ライフサイエンスコーパス: JAK inhibitor

1 T-cell tyrosine phosphatase as an important JAK inhibitor.

2 l lines of various histological origins with JAK inhibitors.

3 ty contribute to the therapeutic efficacy of JAK inhibitors.

4 diagnosis and the development of therapeutic JAK inhibitors.

5 TEER can be suppressed with the treatment of JAK inhibitors.

6 bitor treatment but increased sensitivity to JAK inhibitors.

7 utant allele burden not observed with type I JAK inhibitors.

8 ies in vivo and with distinct sensitivity to JAK inhibitors.

9 d by targeting the JAK pathway using RNAi or JAK inhibitors.

10 therapies markedly improve when treated with JAK inhibitors.

11 d that alopecia areata might be treated with JAK inhibitors.

12 TAT1 in patients' lymphocytes was reduced by JAK inhibitors.

13 chanism of acquisition of resistance against JAK inhibitors.

14 41C and W341C/W791X exhibited sensitivity to JAK inhibitors.

15 hydroxyurea-refractory or intolerant PV with JAK inhibitors.

16 zed cytokine transcription to suppression by Jak inhibitors.

17 lead compound belonging to a novel class of JAK inhibitors.

18 ll molecule Janus family of tyrosine kinase (JAK) inhibitors.

19 itions enhanced sensitivity to Janus kinase (JAK) inhibitors.

20 ng conformation of clinically effective, pan-JAK inhibitor 1 led to identification of a novel, tricyc

21 d or topical delivery resulted in potent pan-JAK inhibitor 2 (PF-06263276), which was advanced into c

22 tibody or administration of a small-molecule JAK inhibitor, abolishes FGF19-induced tumorigenesis, wh

23 Pretreatment with the JAK inhibitor AG-490 20 min before the six occlusion/rep

24 The JAK inhibitor AG490 did not inhibit the tyrosine phospho

25 4 signaling during the decay phase using the JAK inhibitor AG490 or the anti-IL-4R(alpha) Ab M1 abrog

26 Treatment with anti-IL-6 antisera or the JAK inhibitor AG490 or transfection with dominant negati

27 ted with greater sensitivity to the chemical JAK inhibitor AG490.

28 n of kinase activity by staurosporine or the JAK inhibitor, AG490, revealed that maintenance of Stat6

29 roduction was inhibited by the Janus kinase (JAK) inhibitor, AG490, but normal ROS production was obs

30 Treatment of tumor cells with JAK inhibitors also increased susceptibility to NK cell

31 ined AML subset, which uniformly responds to JAK inhibitors and paves the way to personalized clinica

32 nd reduction in disease burden not seen with JAK inhibitors, and deletion of Jak2 following chronic r

33 ponsive to ABL tyrosine kinase inhibitors or JAK inhibitors, and seven had mutations involving the Ra

34 We believe that Jak inhibitors are a good and useful addition to the imm

35 ibitors are now in clinical trials and newer Jak inhibitors are being developed.

36 ed with inflammatory bowel disease (IBD) and JAK inhibitors are being evaluated for therapy targeting

37 The JAK inhibitors are effective in both JAK2-positive and J

38 More specific, novel Jak inhibitors are now in clinical trials and newer Jak

39 because currently available drugs, including JAK inhibitors, are palliative and not shown to be disea

40 JAK inhibitors augmented nuclear levels of NF-ATc1 and c

41 with myelofibrosis (MF) to the Janus kinase (JAK) inhibitor, AZD1480.

42 rts focus on combination trials (including a JAK inhibitor base) or targeting new pathways (ie, telom

43 y phosphorylation-defective STAT3 mutants or JAK inhibitor blocked STAT3 binding to myoferlin and nuc

44 AG 490, a JAK inhibitor, blocked JAK phosphorylation with concomit

45 First-generation pan-Jak inhibitors can be useful for a wide variety of disea

46 The JAK inhibitors consistently alleviate constitutional sym

47 tstanding properties of the kinome-selective JAK inhibitor CP-690550, as well as the challenges in ob

48 th either the PI3K inhibitor LY294002 or the JAK inhibitor CP-690550, suggesting that IL-10-mediated

49 The JAK inhibitors CP-690,550 (tofacitinib) and INCB018424 (

50 lass structure, and JAK3 in complex with PAN-JAK inhibitors CP-690550 ((3R,4R)-3-[4-methyl-3-[N-methy

51 K enzymes followed by a detailed look at the JAK inhibitors currently in the clinic or approved for t

52 nflammatory and immunomodulating activity of JAK inhibitors currently used in the treatment of MF and

53 In addition, JAK inhibitors decreased nuclear localization of NF-kapp

54 Treatment with AG490, a JAK inhibitor, decreased but did not completely abrogate

55 Studies using Pyridine 6 (P6), a pan-JAK inhibitor, demonstrate that the protective effect of

56 iated myelofibrosis, including Janus kinase (JAK) inhibitors, do not induce complete or partial remis

57 tory cytokines at lower therapeutically used JAK inhibitor doses.

58 rapeutic target for Janus-associated kinase (JAK) inhibitor drugs.

