The aml Hub website uses a third-party service provided by Google that dynamically translates web content. Translations are machine generated, so may not be an exact or complete translation, and the aml Hub cannot guarantee the accuracy of translated content. The aml and its employees will not be liable for any direct, indirect, or consequential damages (even if foreseeable) resulting from use of the Google Translate feature. For further support with Google Translate, visit Google Translate Help.
The AML Hub is an independent medical education platform, sponsored by Astellas, Daiichi Sankyo, Johnson & Johnson, Kura Oncology and Syndax, and has been supported through educational grants from Bristol Myers Squibb and the Hippocrate Conference Institute, an association of the Servier Group. The funders are allowed no direct influence on our content. The levels of sponsorship listed are reflective of the amount of funding given. View funders.
Now you can support HCPs in making informed decisions for their patients
Your contribution helps us continuously deliver expertly curated content to HCPs worldwide. You will also have the opportunity to make a content suggestion for consideration and receive updates on the impact contributions are making to our content.
Find out more
Create an account and access these new features:
Bookmark content to read later
Select your specific areas of interest
View aml content recommended for you
FDA grants Fast Track Designation to crenolanib for the treatment of patients with R/R FLT3-Positive AML
On 1st December 2017, the US Food and Drug Administration (FDA) granted crenolanib, a tyrosine kinase inhibitor, Fast Track designation for the treatment of patients with Fms Like Tyrosine Kinase 3 (FLT3) mutation-positive Relapsed or Refractory (R/R) Acute Myeloid Leukemia (AML).1 FLT3 mutations with Internal Tandem Duplications (ITD) occurs in approximately 30% of AML patients. These mutations often lead to poor prognosis and disease relapse in AML patients.2
Crenolanib is a selective and potent inhibitor for Platelet-Derived Growth Factor Receptor (PDGFR) α and β but it also has a high affinity for FLT3. Crenolanib binds to and inhibits both wild-type and mutated forms of FLT3, which can lead to the inhibition of FLT3-related signal transduction pathways.2
At present, crenolanib is being explored in multiple trials for newly diagnosed (NCT02283177) and relapsed/refractory (NCT02298166, NCT02400281, NCT01657682) AML patients with or without FLT3 mutations.
References