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Libri sul tema "Inhibiteurs de JAK/STAT"

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Autore: Grafiati

Pubblicato: 22 giugno 2024

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1

Nicholson, Sandra E., e Nicos A. Nicola, a cura di. JAK-STAT Signalling. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.

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2

Anastasis, Stephanou, a cura di. JAK-STAT pathway in disease. Austin, Tex: Landes Bioscience, 2009.

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3

Decker, Thomas, e Mathias Müller, a cura di. Jak-Stat Signaling : From Basics to Disease. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.

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4

Wilks, Andrew F., e Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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5

Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.

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6

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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7

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.

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8

Stephanou, Anastasis, e Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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9

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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10

H, Bell Jr Richard. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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11

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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12

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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13

Nicola, Nicos A., e Sandra E. Nicholson. JAK-STAT Signalling: Methods and Protocols. Humana Press, 2016.

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14

Decker, Thomas, e Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer, 2012.

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15

Harpur, Ailsa G., e Andrew F. Wilks. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer, 2013.

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16

Decker, Thomas, e Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer London, Limited, 2012.

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17

Decker, Thomas, e Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer, 2012.

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18

Decker, Thomas, e Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer Wien, 2014.

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19

Wilks, Andrew F. Intracellular Signal Transduction: The Jak-Stat Pathway. Springer, 2013.

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20

The Jak-Stat pathway in hematopoiesis and disease. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2002.

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21

Harpur, Ailsa G., e Andrew F. Wilks. The Jak-Stat Pathway (Molecular Biology Intelligence Unit). Springer, 1996.

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22

Ward, Alister C. The Jak-Stat Pathway in Hematopoiesis and Disease (Molecular Biology Intelligence Unit, 20). Springer, 2002.

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23

Ng, Sze-Ling. The Role of IKKepsilon in JAK/STAT Signaling During the Antiviral Immune Response. 2010.

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24

Mahdavi, Alborz. Analysis of transient JAK/STAT signaling kinetics predicts control modules of stem cell fate control. 2006.

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25

Jakstat Signalling Methods And Protocols. Humana Press, 2012.

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26

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Abstract (sommario):

Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.