Anti-leishmanial and anti-trypanosomal activities of 1,4-dihydropyridines: In vitro evaluation and structure–activity relationship study

Independent Analysis of the Flagellum Surface and Matrix Proteomes Provides Insight into Flagellum Signaling in Mammalian-infectious Trypanosoma brucei

“…Flagellum attachment is essential in T. brucei, suggesting that Ca 2ϩ channels might be exploited as targets for therapeutic intervention in trypanosomiases. Indeed, Ca 2ϩ channels are major targets of the pharmaceutical industry for treating of a variety of human diseases (102) and Ca 2ϩ channel blockers have antiprotozoal activity in vitro (103).…”

Investigation into in vitro anti-leishmanial combinations of calcium channel blockers and current anti-leishmanial drugs

“…This is the first report that investigates the in vitro activity of combinations of calcium antagonists and standard drugs for leishmaniasis. Despite the previously observed antileishmanial activity of the CCBs used in the study (Reimão et al 2010), the overall mean ΣFIC and the isobolograms obtained show no physicochemical or biological interactions between the CCBs and the standard drugs.…”

“…Calcium antagonists have shown anti-parasitic properties (Misra et al 1991, Núñez-Vergara et al 1998, Tempone et al 2009, Reimão et al 2010. Other studies have reported that amlodipine reverses the in vitro chloroquine resistance in Plasmodium falciparum and can also increase chloroquine accumulation inside the infected erythrocytes.…”

“…Based on previous reports that demonstrate the antileishmanial activity of several CCBs (Tempone et al 2009, Reimão et al 2010, their in vitro activity when used in combination with standard drugs was explored with the goal of finding new alternatives for the treatment of leishmaniasis.…”

Degradation kinetics and pathways of three calcium channel blockers under UV irradiation

“…As a result, the boatform structure of 1,4-dihydropiridine, which is crucial for the receptor protein (Rojstaczer and Triggle, 1996), was destructed. By contrast, the pharmacophore persisted in the TBPs of the second (A-391) pathway because either the substitution of Cl with OH at Site 5 or the rupture of the aliphatic chain at Sites 7e10 could hardly reduce the therapeutic activity of 1,4-dihydropiridine pharmaceuticals (Yamamoto et al, 2006;Reimao et al, 2010). Therefore, the first pathway is more efficient in eliminating the ecological hazards related to AML.…”