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@ARTICLE{Olubiyi:867774,
author = {Olubiyi, Olujide and Olagunju, Maryam O. and Strodel,
Birgit},
title = {{R}ational {D}rug {D}esign of {P}eptide-{B}ased {T}herapies
for {S}ickle {C}ell {D}isease},
journal = {Molecules},
volume = {24},
number = {24},
issn = {1420-3049},
address = {Basel},
publisher = {MDPI},
reportid = {FZJ-2019-06384},
pages = {4551 -},
year = {2019},
abstract = {Sickle cell disease (SCD) is a group of inherited disorders
affecting red blood cells, which is caused by a single
mutation that results in substitution of the amino acid
valine for glutamic acid in the sixth position of the
β-globin chain of hemoglobin. These mutant hemoglobin
molecules, called hemoglobin S, can polymerize upon
deoxygenation, causing erythrocytes to adopt a sickled form
and to suffer hemolysis and vaso-occlusion. Until recently,
only two drug therapies for SCD, which do not even fully
address the manifestations of SCD, were approved by the
United States (US) Food and Drug Administration. A third
treatment was newly approved, while a monoclonal antibody
preventing vaso-occlusive crises is also now available. The
complex nature of SCD manifestations provides multiple
critical points where drug discovery efforts can be and have
been directed. These notwithstanding, the need for new
therapeutic approaches remains high and one of the recent
efforts includes developments aimed at inhibiting the
polymerization of hemoglobin S. This review focuses on
anti-sickling approaches using peptide-based inhibitors,
ranging from individual amino acid dipeptides investigated
30–40 years ago up to more promising 12- and 15-mers under
consideration in recent years.},
cin = {ICS-6},
ddc = {540},
cid = {I:(DE-Juel1)ICS-6-20110106},
pnm = {553 - Physical Basis of Diseases (POF3-553)},
pid = {G:(DE-HGF)POF3-553},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31842406},
UT = {WOS:000507299600129},
doi = {10.3390/molecules24244551},
url = {https://juser.fz-juelich.de/record/867774},
}