INT158573

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Context Info
Confidence 0.43
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 10
Disease Relevance 8.20
Pain Relevance 3.99

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytoskeleton (Jak3) transcription factor binding (Jak3) cytoplasm (Jak3)
Anatomy Link Frequency
blood 2
B cells 1
Jak3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cytokine 238 99.70 Very High Very High Very High
Inflammation 197 99.30 Very High Very High Very High
Arthritis 384 99.28 Very High Very High Very High
rheumatoid arthritis 178 98.72 Very High Very High Very High
Potency 208 98.60 Very High Very High Very High
abatacept 1 98.56 Very High Very High Very High
psoriasis 24 81.60 Quite High
chemokine 3 75.56 Quite High
Inflammatory response 7 72.24 Quite High
Inflammatory marker 1 69.52 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 197 99.30 Very High Very High Very High
Arthritis 416 99.28 Very High Very High Very High
Hematological Disease 32 98.92 Very High Very High Very High
Rheumatoid Arthritis 179 98.72 Very High Very High Very High
Disease 82 95.16 Very High Very High Very High
Diabetes Mellitus 58 91.32 High High
Immunization 72 89.44 High High
Ganglion Cysts 3 88.72 High High
Pressure And Volume Under Development 24 84.76 Quite High
Psoriasis 24 81.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Based on above and other recent findings, new biological agents targeted to inflammatory cytokines such as tocilizumab, activated T cells (abatacept) or B cells (ocrelizumab), as well as new small molecule drugs such as JAK3 inhibitor, are sure to further facilitate remission without impaired activity of daily life in patients with RA.
Negative_regulation (inhibitor) of JAK3 in B cells associated with inflammation, rheumatoid arthritis, abatacept and cytokine
1) Confidence 0.43 Published 2009 Journal Nippon Rinsho Section Abstract Doc Link 19280922 Disease Relevance 0.35 Pain Relevance 0.28
Results from this study demonstrate a strong PK/PD relationship between inhibition of JAK1 and JAK3, efficacy, and the inhibition of inflammatory cytokines and neutrophilia in the rat AIA model with CP-690,550 (Tables 1 and 2, Figures 1 and 2).
Negative_regulation (inhibition) of JAK3 associated with inflammation, arthritis and cytokine
2) Confidence 0.39 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 1.27 Pain Relevance 0.62
JAK3 (janus kinase 3) expression requires cytokine signaling and inhibition of JAK3 prevents STAT3 activation [36].
Negative_regulation (inhibition) of JAK3 associated with cytokine
3) Confidence 0.32 Published 2008 Journal BMC Med Genomics Section Body Doc Link PMC2442612 Disease Relevance 0.99 Pain Relevance 0.22
The plasma concentration of CP-690,550 at efficacious doses was above the in vitro whole blood IC50 of JAK1 and JAK3 inhibition, but not that of JAK2.


Negative_regulation (inhibition) of JAK3 in blood
4) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Abstract Doc Link PMC2928212 Disease Relevance 1.04 Pain Relevance 0.58
Therefore, exposures of CP-690,550 which are associated with efficacy and PBNC reductions in human RA patients and in the rat AIA model correlate primarily with the inhibition of JAK1 and JAK3 and not that of JAK2, based on the assay results in Table 1.


Negative_regulation (inhibition) of JAK3 associated with rheumatoid arthritis and arthritis
5) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 0.37 Pain Relevance 0.23
Results from this investigation suggest that CP-690,550 is a potent inhibitor of JAK1 and JAK3 with potentially reduced cellular potency for JAK2.
Negative_regulation (inhibitor) of JAK3 associated with potency
6) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Abstract Doc Link PMC2928212 Disease Relevance 1.04 Pain Relevance 0.58
The aim of the current study was to characterize the potency and selectivity of CP-690,550 for the JAK family members and to determine if PBNC reductions in the context of arthritis are related to the anti-inflammatory efficacy of CP-690,550 (through JAK 1 and JAK3 inhibition), or due to inhibition of hematopoiesis through inhibition of JAK2 at efficacious exposures.
Negative_regulation (inhibition) of JAK3 associated with hematological disease, inflammation, arthritis and potency
7) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 1.12 Pain Relevance 0.64
Thirdly, in vitro human selectivity data suggests that clinically efficacious doses of CP-690,550 of up to 30 mg would inhibit the JAK1 and JAK3 enzymes, but not JAK2 (Tables 1 and 2).
Negative_regulation (inhibit) of JAK3
8) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 0.61 Pain Relevance 0.27
These data suggest the importance of JAK1 and JAK3 inhibition for efficacy, since ED50 exposures were below those needed for JAK2 inhibition in whole blood.
Negative_regulation (inhibition) of JAK3 in blood
9) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 0.82 Pain Relevance 0.23
Collectively, results from this investigation suggest that the reductions in PBNC in human RA patients may be an indirect consequence of the anti-inflammatory activity of CP-690,550 and/or the inhibition of JAK1 and JAK3 activity, but not JAK2.
Negative_regulation (inhibition) of JAK3 associated with inflammation and rheumatoid arthritis
10) Confidence 0.29 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2928212 Disease Relevance 0.57 Pain Relevance 0.34

General Comments

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