Books on the topic 'Tissuee inhibitors of metalloproteinase'

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1

Gupta, Satya Prakash, ed. Matrix Metalloproteinase Inhibitors. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0364-9.

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2

Viani, Mary Anne. Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in the hematopoietic microenvironment. Ottawa: National Library of Canada, 2000.

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3

Clendeninn, Neil J., and Krzysztof Appelt. Matrix Metalloproteinase Inhibitors in Cancer Therapy. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/159259011x.

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4

Clendeninn, Neil J., and Krzysztof Appelt, eds. Matrix Metalloproteinase Inhibitors in Cancer Therapy. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1007/978-1-59259-011-7.

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5

McElligott, Anthony M. The role of matrix metalloproteinases and their inhibitors, the tissue inhibitors of metalloproteinases, in renal cell carcinoma cell invasion and metastasis. [S.l: The Author], 1999.

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6

Inhibitors of Metalloproteinases Conference (1996 Banff, Alta.). Tissue inhibitors of metalloproteinases in development and disease: Proceedings of the Inhibitors of Metalloproteinases Conference, Banff, Alberta, Canada, September 25-29, 1996. Edited by Hawkes Susan P, Edwards Dylan R, and Khokha Rama. Australia: Harwood Academic, 2000.

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7

Gupta, Satya Prakash. Matrix metalloproteinase inhibitors: Specificity of binding and structure-activity relationships. Basel: Springer, 2012.

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8

J, Saklatvala, Nagase Hideaki, and Salvesen G, eds. Proteases and the regulation of biological processes. London: Portland Press, 2003.

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9

Reid, Helen M. Tissue inhibitors of matrix metalloproteinases are modulated differently by 12-0-Tetradeconoylphorbol-13-actate (TPA) and 1,1,1-Trichoro-2,2-Bis-(p-Chlorophenyl)-ethane (DDT). [S.l: The Author], 1997.

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10

Matrix Metalloproteinase Conference (1989 Sandestin Beach, Fla.). Matrix metalloproteinases and inhibitors: Proceedings of the Matrix Metalloproteinase Conference held at Sandestin Beach, FL, September 11-15, 1989. Edited by Birkedal-Hansen Henning. Stuttgart: G. Fischer Verlag, 1992.

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11

Tissue Inhibitors of Metalloproteinase in Development and Disease (TIMPs '96). CRC, 2000.

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12

Mohammed, Fazilat Fatima. Tissue inhibitors of metalloproteinases (TIMPS) in hepatic regeneration and tissue homeostasis. 2004.

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13

Tissue inhibitors of metalloproteinases in development and disease: Proceedings of the Inhibitors of Metalloproteinases Conference, held at Banff, Alberta, Canada, September 25-29, 1996. [Amsterdam]: Harwood Academic, 2000.

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14

Matrix Metalloproteinase Inhibitors in Cancer Therapy. Humana Press, 2012.

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15

various. Matrix Metalloproteinase Inhibitors in Cancer Therapy. Humana Press, 2011.

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16

Clendeninn, Neil J., and Krzysztof Appelt. Matrix Metalloproteinase Inhibitors in Cancer Therapy. Humana Press, 2000.

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17

Katherine, Conant, and Gottschall Paul E, eds. Matrix metalloproteinases in the central nervous system. London: Imperial College Press, 2005.

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18

Flenniken, Ann Marie. Expression of tissue inhibitor of metalloproteinases (TIMP) in the mouse. 1990.

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19

Fata, Jimmie Eugene. Tissue inhibitors of metalloproteinases (TIMPs) in mammary gland morphogenesis, differentiation, and apoptosis. 2001.

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20

Gupta, Satya Prakash. Matrix Metalloproteinase Inhibitors: Specificity of Binding and Structure-Activity Relationships. Springer, 2014.

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21

Fedak, Paul William Michael. Mechanisms of cardiac remodeling and failure: Role of the tissue inhibitor of matrix metalloproteinase-3. 2004.

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22

(Editor), Neil J. Clendeninn, and Krzysztof Appelt (Editor), eds. Matrix Metalloproteinase Inhibitors in Cancer Therapy (Cancer Drug Discovery and Development). Humana Press, 2001.

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23

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

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Abstract:
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.
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24

Birkedal-Hansen, Henning. Matrix Metalloproteinases and Inhibitors: Proceedings of the Matrix Metalloproteinase Conference Held at Sandestin Beach, Fl, September 11-15, 1989. Gustav Fischer, 1991.

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