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@ARTICLE{Bukhdruker:885766,
author = {Bukhdruker, Sergey and Varaksa, Tatsiana and Grabovec,
Irina and Marin, Egor and Shabunya, Polina and Kadukova,
Maria and Grudinin, Sergei and Kavaleuski, Anton and Gusach,
Anastasiia and Gilep, Andrei and Borshchevskiy, Valentin and
Strushkevich, Natallia},
title = {{H}ydroxylation of {A}ntitubercular {D}rug {C}andidate,
{SQ}109, by {M}ycobacterial {C}ytochrome {P}450},
journal = {International journal of molecular sciences},
volume = {21},
number = {20},
issn = {1422-0067},
address = {Basel},
publisher = {Molecular Diversity Preservation International},
reportid = {FZJ-2020-04074},
pages = {7683 -},
year = {2020},
abstract = {Spreading of the multidrug-resistant (MDR) strains of the
one of the most harmful pathogen Mycobacterium tuberculosis
(Mtb) generates the need for new effective drugs. SQ109
showed activity against resistant Mtb and already advanced
to Phase II/III clinical trials. Fast SQ109 degradation is
attributed to the human liver Cytochrome P450s (CYPs).
However, no information is available about interactions of
the drug with Mtb CYPs. Here, we show that Mtb CYP124,
previously assigned as a methyl-branched lipid
monooxygenase, binds and hydroxylates SQ109 in vitro. A 1.25
Å-resolution crystal structure of the CYP124–SQ109
complex unambiguously shows two conformations of the drug,
both positioned for hydroxylation of the ω-methyl group in
the trans position. The hydroxylated SQ109 presumably forms
stabilizing H-bonds with its target, Mycobacterial membrane
protein Large 3 (MmpL3). We anticipate that Mtb CYPs could
function as analogs of drug-metabolizing human CYPs
affecting pharmacokinetics and pharmacodynamics of
antitubercular (anti-TB) drugs.},
cin = {IBI-7},
ddc = {540},
cid = {I:(DE-Juel1)IBI-7-20200312},
pnm = {552 - Engineering Cell Function (POF3-552)},
pid = {G:(DE-HGF)POF3-552},
typ = {PUB:(DE-HGF)16},
pubmed = {33081390},
UT = {WOS:000585770700001},
doi = {10.3390/ijms21207683},
url = {https://juser.fz-juelich.de/record/885766},
}