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Inhibitors of tyrosine kinases in the treatment of psoriasis.
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Psoriasis is a heterogenous skin disease, characterized by epidermal hyperproliferation, abnormal keratinization and inflammation. The heterogeneity of the disease results probably from the interaction of multiple gene abnormalities with environmental factors. The new approaches to drug design have
Biological activity of tyrosine kinase inhibitors: novel agents for psoriasis therapy.
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Uncontrolled signaling from protein tyrosine kinases (PTKs) can lead to numerous proliferative and inflammatory diseases, and identification of the specific PTKs that play a key role in a defined disease could potentially lead to a selective therapeutic agent. In psoriasis, the balance of signals
The protein tyrosine phosphatase, non-receptor type 22 R620W polymorphism does not confer susceptibility to psoriasis in the genetic homogeneous population of Crete.
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Recent whole-genome and candidate-gene association studies in patients with psoriasis (PS) have identified a number of single-nucleotide polymorphisms (SNPs) that predispose to disease with moderate risk. Predisposition to PS is known to be affected by genetic variation in human leukocyte antigen-C
Tyrosine phosphorylation in psoriatic T cells is modulated by drugs that induce or improve psoriasis.
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BACKGROUND
The induction of protein tyrosine kinases (PTKs) is known to be a key element in the activation of lymphocytes.
OBJECTIVE
Because immunologic mechanisms are important in the pathogenesis of psoriasis, we examined the time course of tyrosine-phosphorylated proteins (p-tyr) as a marker for
Protein tyrosine phosphatase conjugated with a novel transdermal delivery peptide, astrotactin 1-derived peptide recombinant protein tyrosine phosphatase (AP-rPTP), alleviates both atopic dermatitis-like and psoriasis-like dermatitis.
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BACKGROUND
Atopic dermatitis (AD) and psoriasis are the 2 most common chronic inflammatory skin diseases. There is an unmet medical need to overcome limitations for transcutaneous drug development posed by the skin barrier.
OBJECTIVE
We aimed to identify a novel transdermal delivery peptide and to
Bruton's tyrosine kinase inhibitor suppresses imiquimod-induced psoriasis-like inflammation in mice through regulation of IL-23/IL-17A in innate immune cells.
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Psoriasis is an unchecked chronic inflammation characterized by thick, erythematous, and scaly plaques on the skin. The role of innate immune cells in the pathogenesis of psoriasis is well documented. Bruton's tyrosine kinase (BTK) has been reported to execute important signaling functions in innate
Drug Discovery against Psoriasis: Identification of a New Potent FMS-like Tyrosine Kinase 3 (FLT3) Inhibitor, 1-(4-((1H-Pyrazolo[3,4-d]pyrimidin-4-yl)oxy)-3-fluorophenyl)-3-(5-(tert-butyl)isoxazol-3-yl)urea, That Showed Potent Activity in a Psoriatic Animal Model.
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Psoriasis is a chronic T-cell-mediated autoimmune disease, and FMS-like tyrosine kinase 3 (FLT3) has been considered as a potential molecular target for the treatment of psoriasis. In this investigation, structural optimization was performed on a lead compound,
Phase 2 Trial of Selective Tyrosine Kinase 2 Inhibition in Psoriasis.
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Tyrosine kinase 2 (TYK2) signaling pathways, which mediate cytokine signaling, are implicated in the pathophysiology of psoriasis. Selective inhibitors of TYK2 may be effective in treating psoriasis.
We conducted a phase 2, double-blind trial of a TYK2 inhibitor, BMS-986165, in adults with
Inhibition of spleen tyrosine kinase attenuates psoriasis-like inflammation in mice through blockade of dendritic cell-Th17 inflammation axis.
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Psoriasis is a debilitating autoimmune disease of the skin characterized by acanthosis and hyperkeratosis resulting from excessive growth of keratinocytes in the epidermis and inflammatory infiltrates in the dermis. Innate immune cells such as dendritic cells (DCs), perform a critical role in the
The Protein Tyrosine Phosphatase Nonreceptor 22 (PTPN22) R620W Functional Polymorphism in Psoriasis.
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UNASSIGNED
Psoriasis is a complex autoimmune disease caused by the interaction of genetic and environmental factors. PTPN22 gene polymorphism has been reported to affect psoriasis susceptibility; however, no data are available for Middle Eastern populations.
UNASSIGNED
The aim of this study was to
SU-011248, a vascular endothelial growth factor receptor-tyrosine kinase inhibitor, controls chronic psoriasis.
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[Phenylalanine-tyrosine metabolism in psoriasis vulgaris. Search on a genetic basic defect (author's transl)].
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Protein tyrosine phosphatase gene PTPN22 polymorphism in psoriasis: lack of evidence for association.
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Assessment of the role of spleen tyrosine kinase and zeta-chain-associated 70-kDa protein (tyrosine) kinase in the pathogenesis of psoriasis: A case-controlled study.
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Inhibitors of tyrosine kinases in the treatment of psoriasis.
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