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NDO Home | Contact | Register for NDO Access NNeewwsslleetttteerr Highlights of updates to NDO in March 2015 NDO home | Contact | Register for NDO access in Prescribing Regulatory changes in the EU Outlook 2014 Launched in the UK Apremilast (Otezla) Chronic plaque psoriasis in adults / Psoriatic arthritis in adults – both second-line Bromelain (NexoBrid) Removal of eschar in adults with deep partial- and full-thickness thermal burns Filgrastim biosimilar (Accofil) Neutropenia Follicle stimulating hormone In vitro fertilisation biosimilar (Bemfola) Paclitaxel albumin-bound Advanced non-small cell lung cancer – first-line in combination with carboplatin in (Abraxane) adults unsuitable for surgery or radiation therapy [licence extension/variation] Ruxolitinib (Jakavi) Polycythemia vera in adults resistant to or intolerant of hydroxyurea [licence extension/variation] Approved in the EU Atorvastatin + ezetimibe (Atozet) Hypercholesterolaemia [new formulation] Ciclosporin (Ikervis) Severe 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    Wu et al. Journal of Hematology & Oncology (2018) 11:133 https://doi.org/10.1186/s13045-018-0675-4 REVIEW Open Access FLT3 inhibitors in acute myeloid leukemia Mei Wu1, Chuntuan Li2 and Xiongpeng Zhu2* Abstract FLT3 mutations are one of the most common findings in acute myeloid leukemia (AML). FLT3 inhibitors have been in active clinical development. Midostaurin as the first-in-class FLT3 inhibitor has been approved for treatment of patients with FLT3-mutated AML. In this review, we summarized the preclinical and clinical studies on new FLT3 inhibitors, including sorafenib, lestaurtinib, sunitinib, tandutinib, quizartinib, midostaurin, gilteritinib, crenolanib, cabozantinib, Sel24-B489, G-749, AMG 925, TTT-3002, and FF-10101. New generation FLT3 inhibitors and combination therapies may overcome resistance to first-generation agents. Keywords: FMS-like tyrosine kinase 3 inhibitors, Acute myeloid leukemia, Midostaurin, FLT3 Introduction RAS, MEK, and PI3K/AKT pathways [10], and ultim- Acute myeloid leukemia (AML) remains a highly resist- ately causes suppression of apoptosis and differentiation ant disease to conventional chemotherapy, with a me- of leukemic cells, including dysregulation of leukemic dian survival of only 4 months for relapsed and/or cell proliferation [11]. refractory disease [1]. Molecular profiling by PCR and Multiple FLT3 inhibitors are in clinical trials for treat- next-generation sequencing has revealed a variety of re- ing patients with FLT3/ITD-mutated AML. In this re- current gene mutations [2–4]. New agents are rapidly view, we summarized the preclinical and clinical studies emerging as targeted therapy for high-risk AML [5, 6]. on new FLT3 inhibitors, including sorafenib, lestaurtinib, In 1996, FMS-like tyrosine kinase 3/internal tandem du- sunitinib, tandutinib, quizartinib, midostaurin, gilteriti- plication (FLT3/ITD) was first recognized as a frequently nib, crenolanib, cabozantinib, Sel24-B489, G-749, AMG mutated gene in AML [7].
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