000305425 001__ 305425
000305425 005__ 20251020115508.0
000305425 0247_ $$2doi$$a10.3390/ijms26199811
000305425 0247_ $$2pmid$$apmid:41097076
000305425 0247_ $$2ISSN$$a1422-0067
000305425 0247_ $$2ISSN$$a1661-6596
000305425 037__ $$aDKFZ-2025-02154
000305425 041__ $$aEnglish
000305425 082__ $$a540
000305425 1001_ $$0P:(DE-He78)3caae9893e3b2704f7bb5a9646ef084d$$aJennemann, Richard$$b0$$eFirst author$$udkfz
000305425 245__ $$aThe SGLT2 Inhibitor Dapagliflozin Disrupts the Cell Cycle at High Concentrations Without Altering Glycosphingolipid (De Novo)Biosynthesis.
000305425 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2025
000305425 3367_ $$2DRIVER$$aarticle
000305425 3367_ $$2DataCite$$aOutput Types/Journal article
000305425 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1760947140_1189494$$xLetter
000305425 3367_ $$2BibTeX$$aARTICLE
000305425 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000305425 3367_ $$00$$2EndNote$$aJournal Article
000305425 500__ $$a#EA:A411#LA:A411#
000305425 520__ $$aModern computational screening methods are valuable tools for repurposing approved drugs for novel therapeutic applications. They provide initial insights into alternative uses and may significantly shorten the lengthy process of drug development and regulatory approval. Treatment options for glycosphingolipidoses, lysosomal storage diseases involving glycosphingolipids (GSLs), are currently limited to a few drugs that inhibit de novo GSL biosynthesis, such as eliglustat and miglustat (Zavesca®). In the search for alternative drugs, dapagliflozin emerged as a promising candidate for off-target therapy. In the present study, we investigated whether dapagliflozin can indeed inhibit GSL synthesis, as predicted by previous computational analyses, and compared its effects with those of the glycosphingolipid synthesis inhibitor, the eliglustat analog Genz-123346, in murine 3T3 and Hepa 1-6 cell lines. While Genz-123346 significantly inhibited glycosphingolipid biosynthesis at concentrations as low as 1 µM, dapagliflozin, even up to 50 µM, had no effect on biosynthesis or de novo biosynthesis in either cell line. These results indicate that dapagliflozin, although assessing effects on the cell cycle, including proliferation at high concentrations, is not a suitable candidate for treating glycosphingolipid storage diseases by substrate reduction.
000305425 536__ $$0G:(DE-HGF)POF4-311$$a311 - Zellbiologie und Tumorbiologie (POF4-311)$$cPOF4-311$$fPOF IV$$x0
000305425 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
000305425 650_7 $$2Other$$aGCS-inhibitors
000305425 650_7 $$2Other$$aGenz-123346
000305425 650_7 $$2Other$$adapagliflozin
000305425 650_7 $$2Other$$aeliglustat
000305425 650_7 $$2Other$$aglucosylceramide synthase (GCS)
000305425 650_7 $$2Other$$aglycosphingolipids
000305425 650_7 $$2Other$$amiglustat
000305425 650_7 $$2NLM Chemicals$$aGlucosides
000305425 650_7 $$2NLM Chemicals$$aBenzhydryl Compounds
000305425 650_7 $$2NLM Chemicals$$aGlycosphingolipids
000305425 650_7 $$01ULL0QJ8UC$$2NLM Chemicals$$adapagliflozin
000305425 650_7 $$2NLM Chemicals$$aSodium-Glucose Transporter 2 Inhibitors
000305425 650_7 $$2NLM Chemicals$$aSodium-Glucose Transporter 2
000305425 650_2 $$2MeSH$$aGlucosides: pharmacology
000305425 650_2 $$2MeSH$$aAnimals
000305425 650_2 $$2MeSH$$aBenzhydryl Compounds: pharmacology
000305425 650_2 $$2MeSH$$aGlycosphingolipids: biosynthesis
000305425 650_2 $$2MeSH$$aMice
000305425 650_2 $$2MeSH$$aSodium-Glucose Transporter 2 Inhibitors: pharmacology
000305425 650_2 $$2MeSH$$aCell Cycle: drug effects
000305425 650_2 $$2MeSH$$aCell Line
000305425 650_2 $$2MeSH$$aHumans
000305425 650_2 $$2MeSH$$aSodium-Glucose Transporter 2: metabolism
000305425 7001_ $$0P:(DE-He78)a928ded2085c8911822370cad0b4a728$$aSandhoff, Roger$$b1$$eLast author$$udkfz
000305425 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms26199811$$gVol. 26, no. 19, p. 9811 -$$n19$$p9811$$tInternational journal of molecular sciences$$v26$$x1422-0067$$y2025
000305425 909CO $$ooai:inrepo02.dkfz.de:305425$$pVDB
000305425 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)3caae9893e3b2704f7bb5a9646ef084d$$aDeutsches Krebsforschungszentrum$$b0$$kDKFZ
000305425 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)a928ded2085c8911822370cad0b4a728$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000305425 9131_ $$0G:(DE-HGF)POF4-311$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vZellbiologie und Tumorbiologie$$x0
000305425 9141_ $$y2025
000305425 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)1150$$2StatID$$aDBCoverage$$bCurrent Contents - Physical, Chemical and Earth Sciences$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2024-12-21
000305425 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2024-12-21
000305425 9202_ $$0I:(DE-He78)A411-20160331$$kA411$$lLipid-Pathobiochemie$$x0
000305425 9201_ $$0I:(DE-He78)A411-20160331$$kA411$$lLipid-Pathobiochemie$$x0
000305425 9200_ $$0I:(DE-He78)A411-20160331$$kA411$$lLipid-Pathobiochemie$$x0
000305425 980__ $$ajournal
000305425 980__ $$aVDB
000305425 980__ $$aI:(DE-He78)A411-20160331
000305425 980__ $$aUNRESTRICTED