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 moreCreate an account and access these new features:
Bookmark content to read later
Select your specific areas of interest
View aml content recommended for you
On 7th June 2017, the U.S. Food and Drug Administration (FDA) granted a Fast Track Designation to OXi4503 for the treatment of patients with Acute Myeloid Leukemia (AML).1
OXi4503 (combretastatin A1 di-phosphate) is a dual mechanism vascular disrupting agent that has been shown to destroy tumor vasculature, leading to extensive tumor cell death and necrosis. Additionally, OXi4503 can undergo oxidative stress to quinone intermediate to produce cytotoxicity against tumor cells. Preclinical studies of OXi4503 in AML have shown that this agent could induce phenotypic and molecular remissions in subtypes of AML including Fms Like Tyrosine Kinase 3 (FLT3) mutated AML through multiple mechanisms including vascular disruption and apoptosis. 2
OXi4503 is currently being explored in a phase I/II study (NCT02576301) in patients with Relapsed or Refractory (R/R) AML. The aim of the phase 1 portion of this study is to investigate the maximum tolerated dose of OXi4503 monotherapy and in combination with intermediate-dose cytarabine in R/R AML patients. The aim of the phase II portion of the study is to investigate the overall response rate of OXi4503 in combination with intermediate-dose cytarabine in R/R AML patients after treatment failure of up to 1 prior chemotherapy regimen.
References
Your opinion matters
Approximately what proportion of your patients with FLT3-mutations also have NPM1 and DNMT3A co-mutations?