storage temp. −20°C

solubility ethanol: 10 mg/mL

form solid

color yellow

Safety Information

Hazard Codes Xn,T

Risk Statements 22-36/37/38-46-45

Safety Statements 26-45-53

RIDADR UN 2811 6.1/PG 3

WGK Germany 1

RTECS RR1105000

MSDS Information

RADICICOL Usage And Synthesis

Chemical Properties Solid

Usage Radicicol is a resorcylic acid lactone, produced by several fungal species, that exhibits broad spectrum antifungal and antitumour activity. Radicicol has been the subject of extensive investigation and inhibits protein tyrosine kinase, induces the differentiation of HL-60 cells into macrophages, blocks cell cycle at G1 and G2, suppresses NIH 3T3 cell transformation by diverse oncogenes such as src, ras and mos, and also suppresses the expression of mitogen-inducible cyclooxygenase-2. As a cell differentiation modulator, radicicol has anti-angiogenic activity in vivo, inhibiting the proliferation of plasminogen activator production by vascular endothelial cells.

Usage Radicicol is a resorcylic acid lactone, produced by several fungal species, that exhibits broad spectrum antifungal and antitumor activity. Radicicol has been the subject of extensive investigation and inhibits protein tyrosine kinase, induces the differentiation of HL-60 cells into macrophages, blocks cell cycle at G1 and G2, suppresses NIH 3T3 cell transformation by diverse oncogenes such as src, ras and mos, and also suppresses the expression of mitogen-inducible cyclooxygenase-2. As a cell differentiation modulator, radicicol has anti-angiogenic activity in vivo, inhibiting the proliferation of plasminogen activator production by vascular endothelial cells.

Definition ChEBI: An antifungal macrolactone antibiotic, obtained from Diheterospora chlamydosporia and Chaetomium chiversii that inhibits protein tyrosine kinase and heat shock protein 90 (Hsp90).

Biological Activity Antifungal antibiotic. Inhibits heat shock protein 90 (Hsp90) activity by binding to the ATP-binding pocket, subsequently suppressing cell transformation induced by src, ras and mos. Represses estrogen receptor transcriptional activity and inhibits angiogenesis.

storage temp. −20°C

solubility ethanol: 10 mg/mL

form solid

color yellow

Safety Information

Hazard Codes Xn,T

Risk Statements 22-36/37/38-46-45

Safety Statements 26-45-53

RIDADR UN 2811 6.1/PG 3

WGK Germany 1

RTECS RR1105000

MSDS Information

RADICICOL Usage And Synthesis

Chemical Properties Solid

Usage Radicicol is a resorcylic acid lactone, produced by several fungal species, that exhibits broad spectrum antifungal and antitumour activity. Radicicol has been the subject of extensive investigation and inhibits protein tyrosine kinase, induces the differentiation of HL-60 cells into macrophages, blocks cell cycle at G1 and G2, suppresses NIH 3T3 cell transformation by diverse oncogenes such as src, ras and mos, and also suppresses the expression of mitogen-inducible cyclooxygenase-2. As a cell differentiation modulator, radicicol has anti-angiogenic activity in vivo, inhibiting the proliferation of plasminogen activator production by vascular endothelial cells.

Usage Radicicol is a resorcylic acid lactone, produced by several fungal species, that exhibits broad spectrum antifungal and antitumor activity. Radicicol has been the subject of extensive investigation and inhibits protein tyrosine kinase, induces the differentiation of HL-60 cells into macrophages, blocks cell cycle at G1 and G2, suppresses NIH 3T3 cell transformation by diverse oncogenes such as src, ras and mos, and also suppresses the expression of mitogen-inducible cyclooxygenase-2. As a cell differentiation modulator, radicicol has anti-angiogenic activity in vivo, inhibiting the proliferation of plasminogen activator production by vascular endothelial cells.

Definition ChEBI: An antifungal macrolactone antibiotic, obtained from Diheterospora chlamydosporia and Chaetomium chiversii that inhibits protein tyrosine kinase and heat shock protein 90 (Hsp90).

Biological Activity Antifungal antibiotic. Inhibits heat shock protein 90 (Hsp90) activity by binding to the ATP-binding pocket, subsequently suppressing cell transformation induced by src, ras and mos. Represses estrogen receptor transcriptional activity and inhibits angiogenesis.