ライフサイエンスコーパス: cladribine

1 erienced relapse after their first course of cladribine.

2 ended follow-up of HCL patients treated with cladribine.

3 relapse can be successfully re-treated with cladribine.

4 rferon alfa-2a and alfa-2b, pentostatin, and cladribine.

5 ens the duration of severe neutropenia after cladribine.

6 monocytes, we conducted a phase II trial of cladribine.

7 o relapse can be successfully retreated with cladribine.

8 to chlorambucil, cisplatin, carboplatin, and cladribine.

9 and on MRI findings in patients treated with cladribine.

10 results from the hypomethylating activity of cladribine.

11 ions), in particular synergy with insults by cladribine.

12 iagnosis of hairy cell leukemia treated with cladribine.

13 limod, dimethyl fumarate, teriflunomide, and cladribine.

14 nd poor response to standard treatments like cladribine.

15 stituent at the 2-position present in dG and cladribine.

16 In the first year patients were given cladribine 0.10 mg/kg per day for 7 days as four monthly

17 atients were randomly assigned to first-line cladribine 0.15 mg/kg intravenously days 1-5 with 8 week

18 Of 16 patients who were resistant to cladribine, 11 had a complete remission and 2 had a part

19 Eight patients received cladribine 12 mg/m(2) continuous infusion for 5 days wit

20 om diagnosis, 18 years; and median time from cladribine, 16 years).

21 To assess the efficacy of cladribine (2-chloro-2'-deoxyadenosine) in the treatment

22 high yields of the clinical anticancer drug cladribine (2-chloro-2'-deoxyadenosine).

23 rt efficient syntheses of the clinical agent cladribine (2-chloro-2'-deoxyadenosine, CldAdo), which i

24 Since cladribine (2-chlorodeoxyadenosine [2-CdA]) and mitoxant

25 Cladribine (2-chlorodeoxyadenosine [2-CdA]) is a synthet

26 Cladribine (2-chlorodeoxyadenosine [2-CdA]; Ortho Biotec

27 Cladribine (2-chlorodeoxyadenosine) induces complete rem

28 ability (F value) of 2-chlorodeoxyadenosine (cladribine; 2-CdA) after multiple oral administrations,

29 Having relapsed after prior treatment with cladribine, 24 HCL pts (21 male, 3 female) with a median

30 d to evaluate the effectiveness of high-dose cladribine (2CDA) for treatment of chronic myelogenous l

31 The optimal dose and schedule for cladribine (2CdA) therapy of malignant hematologic disea

32 lity to transport the nucleoside analog drug cladribine, 2CdA, (rCNT2 > > > hCNT2) to identify the cr

33 ents received cladribine 5.25 mg/kg (n=204), cladribine 3.5 mg/kg (n=206), or placebo (n=206).

34 r 96 weeks, 178 (44%) of 402 patients in the cladribine 3.5 mg/kg group and 189 (46%) of 411 patients

35 r 48 weeks, 208 (54%) of 384 patients in the cladribine 3.5 mg/kg group and 222 (56%) of 396 patients

36 r 24 weeks, 266 (67%) of 395 patients in the cladribine 3.5 mg/kg group and 283 (70%) of 406 in the c

37 5.25 mg/kg group, 168 (82%) patients in the cladribine 3.5 mg/kg group, and 162 (79%) patients in th

38 other treatments; 5 pts were retreated with cladribine, 3 underwent splenectomy, and 1 received pent

39 essed for eligibility, 616 patients received cladribine 5.25 mg/kg (n=204), cladribine 3.5 mg/kg (n=2

40 g group and 189 (46%) of 411 patients in the cladribine 5.25 mg/kg group were free from disease activ

41 3.5 mg/kg group and 283 (70%) of 406 in the cladribine 5.25 mg/kg group were free from disease activ

42 g group and 222 (56%) of 396 patients in the cladribine 5.25 mg/kg group were free from disease activ

43 s were reported in 165 (81%) patients in the cladribine 5.25 mg/kg group, 168 (82%) patients in the c

44 Cladribine 5.6 mg/m(2) given IV over 2 hours daily for 5

45 Consolidation was cladribine (5 mg/m(2)) and cytarabine (1 g/m(2) for pati

46 Patients received cladribine (5 mg/m(2)) and cytarabine (1.5 g/m(2) for pa

47 ilure of one prior chemotherapy (n = 2) with cladribine (5.6 mg/m(2) given intravenously over 2 hours

48 day courses of Ara-C (1 g/m(2) per day) plus cladribine (9 mg/m(2) per day) followed by maintenance t

49 2-Chloro-2'-deoxyadenosine [CldAdo (cladribine)], a novel effective antileukemic agent, was

50 Compared with CDAR, delayed rituximab after cladribine achieved lower rate (67% of 21 evaluable pati

51 Cladribine acts in a highly effective subtype-specific m

52 previous observations that single courses of cladribine administered to patients with HCL induce high

53 The median number of cycles of cladribine administered was 2.5 (range, 1-6).

54 In addition, dG and cladribine adopt the anti conformation, in contrast to t

55 ared with 105 historic controls treated with cladribine alone.

