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1  relapse can be successfully re-treated with cladribine.
2 rferon alfa-2a and alfa-2b, pentostatin, and cladribine.
3 ens the duration of severe neutropenia after cladribine.
4  monocytes, we conducted a phase II trial of cladribine.
5 o relapse can be successfully retreated with cladribine.
6 to chlorambucil, cisplatin, carboplatin, and cladribine.
7 and on MRI findings in patients treated with cladribine.
8 iagnosis of hairy cell leukemia treated with cladribine.
9 nd poor response to standard treatments like cladribine.
10 stituent at the 2-position present in dG and cladribine.
11 erienced relapse after their first course of cladribine.
12 ended follow-up of HCL patients treated with cladribine.
13        In the first year patients were given cladribine 0.10 mg/kg per day for 7 days as four monthly
14         Of 16 patients who were resistant to cladribine, 11 had a complete remission and 2 had a part
15                      Eight patients received cladribine 12 mg/m(2) continuous infusion for 5 days wit
16 om diagnosis, 18 years; and median time from cladribine, 16 years).
17                    To assess the efficacy of cladribine (2-chloro-2'-deoxyadenosine) in the treatment
18  high yields of the clinical anticancer drug cladribine (2-chloro-2'-deoxyadenosine).
19 rt efficient syntheses of the clinical agent cladribine (2-chloro-2'-deoxyadenosine, CldAdo), which i
20                                        Since cladribine (2-chlorodeoxyadenosine [2-CdA]) and mitoxant
21                                              Cladribine (2-chlorodeoxyadenosine [2-CdA]) is a synthet
22                                              Cladribine (2-chlorodeoxyadenosine [2-CdA]; Ortho Biotec
23                                              Cladribine (2-chlorodeoxyadenosine) induces complete rem
24 ability (F value) of 2-chlorodeoxyadenosine (cladribine; 2-CdA) after multiple oral administrations,
25   Having relapsed after prior treatment with cladribine, 24 HCL pts (21 male, 3 female) with a median
26 d to evaluate the effectiveness of high-dose cladribine (2CDA) for treatment of chronic myelogenous l
27            The optimal dose and schedule for cladribine (2CdA) therapy of malignant hematologic disea
28 lity to transport the nucleoside analog drug cladribine, 2CdA, (rCNT2 > > > hCNT2) to identify the cr
29 ents received cladribine 5.25 mg/kg (n=204), cladribine 3.5 mg/kg (n=206), or placebo (n=206).
30 r 96 weeks, 178 (44%) of 402 patients in the cladribine 3.5 mg/kg group and 189 (46%) of 411 patients
31 r 48 weeks, 208 (54%) of 384 patients in the cladribine 3.5 mg/kg group and 222 (56%) of 396 patients
32 r 24 weeks, 266 (67%) of 395 patients in the cladribine 3.5 mg/kg group and 283 (70%) of 406 in the c
33  5.25 mg/kg group, 168 (82%) patients in the cladribine 3.5 mg/kg group, and 162 (79%) patients in th
34  other treatments; 5 pts were retreated with cladribine, 3 underwent splenectomy, and 1 received pent
35 essed for eligibility, 616 patients received cladribine 5.25 mg/kg (n=204), cladribine 3.5 mg/kg (n=2
36 g group and 189 (46%) of 411 patients in the cladribine 5.25 mg/kg group were free from disease activ
37  3.5 mg/kg group and 283 (70%) of 406 in the cladribine 5.25 mg/kg group were free from disease activ
38 g group and 222 (56%) of 396 patients in the cladribine 5.25 mg/kg group were free from disease activ
39 s were reported in 165 (81%) patients in the cladribine 5.25 mg/kg group, 168 (82%) patients in the c
40                                              Cladribine 5.6 mg/m(2) given IV over 2 hours daily for 5
41 ilure of one prior chemotherapy (n = 2) with cladribine (5.6 mg/m(2) given intravenously over 2 hours
42 day courses of Ara-C (1 g/m(2) per day) plus cladribine (9 mg/m(2) per day) followed by maintenance t
43          2-Chloro-2'-deoxyadenosine [CldAdo (cladribine)], a novel effective antileukemic agent, was
44 previous observations that single courses of cladribine administered to patients with HCL induce high
45               The median number of cycles of cladribine administered was 2.5 (range, 1-6).
46                          In addition, dG and cladribine adopt the anti conformation, in contrast to t
47 ared with 105 historic controls treated with cladribine alone.
