Tubercidin (Sparsomycin A), an adenosine analogue, is a nucleoside antibiotic. It is incorporated into DNA and inhibits polymerases, thereby inhibiting DNA replication and RNA and protein synthesis. This agent also exhibits antifungal and antiviral activities.

Continuous exposure for 14 days to tubercidin alone is highly toxic to both human CFU-GM and BFU-E. The IC50s of tubercidin are 3.4±1.7 and 3.7±0.2 nM for CFU-GM and BFU-E, respectively. Tubercidin also has a direct dose-dependent inhibitory effect on myeloid and erythroid human bone marrow progenitor cells in vitro[1].

Tubercidin at the dose regimen (5 mg/kg everyday for 4 days) is lethal when used alone. Some of the studies show that the mortality from tubercidin is primarily due to hepatic and renal injuries and, to a lesser extent, damage to the pancreas. Coadministration of NBMPR-P at 25 mg/kg per day completely protects the mice (100% survival) from this lethal dose regimen of tubercidin[1].

Human bone marrow cells were obtained from healthy volunteers. In the protection studies, cells are exposed to 10 nM of tubercidin in the presence or absence of various doses of NBMPR-P. Cells are continuously exposed to drugs for 14 days in a humidified atmosphere of 5% C02-95% air at 37°C. Colonies of CFU-GM (250 cells) and BFU-E (>30 hemoglobinized cells) are counted with an inverted microscope. (Only for Reference)