Effects of formycin B on human lymphocyte deoxyribonucleic acid synthesis

Formycin B-resistant mutants of Chinese hamster ovary cells: novel genetic and biochemical phenotype affecting adenosine kinase.

“…Earlier biochemical studies with these analogs have indicated that unlike formycin A and other adenosine analogs (e.g., toyocamycin and tubercidin), formycin B, which is an analog of inosine, is not phosphorylated in cells (31). However, formycin B has been reported to be a good inhibitor of human purine nucleoside phosphorylase (6,26,28) …”

“…Earlier biochemical studies with these analogs have indicated that unlike formycin A and other adenosine analogs (e.g., toyocamycin and tubercidin), formycin B, which is an analog of inosine, is not phosphorylated in cells (31). However, formycin B has been reported to be a good inhibitor of human purine nucleoside phosphorylase (6,26,28) and polyadenosine diphosphoribose polymerase (20). On the contrary, Osborne et al (23) have found that inhibition of purine nucleoside phosphorylase is a secondary effect of formycin B toxicity, but the primary site of action of formycin B was not identified in these studies.…”

American Leishmania spp: Formycin B treatment of cutaneous leishmaniasis in mice

“…Variations in the number of doses (for example, only 10 consecutive doses or 20 doses given in 2 periods separated by a 2-week interval), shortened the leishmanistatic period. Furthermore, a dose of 5 mg FoB/kg body weight given as 20 consecutive injections diminished the leishmanistatic period (Table 1, see LMA, EB and LR isolates) suggesting, for example, an inhibitory effect on the host immune response (Osborne, Sullivan & Scott, 1980;Cowan, Cashman & Ammann, 1981). However, the FoB dose found to be optimal for the treatment of experimental leishmanial infection was about 200-fold lower than that reported as being toxic for mice (Ishizuka et al 1968).…”