48 ssover study was started in 1992 to evaluate cladribine, an immunosuppressive drug, in the treatment
49     An international phase 2 study combining cladribine and cytarabine (Ara-C) was initiated for pati
50                                              Cladribine and interferon alpha were therapeutically the
51              Although the nucleoside analogs cladribine and pentostatin produce high response rates i
52 eatment with the nucleoside purine analogues cladribine and pentostatin results in lengthy remissions
53 ed a study of priming filgrastim followed by cladribine and then filgrastim again to determine if fil
54 Thirty-five patients received filgrastim and cladribine and were compared with 105 historic controls
55  antineoplastic, 2-chloro-2'-deoxyadenosine (cladribine) and puromycin, a protein synthesis inhibitor
56 lzomib), nucleoside analogs (fludarabine and cladribine), and ibrutinib.
57 ncer nucleoside drugs, including cytarabine, cladribine, and fludarabine.
58 ssion-free survival (P = .007) after initial cladribine, and shorter overall survival from diagnosis
59                     Thus, the combination of cladribine/Ara-C is effective therapy for refractory mul
60 s with hairy cell leukemia were treated with cladribine at 0.087 or 0.1 mg/kg body weight per day by
61 showed that short-course oral treatment with cladribine at cumulative doses of 3.5 and 5.25 mg/kg ove
62 able patients treated with second courses of cladribine at first relapse, 33 (62%) achieved complete
63 f purine nucleoside analogs (pentostatin and cladribine) changed the natural history of this rare dis
64  of phase 3 trials and cross-study analyses, cladribine compared favorably with fludarabine, another
65                                  A course of cladribine constituted a 7-day continuous intravenous in
66 urvival for all patients following the first cladribine course was 231 months, and 251 months from di
67           From the 358-person Scripps Clinic cladribine database, we identified 19 patients in contin
68 le, has only modest single-agent activity in cladribine-failed HCL patients when compared with other
69                 Best responses to BL22 after cladribine failure are achieved before the patients deve
70 y to determine the feasibility and safety of cladribine followed by rituximab in patients with hairy
71                               Treatment with cladribine followed by rituximab is effective tk;4and ma
72 pproved novel agents may act in synergy with cladribine for these conditions and should be incorporat
73 /=40 years of age at diagnosis) treated with cladribine from the Scripps Clinic HCL Database, of whom
74 dverse events that were more frequent in the cladribine groups included lymphocytopenia (21.6% in the
75 nine patients with HCL who were treated with cladribine had at least 7 years of follow-up.
76                                              Cladribine has been noted to have particular activity am
77                                              Cladribine has high efficacy and a favorable acute and l
78                                        Thus, cladribine has major activity in adult LCH and warrants
79                                              Cladribine has moderate clinical efficacy in the treatme
80 o treatment with purine analogues, including cladribine, has a poor prognosis.
81 rete et al report the safety and efficacy of cladribine in 68 adult patients with mastocytosis.
82 ately 10-fold loss of cytostatic activity of cladribine in MCF-7.Hyor cells and observed a rapid and
83 he routine adjunctive use of filgrastim with cladribine in the treatment of HCL cannot be recommended
84 cal advantage from the use of filgrastim and cladribine in the treatment of HCL.
85 toreductive therapies (eg, interferon-alpha, cladribine) in this setting.
86                            Single courses of cladribine induce high rates of complete and durable res
87 t B-cell disorder in which single courses of cladribine induce high rates of complete responses.
88          The purine analogs, pentostatin and cladribine, induce high remission rates when used as fir
89                            Single courses of cladribine induced long-lasting complete responses in th
90                                              Cladribine induces protracted remissions in patients wit
91                                        While cladribine is best known for the treatment of hairy cell
92                Kinetic analysis reveals that cladribine is phosphorylated at the highest efficiency w
93                                      Because cladribine is potently toxic to monocytes, we conducted
94 e analog 2-chloro-2'-deoxyadenosine (CldAdo; cladribine) is effective in the treatment of hairy cell
95 re stratified into three groups: response to cladribine less than 1 year, those with a response lasti
96 e initial very high response rates following cladribine, many patients (pts) ultimately relapse.
