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(1) Background: Leishmaniasis refers to a group of anthropozoonotic diseases caused by Leishmania. The major chemotherapeutic agent used for its treatment is Glucantime ®® , but the search continues for new compounds that are economically viable and act on the protozoan without causing damage to the host cell. As an alternative approach, this study used a combination of copaiba oil (CO) and kojic acid (KA) to determine their in vitro action on host cells, on the Leishmania (Leishmania) amazonensis protozoan and its interaction with macrophages. (2) Methods: In vitro culture, analysis of cytokine release and microscopy assays were performed. Statistical analysis was performed with ANOVA (GraphPad Prism). (3) Results: The combination did not induce cytotoxic effects on macrophages after treatment but promoted morphological changes in the protozoan, such as nuclear alterations (apoptotic characteristics), alterations in the cellular body and an increase in the number of electrodense structures and acidocalcisomes, observed mainly at the concentrations of CO20KA50 and CO30KA50 μg/mL. We observed reductions in the intracellular amastigote number and in the production of proinflammatory cytokines, such as IL-6 and TNF-α, after treatment with CO30KA at 50 µg/mL. (4) Conclusions: We report here, for the first time, that the combination of CO and KA may be a promising approach against Leishmania (Leishmania) amazonensis .

Chromoblastomycosis (CBM) is a chronic human subcutaneous mycosis caused by various aetiologic agents. CBM does not have an established treatment but may be managed using antifungal agents, surgical removal of the lesions, or cryotherapy. Kojic acid (KA), a known tyrosinase inhibitor with a variety of biological actions, including fungistatic action against the fungus Cryptococcus neoformans, mediated by inhibiting melanin production, seems to be an alternative to improve the treatment of CBM. The aim of the present study was to analyze the action of KA against the pathogenic fungus Fonsecaea sp., an aetiological agent of CBM. The fungal culture was incubated with KA, and the amount of melanin was assessed, followed by cytochemical detection. Subsequently, the samples were analyzed by light microscopy, transmission and scanning electron microscopy. Culture analysis revealed that 100 g/mL KA significantly decreased the melanization of the fungus and the exocytosis of melanin into the culture supernatant. Additionally, KA induced less growth of biofilm formation and intense disruption of the cell wall, and decreased the number of melanin-containing vesicles in the culture supernatant. Finally, KA inhibited fungal filamentation in culture and the subsequent phagocytosis process. Thus, KA may be a promising substance to help in the treatment of CBM.