59 nhibited JAK/STAT signaling in AML LSCs, and JAK inhibitors effectively inhibited FLT3-mutated AML LS

60 Ruxolitinib and most other JAK inhibitors exert a salutary effect on constitutional

61 of CP-690,550 1, a potential first-in-class JAK inhibitor for treatment of autoimmune diseases and o

62 ded on what the past decade of research with JAK inhibitors for inflammatory indications has taught a

63 points that will support labeling claims for JAK inhibitors for the aforementioned indications.

64 neoplasms and implicates the clinical use of JAK inhibitors for this disease.

65 led to clinical development of Janus kinase (JAK) inhibitors for treatment of MPN.

66 synergistic administration of PI3K/mTOR and JAK inhibitors further abrogated leukemia development.

67 JAK inhibitors have been developed as antiinflammatory a

68 Although JAK inhibitors have important benefits in myelofibrosis

69 ot fully delineated, and clinically utilized JAK inhibitors have limited ability to reduce disease bu

70 onsistent with the clonal complexity of MPN, JAK inhibitors have not thus far shown disease-modifying

71 hanism of action of successful Janus kinase (Jak) inhibitors have revealed that, apart from T and B c

72 recently, clinical trials with Janus kinase (JAK) inhibitors have shown that cytokine receptors that

73 le cytokine signaling pathways, and as such, JAK inhibitors hold promise for treatment of autoimmune

74 The combination of JAK inhibitor I and ABT-737 reduced the number of erythr

75 , as demonstrated in vitro by treatment with JAK inhibitor I and in vivo by treatment with the JAK/ST

76 However, both JAK inhibitor I and PI3K inhibitor had no effect on the

77 Inhibition of Jak kinase activity with Jak inhibitor I completely reversed the neuroprotective

78 Transfected siRNAs of JAK molecules and JAK inhibitor I decreased IL-17A-induced gene expression

79 diated reprogramming was enhanced 10-fold on JAK inhibitor I treatment.

80 JAK1/2 inhibitors (such as ruxolitinib and JAK inhibitor I) strongly stimulate VSV replication and

81 indicated by studies with cycloheximide, the JAK inhibitor I, and small interfering RNA against STAT1

82 tworks and providing a rationale for testing JAK inhibitors in clinical trials.

83 K3/STAT6 and we propose a potential role for JAK inhibitors in combination with BCR kinase inhibitors

84 it balance favors use of currently available JAK inhibitors in only a select group of patients with m

85 y companies both on expanding the utility of JAK inhibitors in other auto-immune indications and in d

86 Importantly, JAK inhibitors increased proinflammatory cytokines secre

87 Furthermore, the palliative value of JAK inhibitors is diminished by notable side effects, in

88 Built on these findings, we showed that JAK inhibitor (JAKi) significantly reduced aberrant HSPC

89 mmatory secretome of senescent cells using a JAK inhibitor (JAKi).

90 Recently the first Jak inhibitor (jakinib) has been approved by the FDA and

91 emplified by the bench-to-bedside success of Jak inhibitors ('jakinibs') and pathway-targeting drugs.

92 JAK inhibitors may be a viable therapeutic option for th

93 We speculate that SASP inhibition by JAK inhibitors may contribute to alleviating frailty.

94 protein that was down-regulated during "all JAKs inhibitor"-mediated endoreduplication.

95 his study was to examine the effects of both JAK inhibitors on inflammatory and tumor necrosis factor

96 1), so we tested the effect of Janus kinase (JAK) inhibitors on STAT1 phosphorylation in lymphocytes

97 ad no effect on pSTAT3 levels, whereas a pan-JAK inhibitor (P6) blocked activation of STAT3 and inhib

98 JAK inhibitor, would demonstrate activity in JAK inhibitor persistent cells, murine MPN models, and M

99 s were sensitive to CHZ868, including type I JAK inhibitor persistent cells.

100 alone, conventional or investigational (eg, JAK inhibitors, pomalidomide) drug therapy, allogenic st

101 sing the therapeutic value of new drugs (eg, JAK inhibitors, pomalidomide) or allogeneic stem-cell tr

102 fication of structurally novel Janus kinase (JAK) inhibitors predicted to bind beyond the ATP binding

103 r of transcription (STAT) pathway, and a pan-JAK inhibitor protected CGNs from Rac inhibition.

104 at monotherapy of mice with tofacitinib (the JAK inhibitor) quells Ab responses to an immunotoxin der

105 Although clinically tested JAK inhibitors reduce splenomegaly and systemic symptoms

106 JAK inhibitors represent a class of immunomodulatory dru

107 Preincubation with a non-selective JAK inhibitor restored glucose uptake and Akt phosphoryl

108 We recently showed that chronic exposure to JAK inhibitors results in inhibitor persistence via JAK2

109 JAK inhibitors reversed the macrophage-induced antiviral

110 therefore, investigated the efficacy of the JAK inhibitor ruxolitinib and the mTOR inhibitor rapamyc

111 Although the JAK inhibitor ruxolitinib was recently approved for use

112 The Janus kinase (JAK) inhibitor ruxolitinib is the only approved therapy

113 The Janus kinase (JAK)-inhibitor ruxolitinib decreases constitutional symp

114 Unexpectedly, another JAK inhibitor, ruxolitinib (RUX), was ineffective in 8 o

115 ressing cells are much more sensitive to the JAK inhibitor, ruxolitinib, than JAK2V617F-expressers, s

116 A knockdown, we have demonstrated that these JAK inhibitor-sensitive cells are dependent on both JAK1

117 or IL-2Rgamma induced cell death in selected JAK inhibitor-sensitive cells.

