Halofuginone HBr
Prolyl-tRNA synthase inhibitor / Potent and selective prolyl-tRNA synthetase (PRS) inhibitor (Ki=18.3 nM) derived from febrifugine.1 Also attenuates TGF-β signaling, including reversibly reducing Smad3 protein levels and inhibiting fibroblast differentiation.2 Blocks fibrosis, angiogenesis, and tumor progression.2,3 Inhibition of PRS results in amino acid starvation which activates the integrated stress response (ISR) and mTOR signaling4 and thus preventing differentiation of TH17 cells, suppressing the autoimmune response5. Reduces TMPRSS2 protein levels via enhanced ubiquitination and proteasomal degradation, limiting SARS-CoV-2 cellular entry.6
Biochemicals & reagents
64924-67-0
NSC 713205
1 Keller et al. (2012), Halofuginone and other febrifugine derivatives inhibit prolyl-tRNA synthetase; Nat. Chem. Biol., 8 311 2 Nelson et al. (2012), Halofuginone down-regulates Smad3 expression and inhibits the TGß-induced expression of fibrotic markers in human corneal fibroblasts; Mol. Vis., 18 479 3 Elkin et al. (2000), Halofuginone: a potent inhibitor of critical steps in angiogenesis progression. FASEB J., 14 2477 4 Misra et al. (2021), Discordant regulation of eIF2 kinase GCN2 and mTORC1 during nutrient stress; Nucleic Acids Res., 49 5726 5 Sundrud et al. (2009), Halofuginone inhibits Th17 cell differentiation by activating the amino acid starvation response; Science, 324 1334 6 Chen et al. (2021), A high-throughput screen for TMPRSS2 expression identifies FDA-approved compounds that can limit SARS-CoV-2 entry; Nat. Commun., 12 3907
-20°C
PATHWAY: Protein synthesis; TGF-beta; mTOR -- RESEARCH AREA: Immunology; Angiogenesis; Cellular stress -- DISEASE AREA: Cancer; ParasitesInflammation; Infectious disease