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A number of novel therapies for ITP are currently being developed based upon the current pathophysiology of ITP. Many therapies are targetted at reducing platelet destruction by decreasing anti\u2010platelet antibody production by immunosuppression with monoclonal antibodies targetted against CD40, CD38 and the immunoproteasome or physically reducing the anti\u2010platelet antibody concentration by inhibition of the neonatal Fc receptor. Others target the phagocytic system by inhibiting Fc\u03b3R function with staphylococcal protein A, hypersialylated IgG, polymeric Fc fragments, or Bruton kinase. With a recognition that platelet destruction is also mediated by complement, inhibitors of C1s are also being tested. Inhibition of platelet desialylation may also play a role. Other novel therapies promote platelet production with new oral thrombopoietin receptor agonists or the use of low\u2010level laser light to improve mitochondrial activity and prevent megakaryocyte apoptosis. This review will focus on these novel mechanisms for treating ITP and assess the status of treatments currently under development. Successful new treatments for ITP might also provide a pathway to treat other autoimmune disorders.<\/jats:p>","DOI":"10.1111\/bjh.17872","type":"journal-article","created":{"date-parts":[[2021,10,8]],"date-time":"2021-10-08T04:21:28Z","timestamp":1633666888000},"page":"1311-1328","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Novel therapies for immune thrombocytopenia"],"prefix":"10.1111","volume":"196","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2084-8810","authenticated-orcid":false,"given":"David J.","family":"Kuter","sequence":"first","affiliation":[{"name":"Hematology Division Massachusetts General Hospital Harvard Medical School  Boston MA 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