In-vitro antileishmanial potential of peptide drug hirudin
Research article published in Chemical biology & drug design (2017)
Abstract
Hirudin is clinically an important drug used for the treatment of cardiac diseases, but has never been elucidated for antileishmanial potential. This study was designed to determine the therapeutic utility of hirudin against leishmaniasis. Binding affinities of 28 potent proteinase inhibitors were screened computationally against leishmanolysin (GP63), out of which hirudin exhibited higher binding affinity with GP63 and good expected IC50 values. Experimentally, hirudin showed most promising activity against promastigote and axenic amastigote forms of leishmanial parasites with IC50 values of 0.60 ± 0.36 μg/mL and 0.43 ± 0.23 μg/mL, respectively, in a dose- and time-dependent assay. The cytotoxicity assay revealed no adverse effects on human macrophages with LD50 value of 860.11 ± 53.44 μg/mL. Hirudin caused leishmanial cell death mainly by apoptosis and membrane permeability. In spite of the basic knowledge obtained, hirudin mechanism is considerably less prone to the induction of resistance than classical drugs. Collectively, this study fosters further studies for the hirudin as new antileishmania lead with a new mode of action.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
Hirudin is clinically an important drug used for the treatment of cardiac diseases, but has never been elucidated for antileishmanial potential. This study was designed to determine the therapeutic utility of hirudin against leishmaniasis.
Why This Matters for Hirudotherapy
This study screened hirudin against the parasite enzyme leishmanolysin (GP63) computationally and then tested it in the laboratory, reporting activity against promastigote and axenic amastigote forms of Leishmania (IC50 ~0.60 and ~0.43 µg/mL) with no observed toxicity to human macrophages (LD50 ~860 µg/mL), and proposing apoptosis and membrane permeabilization as the mechanism of parasite death. For ASH it widens the leech-secretome drug-discovery story beyond anticoagulation, suggesting hirudin — already known as a thrombin inhibitor — may have an entirely separate antiparasitic mode of action worth exploring against leishmaniasis. This is strictly an in-vitro and in-silico screen: the results come from cultured parasites and cells, not animals or patients, so they establish a research lead only and cannot support any claim that hirudin or leech therapy treats leishmaniasis in humans.
Citation
In-vitro antileishmanial potential of peptide drug hirudin.
Khan H et al. · Chemical biology & drug design, 2017
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