118 n mutations were found in some, but not all, JAK inhibitor-sensitive cells.

119 JAK inhibitor sensitivity correlated with the STAT3 phos

120 ras/Irs-1(+/+) and Kras/Irs-1(-/-) mice with JAK inhibitors significantly reduced tumor burden, most

121 servations also support the incorporation of JAK inhibitors such as ruxolitinib into future clinical

122 ent TS1 clones can be efficiently blocked by JAK inhibitors such as ruxolitinib or CMP6 in short-term

123 tudies evaluating the safety and efficacy of JAK inhibitors, such as ruxolitinib, and evaluate their

124 Our findings demonstrate that JAK inhibitors suppress macrophage activation and attenu

125 JAK inhibitor suppressed senescent cell activin A produc

126 Remarkably, administration of anti-miR-9 or JAK inhibitors suppressed MV-induced cell migration in v

127 JAK inhibitors suppressed the activation and expression

128 A Janus kinase (JAK) inhibitor synergistically potentiated effects of ST

129 aling inhibitor tofacitinib, a Janus kinase (JAK) inhibitor targeting JAK3 and JAK1.

130 ed a uniform and specific sensitivity to all JAK inhibitors tested irrespective of their CSF3R mutati

131 these results show that 6BIO is a novel pan-JAK inhibitor that can selectively inhibit STAT3 signali

132 We found that 6BIO is a pan-JAK inhibitor that induces apoptosis of human melanoma c

133 why would they choose ruxolitinib over other JAK inhibitors that are freely available for use in a re

134 d that MPN cells become persistent to type I JAK inhibitors that bind the active conformation of JAK2

135 defense and a negative role of an intrinsic JAK inhibitor, the suppressor of cytokine signaling (SOC

136 m which CM was derived had been treated with JAK inhibitors, the resulting CM was much less proinflam

137 Therefore, JAK inhibitor therapy might benefit patients with ALK- A

138 eligibility criteria; 48% had received prior JAK inhibitor therapy.

139 ependent ALL and can overcome persistence to JAK-inhibitor therapy in ALL cells.

140 The administration of JAK inhibitor to aged mice for 10 wk alleviated both adi

141 erefore, the ability of structurally diverse JAK inhibitors to block IL-6-induced MMP-9 expression wa

142 These findings highlight the potential of JAK inhibitors to counteract stroma-induced resistance t

143 uppressive drugs targeting this pathway, the JAK inhibitor tofacitinib (CP-690,550) and the anti-inte

144 The JAK inhibitor tofacitinib effectively suppresses tissue-

145 These results suggest that the JAK inhibitor tofacitinib suppresses osteoclast-mediated

146 treatment of T cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionately altered th

147 btained with a second structurally unrelated Jak inhibitor, Tofacitinib.

148 JAK inhibitor treatment is limited by the variable devel

149 at the thrombocytopenia frequently seen with JAK inhibitor treatment is not due to JAK2 inhibition in

150 e 3 Controlled Myelofibrosis Study with Oral JAK Inhibitor Treatment-I trial, patients with MF, post-

151 -I (Controlled Myelofibrosis Study With Oral JAK Inhibitor Treatment-I) is a double-blind, placebo-co

152 sitivity of JAK1-mutated primary SS cells to JAK inhibitor treatment.

153 sis Study With Oral Janus-associated Kinase (JAK) Inhibitor Treatment-II (the COMFORT-II Trial), comp

154 Here, we review the current experience with JAK inhibitors used for the treatment of myelofibrosis a

155 Moreover, JAK inhibitors were effective in prolonging survival of

156 The in vivo effects of JAK inhibitors were evaluated in the K/BxN serum-transfe

157 G2-M arrest and endoreduplication induced by JAK inhibitors were reduced in cells pretreated with PD9

158 ain that confer resistance across a panel of JAK inhibitors, whether present in cis with JAK2 V617F (

159 y reduced after 7 days of treatment with the JAK inhibitor, which correlated with reduced numbers of

160 leukemia transformation, but it appears that JAK inhibitors will offer an important palliative option

161 of indazoles was identified as selective pan-JAK inhibitors with a type 1.5 binding mode.

162 rent therapeutic results, the combination of JAK inhibitors with other agents is currently being test

163 cal trials for patients with MF focus on new JAK inhibitors with potentially less myelosuppression( p

164 ore, it is of interest to identify optimized JAK inhibitors with unique profiles to maximize therapeu

165 We investigated whether CHZ868, a type II JAK inhibitor, would demonstrate activity in JAK inhibit

166 kinase inhibitors, the first such drug (the JAK inhibitor Xeljanz, tofacitinib) was approved by the