Diethylcarbamazine

Diethylcarbamazine is an orally active microfilaricidal agent used originally in onchocerciasis and lymphatic filiariasis. Diethylcarbamazine reduces eosinophil trafficking to the lung tissue and exerts anti-allergic effects. Diethylcarbamazine reduces serum levels of leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without altering body, liver, or adipose tissue weights. Diethylcarbamazine enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits actinomycetoma lesion development. Diethylcarbamazine can be used for the researches of bronchial asthma, insulin resistance and infection^[1][2][3]. In Vitro:Diethylcarbamazine (0-40 mM; 60 min) cross-reacts with rabbit anti-MPCA-BSA polyclonal IgG antibodies in an inhibition ELISA^[1]. In Vivo:Diethylcarbamazine (citrate) (12 mg/kg; p.o.) exerts anti-allergic effects in Ovalbumin (HY-W250978)-induced asthmatic mice, with pre-treatment with 40 mg/kg quercetin significantly potentiating these effects, as evidenced by reduced serum Th2 cytokines, BALF IgE, lung eosinophil markers, and complete resolution of histopathological lung damage^[1].
Diethylcarbamazine (12-200 mg/kg; p.o.; twice weekly; 12 weeks) significantly ameliorates high-fat diet-induced insulin resistance in male Swiss mice via suppression of adipose tissue inflammation at the optimal 50 mg/kg dose, without affecting body or tissue weights, with significant reductions in serum glucose, insulin, triglycerides, proinflammatory mediators, liver cyclooxygenase activity, and NF-κBp65 nuclear translocation^[2].
Diethylcarbamazine (6 mg/kg; p.o.; daily; 1 week) inhibits actinomycetoma development in BALB/c mice, with a statistically significant reduction in lesion size, and enhances cellular immune responses including neutrophil reactive oxygen intermediate production and lymphocyte proliferation^[3].