Case reportSU-011248, a vascular endothelial growth factor receptor-tyrosine kinase inhibitor, controls chronic psoriasis
Section snippets
Discussion
To the authors’ knowledge, this case report is the first to document the improvement in chronic cutaneous psoriasis after systemic therapy with the VEGFR-TK inhibitor, SU-011248, during second-line monotherapy for treatment of recurrent metastatic RCC. Exacerbation of psoriasis during IFN-α therapy has been previously reported,1 and the initial improvement in psoriasis during the first cycle of sunitinib therapy could have been related to the withdrawal of IFN-α treatment. However, subsequent
Conclusion
VEGFR-TK inhibitors may have a therapeutic effect in chronic cutaneous psoriasis. Additional collection of similar case reports is encouraged to provide a rationale for conducting a clinical study of angiogenesis inhibitors in the treatment of refractory psoriasis.
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Nintedanib ameliorates imiquimod-induced psoriasis in mice by inhibiting NF-κB and VEGFR2 signaling
2021, International ImmunopharmacologyCitation Excerpt :In addition, nintedanib inhibited angiogenesis by downregulating the activation of p-VEGFR2 in IMQ-induced mice. Several case studies reported the attenuation of psoriatic disease in patients with cancer after treatment with anti-VEGFA antibodies or anti-VEGFA receptor small-molecule inhibitors [11,19–22]. The use of anti-VEGFA inhibitors in different mouse models of psoriasis induced the regression of the psoriasis phenotypes, including epidermal hyperproliferation, thickness, altered differentiation, dermal immune infiltration, and increased angiogenesis [13,14,34,35].
Topical Sunitinib ointment alleviates Psoriasis-like inflammation by inhibiting the proliferation and apoptosis of keratinocytes
2018, European Journal of PharmacologyCitation Excerpt :VEGF receptor tyrosine kinase inhibitors can effectively treat psoriasis, this may be attributed to the antiangiogenic activity of Sunitinib by inhibition of VEGF receptors (Su et al., 2009). EGF could induce HaCaT cells to a highly proliferation state (Keshtgarpour and Dudek, 2007; Jiang et al., 2012). In this study, therefore, we chose EGF co-cultured HaCat cells (HaCaT/E), which was used as a cell model of psoriasis keratinocyte, to imitate the highly proliferative state of psoriatic keratinocytes.
Angiogenesis in Dermatology – Insights of Molecular Mechanisms and Latest Developments
2017, Actas Dermo-SifiliograficasCitation Excerpt :Different case reports with angiogenesis-inhibitors given for cancer therapy in patients with psoriasis have been published. Sunitinib (Sutent), a potent VEGFR – inhibitor in the treatment for renal cell carcinoma, could almost clear chronic large psoriatic plaques in a patient, as reported in 2007 by Keshtagarpour and Arkadius.24 In 2009 another report of a patient presenting complete remission of chronic psoriasis while receiving Bevacizumab (anti-VEGF Ab) for colon cancer therapy was published.25
Cannabinoids: Possible agents for treatment of psoriasis via suppression of angiogenesis and inflammation
2017, Medical HypothesesCitation Excerpt :According to Datta-Mitra’s study on a PS patient with renal cancer which was treated by an anti-VEGF monoclonal anti-body (Bevacizumab®), a complete remission of PS and psoriatic arthritis was observed [42]. Additionally, in two cases with psoriasis who received Sunitinib (a tyrosine kinase inhibitor of VEGFR) an acceptable improvement in their condition was observed [43,44]. Monoclonal antibodies against TNF-α such as Infliximab® has been confirmed as a systemic treatment for adults’ psoriasis by food and drug administration (FDA) in 2006 [45].
Tyrosine kinases in inflammatory dermatologic disease
2011, Journal of the American Academy of DermatologyImprovement of psoriasis during sunitinib therapy for renal cell carcinoma
2010, American Journal of the Medical Sciences