56 ssover study was started in 1992 to evaluate cladribine, an immunosuppressive drug, in the treatment

57 Of the 1587 patients (485 taking cladribine and 1102 taking S1PRMs), matching yielded 475

58 opoietic stem cell transplant is superior to cladribine and alemtuzumab at suppressing relapses and e

59 ansplant vs. immune-reconstitution therapies cladribine and alemtuzumab.

60 An international phase 2 study combining cladribine and cytarabine (Ara-C) was initiated for pati

61 es (hematopoietic stem-cell transplantation, cladribine and cytarabine, anti-MEK agent, vinblastine,

62 Cladribine and interferon alpha were therapeutically the

63 Although the nucleoside analogs cladribine and pentostatin produce high response rates i

64 eatment with the nucleoside purine analogues cladribine and pentostatin results in lengthy remissions

65 frontline chemotherapy with purine analogs (cladribine and pentostatine).

66 m cell transplantation, the oral formulation cladribine and the monoclonal antibodies alemtuzumab, ri

67 ed a study of priming filgrastim followed by cladribine and then filgrastim again to determine if fil

68 Thirty-five patients received filgrastim and cladribine and were compared with 105 historic controls

69 fically deplete lymphocytes (alemtuzumab and cladribine) and autologous haematopoietic stem cell tran

70 antineoplastic, 2-chloro-2'-deoxyadenosine (cladribine) and puromycin, a protein synthesis inhibitor

71 lzomib), nucleoside analogs (fludarabine and cladribine), and ibrutinib.

72 1-phosphate receptor modulators, fumarates, cladribine, and 3 types of monoclonal antibodies.

73 ncer nucleoside drugs, including cytarabine, cladribine, and fludarabine.

74 ssion-free survival (P = .007) after initial cladribine, and shorter overall survival from diagnosis

75 Thus, the combination of cladribine/Ara-C is effective therapy for refractory mul

76 s with hairy cell leukemia were treated with cladribine at 0.087 or 0.1 mg/kg body weight per day by

77 showed that short-course oral treatment with cladribine at cumulative doses of 3.5 and 5.25 mg/kg ove

78 able patients treated with second courses of cladribine at first relapse, 33 (62%) achieved complete

79 f purine nucleoside analogs (pentostatin and cladribine) changed the natural history of this rare dis

80 othesized that the addition of venetoclax to cladribine (CLAD)/low-dose araC (low-dose cytarabine [LD

81 of phase 3 trials and cross-study analyses, cladribine compared favorably with fludarabine, another

82 A course of cladribine constituted a 7-day continuous intravenous in

83 g that this group specifically benefits from cladribine-containing therapy.

84 urvival for all patients following the first cladribine course was 231 months, and 251 months from di

85 8, mortality first declined with combination cladribine-cytarabine therapy and then with MAPK inhibit

86 d with daunorubicine + cytarabine (DA), DA + cladribine (DAC), or DA + fludarabine.

87 factor and idarubicin (FLAG-Ida) or DA with cladribine (DAC).

88 From the 358-person Scripps Clinic cladribine database, we identified 19 patients in contin

89 le, has only modest single-agent activity in cladribine-failed HCL patients when compared with other

90 Best responses to BL22 after cladribine failure are achieved before the patients deve

91 y to determine the feasibility and safety of cladribine followed by rituximab in patients with hairy

92 Treatment with cladribine followed by rituximab is effective tk;4and ma

93 pproved novel agents may act in synergy with cladribine for these conditions and should be incorporat

94 /=40 years of age at diagnosis) treated with cladribine from the Scripps Clinic HCL Database, of whom

95 dverse events that were more frequent in the cladribine groups included lymphocytopenia (21.6% in the

96 nine patients with HCL who were treated with cladribine had at least 7 years of follow-up.

