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@ARTICLE{Hedrich:162807,
author = {Hedrich, Ulrike B S and Lauxmann, Stephan and Wolff, Markus
and Synofzik, Matthis and Bast, Thomas and Binelli, Adrian
and Serratosa, José M and Martínez-Ulloa, Pedro and Allen,
Nicholas M and King, Mary D and Gorman, Kathleen M and Zeev,
Bruria Ben and Tzadok, Michal and Wong-Kisiel, Lily and
Marjanovic, Dragan and Rubboli, Guido and Sisodiya, Sanjay M
and Lutz, Florian and Ashraf, Harshad Pannikkaveettil and
Torge, Kirsten and Yan, Pu and Bosselmann, Christian and
Schwarz, Niklas and Fudali, Monika and Lerche, Holger},
title = {4-{A}minopyridine is a promising treatment option for
patients with gain-of-function {KCNA}2-encephalopathy.},
journal = {Science translational medicine},
volume = {13},
number = {609},
issn = {1946-6242},
address = {Washington, DC},
publisher = {AAAS},
reportid = {DZNE-2021-01462},
pages = {eaaz4957},
year = {2021},
abstract = {Developmental and epileptic encephalopathies are
devastating disorders characterized by epilepsy,
intellectual disability, and other neuropsychiatric
symptoms, for which available treatments are largely
ineffective. Following a precision medicine approach, we
show for KCNA2-encephalopathy that the K+ channel blocker
4-aminopyridine can antagonize gain-of-function defects
caused by variants in the KV1.2 subunit in vitro, by
reducing current amplitudes and negative shifts of
steady-state activation and increasing the firing rate of
transfected neurons. In n-of-1 trials carried out in nine
different centers, 9 of 11 patients carrying such variants
benefitted from treatment with 4-aminopyridine. All six
patients experiencing daily absence, myoclonic, or atonic
seizures became seizure-free (except some remaining provoked
seizures). Two of six patients experiencing generalized
tonic-clonic seizures showed marked improvement, three
showed no effect, and one worsening. Nine patients showed
improved gait, ataxia, alertness, cognition, or speech.
4-Aminopyridine was well tolerated up to 2.6 mg/kg per day.
We suggest 4-aminopyridine as a promising tailored treatment
in KCNA2-(gain-of-function)–encephalopathy and provide an
online tool assisting physicians to select patients with
gain-of-function mutations suited to this treatment.},
keywords = {4-Aminopyridine: therapeutic use / Brain Diseases /
Epilepsy / Gain of Function Mutation / Humans / Kv1.2
Potassium Channel: genetics / Mutation / KCNA2 protein,
human (NLM Chemicals) / Kv1.2 Potassium Channel (NLM
Chemicals) / 4-Aminopyridine (NLM Chemicals)},
cin = {AG Gasser 1},
ddc = {500},
cid = {I:(DE-2719)1210000},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34516822},
doi = {10.1126/scitranslmed.aaz4957},
url = {https://pub.dzne.de/record/162807},
}