Radicicol
HSP90 inhibitor / Radicicol inhibits heat shock protein 90 (Hsp90) activity by binding to the ATP-binding pocket.1 In cells Hsp90 client proteins such as Raf kinase2, HIF-1α3 and estrogen receptor4 are destabilized and proteolytically degraded. Inhibits expression of COX-2 without affecting COX-1 expression in LPS-stimulated macrophages (IC50=27 nM).5 Inhibits angiogenesis.6
Biochemicals & reagents
12772-57-5
Monorden
1) Schulte et al. (1999), Interaction of radicicol with members of the heat shock protein 90 family of molecular chaperones; Mol.Endocrinol. 13 1435 2) Soga et al. (1998), Radicicol leads to selective depletion of Raf kinase and disrupts K-Ras-activated aberrant signaling pathway; J.Biol.Chem. 273 822 3) Hur et al. (2002) Reduction of hypoxia-induced transcription through the repression of hypoxia-inducible factor-1alpha/aryl hydrocarbon receptor nuclear translocator DNA binding by the 90-kDa heat-shock protein inhibitor radicicol; Mol.Pharmacol. 62 975 4) Lee et al. (2002) Radicicol represses the transcriptional function of the estrogen receptor by suppressing the stabilization of the receptor by heat shock protein 90; Mol.Cell.Endocrinol. 188 47 5) Chanmugam et al. (1995) Radicicol, a protein tyrosine kinase inhibitor, suppresses the expression of mitogen-inducible cyclooxygenase in macrophages stimulated with lipopolysaccharide and in experimental glomerulonephritis; J.Biol.Chem. 270 5418 6) Oikawa et al. (1993) Radicicol, a microbial cell differentiation modulator, inhibits in vivo angiogenesis; Eur.J.Pharmacol. 241 221
-20°C
TARGET: HSP (Heat shock protein); Kinase -- PATHWAY: Autophagy -- RESEARCH AREA: Angiogenesis; Oxidative stress; Ubiquitin/Proteasome; Cell death -- DISEASE AREA: Cancer; Infectious disease