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@ARTICLE{Cologni:1030251,
author = {Cologni, Roberta and Holschbach, Marcus and Schneider,
Daniela and Bier, Dirk and Schulze, Annette and Stegmayr,
Carina and Endepols, Heike and Ermert, Johannes and
Neumaier, Felix and Neumaier, Bernd},
title = {{P}reparation and {P}reclinical {E}valuation of
18{F}-{L}abeled {O}lutasidenib {D}erivatives for
{N}on-{I}nvasive {D}etection of {M}utated {I}socitrate
{D}ehydrogenase 1 (m{IDH}1)},
journal = {Molecules},
volume = {29},
number = {16},
issn = {1420-3049},
address = {Basel},
publisher = {MDPI},
reportid = {FZJ-2024-05268},
pages = {3939},
year = {2024},
note = {This research was funded by Deutsche Forschungsgemeinschaft
(DFG), grant number NE 890/9-1, and by the Helmholtz
European Partnering program (‘Innovative high-performance
computing approaches for molecular neuromedicine’).},
abstract = {Mutations of isocitrate dehydrogenase 1 (IDH1) are key
biomarkers for glioma classification, but current methods
for detection of mutated IDH1 (mIDH1) require invasive
tissue sampling and cannot be used for longitudinal studies.
Positron emission tomography (PET) imaging with
mIDH1-selective radioligands is a promising alternative
approach that could enable non-invasive assessment of the
IDH status. In the present work, we developed efficient
protocols for the preparation of four 18F-labeled
derivatives of the mIDH1-selective inhibitor olutasidenib.
All four probes were characterized by cellular uptake
studies with U87 glioma cells harboring a heterozygous IDH1
mutation (U87-mIDH) and the corresponding wildtype cells
(U87-WT). In addition, the most promising probe was
evaluated by PET imaging in healthy mice and mice bearing
subcutaneous U87-mIDH and U87-WT tumors. Although all four
probes inhibited mIDH1 with variable potencies, only one of
them ([18F]mIDH-138) showed significantly higher in vitro
uptake into U87-mIDH compared to U87-WT cells. In addition,
PET imaging with [18F]mIDH-138 in mice demonstrated good in
vivo stability and low non-specific uptake of the probe, but
also revealed significantly higher uptake into U87-WT
compared to U87-mIDH tumors. Finally, application of a
two-tissue compartment model (2TCM) to the PET data
indicated that preferential tracer uptake into U87-WT tumors
results from higher specific binding rather than from
differences in tracer perfusion. In conclusion, these
results corroborate recent findings that mIDH1-selective
inhibition may not directly correlate with mIDH1-selective
target engagement and indicate that in vivo engagement of
wildtype and mutated IDH1 may be governed by factors that
are not faithfully reproduced by in vitro assays, both of
which could complicate development of PET probes.},
cin = {INM-5},
ddc = {540},
cid = {I:(DE-Juel1)INM-5-20090406},
pnm = {5253 - Neuroimaging (POF4-525)},
pid = {G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)16},
pubmed = {39203017},
UT = {WOS:001306947000001},
doi = {10.3390/molecules29163939},
url = {https://juser.fz-juelich.de/record/1030251},
}