1 ized that these lymphocytes would respond to 
forodesine.                                             
 
     2 LL lymphocytes with 10 or 20 microM dGuo and 
forodesine (
2 microM) resulted in accumulation of higher
 
     3 h progressive disease were eligible for oral 
forodesine (
200 mg/d) for up to 24 weeks.               
 
     4 were treated with an intravenous infusion of 
forodesine (
40 mg/m2) on day 1; treatment continued on d
 
     5                         Median peak level of 
forodesine (
5.4 microM) was achieved at the end of infus
 
     6 e-based synthesis of immucillin-H (BCX-1777, 
forodesine), 
a transition-state analog of PNP.          
 
     7                                              Forodesine, 
a potent inhibitor of PNP, was designed base
 
     8                                              Forodesine, 
a purine nucleoside phosphorylase inhibitor,
 
     9 onversely, MSC viability was not affected by 
forodesine and dGuo.                                    
 
    10 rom 12 patients with CLL were incubated with 
forodesine and dGuo.                                    
 
    11 ical mechanism for MSC-derived resistance to 
forodesine and emphasizes the need to move toward combin
 
    12 d on these data, a phase 2 clinical trial of 
forodesine has been initiated for CLL patients.         
 
    13                                              Forodesine has biologic activity in CLL; pharmacodynamic
 
    14               Initial clinical data indicate 
forodesine has significant activity on circulating CLL c
 
    15 odynamic effectiveness of the PNP inhibitor, 
forodesine; 
however, regrowth of leukemia cells in the b
 
    16 fere with the purine metabolic pathway (e.g. 
forodesine), 
immunomodulatory agents, proapoptotic small
 
    17                  A phase 1 clinical trial of 
forodesine in T-cell malignancies demonstrated significa
 
    18 al studies provided the rationale for use of 
forodesine in T-cell malignancies.                      
 
    19            Previous studies established that 
forodesine in the presence of deoxyguanosine (dGuo) inhi
 
    20          We demonstrate that spontaneous and 
forodesine-
induced apoptosis of CLL cells was significan
 
    21  MSC-induced biochemical changes antagonized 
forodesine-
induced CLL cell apoptosis.                  
 
    22 the impact of marrow stromal cells (MSCs) on 
forodesine-
induced response in CLL lymphocytes.         
 
    23            Also, MSCs rescued CLL cells from 
forodesine-
induced RNA- and protein-synthesis inhibition
 
    24                                              Forodesine is a new and potent purine nucleoside phospho
 
    25                                              Forodesine-
promoted dGuo triphosphate (dGTP) accumulatio
 
    26                        Steady-state level of 
forodesine ranged from 200 to 1300 nM and did not reach 
 
    27 /m2) on day 1; treatment continued on day 2; 
forodesine was administered every 12 hours for an additi