97 Cladribine has been noted to have particular activity am

98 Cladribine has high efficacy and a favorable acute and l

99 Thus, cladribine has major activity in adult LCH and warrants

100 Cladribine has moderate clinical efficacy in the treatme

101 o treatment with purine analogues, including cladribine, has a poor prognosis.

102 Single-agent purine analog, usually cladribine, has been the standard first-line therapy of

103 Because some oral treatments, such as cladribine, have long-lasting effects on the immune syst

104 d 3 days of an anthracycline ("7+3") CLAG-M (cladribine, high-dose cytarabine, granulocyte colony-sti

105 to intensive chemotherapy (the CLIA regimen [cladribine, high-dose cytarabine, idarubicin]).

106 was mainly driven by reduced PIRA risk with cladribine (HR, 0.40; 95% CI, 0.20-0.79; P = .009), with

107 rete et al report the safety and efficacy of cladribine in 68 adult patients with mastocytosis.

108 staurin compensated the inferior efficacy of cladribine in first- and second-line treatment.

109 ately 10-fold loss of cytostatic activity of cladribine in MCF-7.Hyor cells and observed a rapid and

110 we compared the efficacy of midostaurin and cladribine in patients with advanced systemic mastocytos

111 midostaurin revealed superior efficacy over cladribine in patients with AdvSM.

112 he routine adjunctive use of filgrastim with cladribine in the treatment of HCL cannot be recommended

113 cal advantage from the use of filgrastim and cladribine in the treatment of HCL.

114 toreductive therapies (eg, interferon-alpha, cladribine) in this setting.

115 Single courses of cladribine induce high rates of complete and durable res

116 t B-cell disorder in which single courses of cladribine induce high rates of complete responses.

117 The purine analogs, pentostatin and cladribine, induce high remission rates when used as fir

118 Single courses of cladribine induced long-lasting complete responses in th

119 Cladribine induces protracted remissions in patients wit

120 While cladribine is best known for the treatment of hairy cell

121 chieving MRD-free CR of HCL after first-line cladribine is greatly enhanced by concurrent rituximab a

122 Kinetic analysis reveals that cladribine is phosphorylated at the highest efficiency w

123 Because cladribine is potently toxic to monocytes, we conducted

124 e analog 2-chloro-2'-deoxyadenosine (CldAdo; cladribine) is effective in the treatment of hairy cell

125 re stratified into three groups: response to cladribine less than 1 year, those with a response lasti

126 e initial very high response rates following cladribine, many patients (pts) ultimately relapse.

127 bine/melphalan combination and 87.5% for the cladribine/melphalan combination.

128 tially (midostaurin-cladribine, n = 30, 57%; cladribine-midostaurin, n = 23, 43%).

129 Compared with cladribine monotherapy, CDAR led to brief grade 3/4 thro

130 At 6 months after CDAR versus cladribine monotherapy, CR rates were 100% versus 88% (P

131 for relapsed/refractory HCL after first-line cladribine (n = 3) or after multiple lines of therapy (n

132 (n = 23, 17%), or sequentially (midostaurin-cladribine, n = 30, 57%; cladribine-midostaurin, n = 23,

133 e 3 study we investigated the effect of oral cladribine on conversion to clinically definite MS in pa

134 mparison of efficacy between midostaurin and cladribine on response (eg, organ dysfunction, bone marr

135 we therefore aimed to assess the effects of cladribine on this composite outcome measure by doing a

136 treated with midostaurin only (n = 63, 45%), cladribine only (n = 23, 17%), or sequentially (midostau

137 Midostaurin only was superior to cladribine only with effects from responses on MC and no

138 tologous hematopoietic stem cell transplant, cladribine or alemtuzumab, with a minimum of 2-month fol

139 tment-naive patients with RRMS who initiated cladribine or an S1PRM (fingolimod, ozanimod, or ponesim

140 Initiation of cladribine or an S1PRM, with duration reflecting clinica

141 ate whether the addition of a purine analog, cladribine or fludarabine, to the standard induction reg

142 d-up for a mean of 3.8-3.9 (stem cell), 1.9 (cladribine) or 4.5 years (alemtuzumab).

143 (daunorubicin plus cytarabine), DAC (DA plus cladribine), or DAF (DA plus fludarabine).

144 T1), accumulation of [(3)H]cytarabine, [(3)H]cladribine, or [(3)H]fludarabine was reduced by each of

145 nhanced cytotoxicity induced by fludarabine, cladribine, or chlorambucil.

146 rtial response (PR) after a single course of cladribine (overall response rate, 100%).

