Kojic acid is a fungal metabolite that inhibits tyrosinase, an enzyme involved in melanin synthesis, with an IC50 value of 30.6 μM for mushroom tyrosinase.

Kojic acid（KA）（50 μg/mL）在体外实验中，分别减少了promastigotes和amastigotes生长62%（IC50 34 μg/mL）和79%（IC50 27.84 μg/mL）。KA处理后的amastigotes表现出鞭毛囊内有囊泡体出现，以及线粒体内部出现明显的液泡化和肿胀。在寄生虫与宿主细胞的体外相互作用中，KA能逆转由寄生虫促进的超氧阴离子（O2-）的抑制机制。

在KA局部涂故治疗感染动物4周后，观察到一个愈合过程，其特点是胶原纤维的高产生以及寄生虫负担的减少。这展示了KA作为抗利什曼病化合物的巨大潜力[1]。

Amazonensis promastigotes (10^6 parasites/mL) were inoculated in a 24-well plate containing RPMI medium supplemented with 10% inactivated fetal bovine serum treated with different concentrations of KA and incubated at 25 °C for 5 days without medium replacement. Every 24 h after treatment, aliquots were harvested and the effect of Kojic acid on promastigotes growth was evaluated using a Neubauer chamber and compared with untreated parasites culture. The cultures were performed in triplicate[1].

Animals (eight-week-old female Golden hamsters) were infected with 10^6 of L. amazonensis promastigotes/mL during the stationary growth phase with a maximum volume of 0.2 mL on both hind paws.?Animals were separated in 3 groups: untreated (n?=?5);?KA-treated 100 mg/kg/day (n?=?5) and KA vehicle (n?=?5).?KA topical formulation treatment was initiated after 5 weeks of infection.?The KA formulation and vehicle was applied topically to all lesions once daily for 4 weeks.?Control groups were also maintained in parallel.?During the treatment period, the lesion size was measured weekly using a caliper.?Width and height of both hind paws were used to calculate the lesion area (mm^2)[1].