97 bine/melphalan combination and 87.5% for the cladribine/melphalan combination.
98 for relapsed/refractory HCL after first-line cladribine (n = 3) or after multiple lines of therapy (n
99 e 3 study we investigated the effect of oral cladribine on conversion to clinically definite MS in pa
100  we therefore aimed to assess the effects of cladribine on this composite outcome measure by doing a
101 ate whether the addition of a purine analog, cladribine or fludarabine, to the standard induction reg
102 (daunorubicin plus cytarabine), DAC (DA plus cladribine), or DAF (DA plus fludarabine).
103 T1), accumulation of [(3)H]cytarabine, [(3)H]cladribine, or [(3)H]fludarabine was reduced by each of
104 nhanced cytotoxicity induced by fludarabine, cladribine, or chlorambucil.
105 rtial response (PR) after a single course of cladribine (overall response rate, 100%).
106             Many treatments exist, including cladribine, pentostatin, interferon-alpha, splenectomy,
107 nfusions of 0.10 mg, 0.05 mg, and 0.05 mg of cladribine per kg of body weight per day for 7 consecuti
108                                              Cladribine provides immunomodulation through selective t
109 e analogues of medicinal importance, such as cladribine, require phosphorylation by deoxycytidine kin
110                                     However, cladribine's impressive activity in other lymphoprolifer
111  single-arm phase 2 trials have demonstrated cladribine's potency across the full spectrum of lymphoi
112                                Both doses of cladribine significantly delayed MS diagnosis compared w
113 ents, the condition of patients who received cladribine stabilized or even improved slightly.
114                  Among patients who received cladribine tablets (either 3.5 mg or 5.25 mg per kilogra
115 io to receive one of two cumulative doses of cladribine tablets (either 3.5 mg or 5.25 mg per kilogra
116 ng were randomly assigned (1:1:1) to receive cladribine tablets at cumulative doses of 5.25 mg/kg or
117                               The effects of cladribine tablets on freedom from disease activity were
118                               Treatment with cladribine tablets significantly increased the proportio
119                               Treatment with cladribine tablets significantly reduced relapse rates,
120 s clinical and MRI measurements, the phase 3 Cladribine Tablets Treating Multiple Sclerosis Orally (C
121       We assessed the effect of two doses of cladribine tablets versus placebo on the proportion of p
122 .26 x 10(9)/L (2.5-fold increase), and after cladribine, the median nadir ANC in the filgrastim-treat
123                                              Cladribine therapy in first-line treatment or later.
124             Response to initial single-agent cladribine therapy is suboptimal; these patients should
125              Their median age at the time of cladribine therapy was 62 years (age range, 40-78 years)
126              Among patients who responded to cladribine therapy, the median duration of clinical resp
127          We attribute this to the ability of cladribine to combine advantageous properties from dA (f
128 iency of PNPHyor-catalyzed phosphorolysis of cladribine to its less toxic base 2-chloroadenine (Km =
129                              The addition of cladribine to the standard induction regimen is associat
130  could clarify the potential effects of oral cladribine treatment in the early stages of MS.
131                                              Cladribine treatment of hairy cell leukemia (HCL) is com
132 dicate that HCL is potentially curable after cladribine treatment.
133 nd -1 and then again after the completion of cladribine until the absolute neutrophil count (ANC) was
134                                              Cladribine was administered at 0.1 mg/kg/d by continuous
135                                              Cladribine was administered to 13 LCH patients at 0.14 m
136  small study of patients with de novo B-PLL, cladribine was an active agent that induced a high overa
137        At trial termination on Oct 25, 2011, cladribine was associated with a risk reduction versus p
138 ationally designed antineoplastic therapies, cladribine was identified as a lymphocyte-specific agent
139                        The safety profile of cladribine was similar to that noted in a trial in patie
140                                              Cladribine was the most commonly used chemotherapeutic a
141                                              Cladribine was used as the first-line treatment in 9 pat
142 atients who had been treated previously with cladribine were crossed over to placebo.
143 nders subsequent to a single 7-day course of cladribine were without minimal residual disease (MRD) a

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