and antimonials in Escherichia coli, is allosterically activ
37 responsible for resistance to arsenicals and antimonials in Escherichia coli.
38 on that confers resistance to arsenicals and antimonials in Escherichia coli.
39 atment options remain limited to pentavalent antimonials, liposomal amphotericin B, and miltefosine.
40 ted in deglutathionylation and activation of antimonial prodrugs used to treat leishmaniasis.
41 ficant role in the development of Leishmania antimonial resistance in Bihar because inadequate treatm
42 might have contributed to the development of antimonial resistance in Leishmania parasites in Bihar.
43 coli plasmid R773 that confers arsenical and antimonial resistance is negatively regulated by the Ars
44 s not exclusive to India, whereas widespread antimonial resistance is.
45  cure by chemotherapy (primarily pentavalent antimonials [Sb(V)]).
46 ficantly more effective than the pentavalent antimonial sodium stibogluconate (70 mg/kg) for the trea
47   The current standard to assess pentavalent antimonial (SSG) susceptibility of Leishmania is a labor
48 he associations between arsenic exposure and antimonial treatment failure and death in the leishmania
49 ia strains are frequently cross-resistant to antimonials, we considered the possibility that Sb(V) is
50 nfer high level resistance to arsenicals and antimonials, while the chromosomally encoded ars operon