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The causative protein of prion disease is the prion protein (PrP), and structural transition of PrP from the normal helix rich form (PrP<jats:sup>C<\/jats:sup>) to the abnormal \u03b2-sheet rich form (PrP<jats:sup>Sc<\/jats:sup>) occurs in prion disease. While so far numerous therapeutic agents for prion diseases have been developed, none of them are still useful. A fluorinated alcohol, hexafluoro isopropanol (HFIP), is a precursor to the inhalational anesthetic sevoflurane and its metabolites. HFIP is also known as a robust \u03b1-helix inducer and is widely used as a solvent for highly aggregated peptides. Here we show that the \u03b1-helix-inducing activity of HFIP caused the conformational transformation of the fibrous structure of PrP into amorphous aggregates in vitro. HFIP added to the ScN2a cell medium, which continuously expresses PrP<jats:sup>Sc<\/jats:sup>, reduced PrP<jats:sup>Sc<\/jats:sup> protease resistance after 24-h incubation. It was also clarified that ScN2a cells are more susceptible to HFIP than any of the cells being compared. Based on these findings, HFIP is expected to develop as a therapeutic agent for prion disease.<\/jats:p>","DOI":"10.1007\/s11064-021-03344-8","type":"journal-article","created":{"date-parts":[[2021,5,27]],"date-time":"2021-05-27T08:02:43Z","timestamp":1622102563000},"page":"2056-2065","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Volatile Anesthetic Sevoflurane Precursor 1,1,1,3,3,3-Hexafluoro-2-Propanol (HFIP) Exerts an Anti-Prion Activity in Prion-Infected Culture Cells"],"prefix":"10.1007","volume":"46","author":[{"given":"Takuto","family":"Shimizu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emiko","family":"Nogami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuka","family":"Ito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuo","family":"Morikawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaki","family":"Nagane","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadashi","family":"Yamashita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsuyoshi","family":"Ogawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fuyuki","family":"Kametani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hisashi","family":"Yagi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1630-663X","authenticated-orcid":false,"given":"Naomi","family":"Hachiya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,5,27]]},"reference":[{"key":"3344_CR1","doi-asserted-by":"publisher","first-page":"13363","DOI":"10.1073\/pnas.95.23.13363","volume":"95","author":"SB Prusiner","year":"1998","unstructured":"Prusiner SB (1998) Prions. 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