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Axitinib Shown to Be Active in Resistant CML and B-ALL

Axitinib (Inlyta, Pfizer Inc), already approved for the second-line treatment of advanced renal cell carcinoma (RCC), has surprisingly been shown to inhibit the BCR-ABL1 (T315I) mutation in cells of patients with chronic myelogenous leukemia (CML) and Philadelphia chromosome–positive B-cell acute lymphoblastic leukemia (B-ALL). This mutation renders these diseases resistant to most current treatments, so axitinib offers hope as a new therapy.

This was an unexpected finding and makes axitinib the first vascular endothelial growth factor receptor (VEGFR) inhibitor to show activity in BCR-ABL (T315I) CML and B-ALL.

The new observations were reported in a study published online February 9 in Nature and resulted from a collaboration between researchers from the Institute for Molecular Medicine Finland (FIMM) at the University of Helsinki, the Helsinki University Central Hospital Comprehensive Cancer Center, and Pfizer's research team
read full article:
http://www.medscape.com/viewarticle/839507?src=sttwit

I was just about to post a very similar article!

Here's the one I read:

http://www.news-medical.net/news/20150210/Researchers-identify-axitinib-...

It's very promising that there's still new developments, and plenty of scope for new therapies for us all.

David.

Thanks David,
Thanks for the link to this article.

I think for resistant CML there is still a lot of work going on- this will no doubt benefit all of us in the longer run.

'.... By virtue of its distinct pharmacological profile and by preclinical pharmacological studies demonstrating an additive effect, a combination of ABL001 and a tyrosine-kinase inhibitor (TKI) has the potential to achieve a deeper molecular response in a higher proportion of CML patients as compared to single agent TKI therapy. Such a combination has the added advantage of targeting the ABL kinase domain at two distinct locations, theoretically preventing single point mutation-associated treatment resistance. The prediction is that a nilotinib/ABL001 combination will increase the percentage of patients who achieve a complete molecular response (CMR) and decrease the time to CMR, thereby increasing the possibility of achieving sustained treatment-free remissions in these patients. In addition, some patients may be intolerant of therapy with TKIs or may develop mutations that promote resistance to TKI therapy. In these patients, ABL001 may provide a novel therapeutic option.'

https://clinicaltrials.gov/ct2/show/NCT02081378

Sandy