The selectivity of RM-A to OCs is attributed to the three carboxyl moieties in its structure 4, making it highly hydrophilic and difficult to penetrate the cell membrane. RM-A is at least 100 times more cytotoxic to OCs than to a number of other types of cells, including OC progenitor cells, highlighting its potential in the development of anti-osteoporosis therapeutics 4, 5. Later, RM-A was found to potently induce the apoptosis of osteoclasts (OCs) and suppress bone loss in ovariectomized mice 4. Reveromycin A could inhibit the proliferation of human tumour KB and K562 cells in vitro 2 and ovarian cancer and prostate cancer growth in vivo 3. 1a) was originally isolated from Streptomyces reveromyceticus SN-593 in a study screening antitumour compounds in the early 1990s by the RIKEN Antibiotics Laboratory 1. The polyketide reveromycin A (RM-A) (Fig.
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