Radicicol from Diheterospora chlamydosporia 

Antifungal macrolactone antibiotic that inhibits protein tyrosine kinase. Radicicol induces the differentiation of HL-60 cells into macrophages, blocking cell cycle at G1 and G2. It 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 and plasminogen activator production by vascular endothelial cells.

Photosensitive

solid

yellow

ethanol: 10 mg/mL

−20°C

Shimada, Y., et al., Induction of differentiation of HL-60 cells by the anti-fungal antibiotic, radicicol. J. Antibiot. 48, 824-830, (1995) abstract

Zhao, J.F., et al., Suppression of RAS and MOS transformation by radicicol. Oncogene 11, 161-173, (1995) abstract

Pillay, I., et al., Radicicol inhibits tyrosine phosphorylation of the mitotic Src substrate Sam68 and retards subsequent exit from mitosis of Src-transformed cells. Cell. Growth Differ. 7, 1487-1499, (1996) abstract

Oikawa, T., et al., Radicicol a microbial cell differentiation modulator inhibits in vivo angiogenesis. Eur. J. Pharmacol. 241, 221, (1993) abstract

Chanmugan, P., 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, (1995) abstract

Xn

22-36/37/38

26

UN 2811 6.1/PG 3

1

RR1105000