147 Many treatments exist, including cladribine, pentostatin, interferon-alpha, splenectomy,

148 nfusions of 0.10 mg, 0.05 mg, and 0.05 mg of cladribine per kg of body weight per day for 7 consecuti

149 ored, including high-dose anti-CD20 therapy, cladribine, proteasome inhibitors, BTK inhibitors, CNS-p

150 Cladribine provides immunomodulation through selective t

151 e analogues of medicinal importance, such as cladribine, require phosphorylation by deoxycytidine kin

152 ML cells with R140Q or R172K IDH2 mutations, cladribine restrained mutations-related DNA hypermethyla

153 combinations (in vitro and in mice) included cladribine, romidepsin ([H]DAC), venetoclax (BCL2), and/

154 However, cladribine's impressive activity in other lymphoprolifer

155 single-arm phase 2 trials have demonstrated cladribine's potency across the full spectrum of lymphoi

156 Cladribine sensitivity correlated with expression of its

157 After 36 months, patients treated with cladribine showed higher relapse risk (HR, 1.81; 95% CI,

158 Both doses of cladribine significantly delayed MS diagnosis compared w

159 ents, the condition of patients who received cladribine stabilized or even improved slightly.

160 Compared to cladribine, stem cell transplant was associated with a l

161 Among patients who received cladribine tablets (either 3.5 mg or 5.25 mg per kilogra

162 io to receive one of two cumulative doses of cladribine tablets (either 3.5 mg or 5.25 mg per kilogra

163 ng were randomly assigned (1:1:1) to receive cladribine tablets at cumulative doses of 5.25 mg/kg or

164 The effects of cladribine tablets on freedom from disease activity were

165 Treatment with cladribine tablets significantly increased the proportio

166 Treatment with cladribine tablets significantly reduced relapse rates,

167 s clinical and MRI measurements, the phase 3 Cladribine Tablets Treating Multiple Sclerosis Orally (C

168 changes in immune cell composition following cladribine tablets treatment and reveal immune homeostas

169 We assessed the effect of two doses of cladribine tablets versus placebo on the proportion of p

170 ing multiple sclerosis patients treated with cladribine tablets.

171 identify a promising therapeutic candidate, cladribine, that has not previously been linked to HCC t

172 .26 x 10(9)/L (2.5-fold increase), and after cladribine, the median nadir ANC in the filgrastim-treat

173 Cladribine therapy in first-line treatment or later.

174 Response to initial single-agent cladribine therapy is suboptimal; these patients should

175 Their median age at the time of cladribine therapy was 62 years (age range, 40-78 years)

176 Among patients who responded to cladribine therapy, the median duration of clinical resp

177 We attribute this to the ability of cladribine to combine advantageous properties from dA (f

178 We next evaluated the effect of addition of cladribine to induction regimen on the patients' outcome

179 iency of PNPHyor-catalyzed phosphorolysis of cladribine to its less toxic base 2-chloroadenine (Km =

180 The addition of cladribine to the standard induction regimen is associat

181 The matching of 143 (stem cell) to 283 cladribine-treated patients and of 134 (stem cell) to 56

182 could clarify the potential effects of oral cladribine treatment in the early stages of MS.

183 Cladribine treatment of hairy cell leukemia (HCL) is com

184 dicate that HCL is potentially curable after cladribine treatment.

185 nd -1 and then again after the completion of cladribine until the absolute neutrophil count (ANC) was

186 For the cladribine vs S1PRM groups, no significant differences w

187 ally crucial, yet robust comparative data on cladribine vs sphingosine-1-phosphate receptor modulator

188 Cladribine was administered at 0.1 mg/kg/d by continuous

189 Cladribine was administered to 13 LCH patients at 0.14 m

190 small study of patients with de novo B-PLL, cladribine was an active agent that induced a high overa

191 Cladribine was associated with a lower risk of disabilit

192 At trial termination on Oct 25, 2011, cladribine was associated with a risk reduction versus p

193 These findings suggest cladribine was associated with superior effectiveness in

194 ationally designed antineoplastic therapies, cladribine was identified as a lymphocyte-specific agent

195 The safety profile of cladribine was similar to that noted in a trial in patie

196 Cladribine was the most commonly used chemotherapeutic a

197 Cladribine was used as the first-line treatment in 9 pat

198 atients who had been treated previously with cladribine were crossed over to placebo.

199 Clofarabine and cladribine were ENT1 and ENT2 substrates, whereas nevira

200 nders subsequent to a single 7-day course of cladribine were without minimal residual disease (MRD) a

201 estigations of induction protocols combining cladribine with IDH1/2 inhibitors in IDH2-mutant.