Antiparasitic agent-44

C57BL/6 (female, 8 weeks old, 32.27 g)^[1]

100 mg/kg (monotherapy); 50 mg/kg (in combination with 100 mg/kg benznidazole); 100 mg/kg (in combination with 100 mg/kg benznidazole)

p.o.; daily; 10 days

Reduced mean parasitemia from 21.68 × 10⁴ to 3.88 × 10³, and peak parasitemia from 4.61 × 10⁵ to 1.70 × 10⁴ (100 mg/kg monotherapy).
Reduced skeletal muscle parasite load compared to untreated infected mice (100 mg/kg monotherapy).
Attenuated skeletal muscle oxidative stress markers (ROS, nitric oxide, advanced oxidation protein products, protein carbonyl, lipid hydroperoxides) compared to untreated infected mice (100 mg/kg monotherapy).
Reduced skeletal muscle inflammatory markers (interstitial cellularity, MPO activity, NAG activity, IFN-γ, TNF, IL-6, IL-10 levels) compared to untreated infected mice (100 mg/kg monotherapy).
Mitigated skeletal muscle microstructural damage (reduced stroma volume density, restored myocyte thickness and cross-sectional area) compared to untreated infected mice (100 mg/kg monotherapy).
Reduced mean parasitemia to 0.35 × 10² and peak parasitemia to 1.06 × 10³, which was significantly lower than compound ME monotherapy, benznidazole monotherapy, and the 50 mg/kg compound ME + 100 mg/kg benznidazole combination (100 mg/kg + 100 mg/kg benznidazole).
Reduced skeletal muscle parasite load to levels significantly lower than all other treatment groups (100 mg/kg + 100 mg/kg benznidazole).
Attenuated skeletal muscle ROS, advanced oxidation protein products, and lipid hydroperoxide levels to levels significantly lower than all other treatment groups (100 mg/kg + 100 mg/kg benznidazole).
Reduced skeletal muscle interstitial cellularity, MPO activity, IFN-γ, TNF, and IL-10 levels to levels significantly lower than all other treatment groups (100 mg/kg + 100 mg/kg benznidazole).
Preserved skeletal muscle microstructure to a pattern nearly identical to uninfected control mice, with minimal stroma expansion and no visible T. cruzi nests (100 mg/kg + 100 mg/kg benznidazole).