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- W2089849103 abstract "Introduction: The non-receptor tyrosine kinase, spleen tyrosine kinase (Syk), is primarily expressed in haematopoietic cells and appears to be particularly important in B cells. Syk is involved in signal transduction processes and appears to regulate allergic, inflammatory and autoimmune responses. It also appears to play a significant role in the development of haematological malignancies. Inhibitors of Syk are potentially useful in treating asthma, rheumatoid arthritis, lupus, chronic lymphocytic leukaemia and lymphomas. Areas covered: This article reviews the increasing number of patent filings between 2010 and 2013 claiming Syk inhibitors and focuses on the multiple structural classes of Syk inhibitors disclosed. It also comments on recent developments with Syk inhibitors, both clinical results and licensing deals. Expert opinion: The increased interest in the identification of Syk inhibitors has seen a sharp increase in patent filings claiming such compounds. However, the number of these is well below that of filings relating to other pro-inflammatory kinases (p38, JAK). These filings have also claimed an increasingly diverse range of chemical classes moving away from the 2,4-diaminopyrimidine motif present in drugs such as fostamatinib and PRT-06207. Many of the claimed compounds are Syk inhibitors with potencies considerably better than fostamatinib. However, good kinase selectivity is also likely to be essential if a Syk inhibitor is to prove useful enough to emulate the JAK inhibitor tofacitinib in gaining marketing authorisation. Recent clinical failures with Syk inhibitors are expected to result in a decrease in the rate of patent filings claiming Syk inhibitors." @default.
- W2089849103 created "2016-06-24" @default.
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- W2089849103 date "2014-02-20" @default.
- W2089849103 modified "2023-10-17" @default.
- W2089849103 title "Spleen tyrosine kinase inhibitors: a review of the patent literature 2010 – 2013" @default.
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- W2089849103 doi "https://doi.org/10.1517/13543776.2014.890184" @default.
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