Therapeutic for Acute Myeloid Leukemia and Other Cancers

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2016-SINT-67603
Acute myeloid leukemia (AML) has a five-year survival rate of 25 percent. Patients develop resistance to the current standard AML drug, ara-C, both alone and in combination with other cancer drugs. In AML as well as a number of other cancers, the disease is driven by protein kinases like FLT-3 and TrkC. Another structure implicated in cancer is the G-quadruplex formed through DNA interactions. This biology can be taken advantage of to design a more effective treatment for AML.

A Purdue University researcher has developed a series of new compounds that inhibit the FLT-3 and TrkC protein kinases and bind to G-quadruplexes. These compounds display activity in AML cell lines with nanomolar IC50 values. In addition to their effectiveness against cancer cell lines, these compounds have been designed to be metabolically stable. It is anticipated that these compounds will have superior performance against AML compared to the standard treatment. The mechanisms that drive AML also drive many cancers, so these dual protein kinase inhibitors/G-quadruplex binders have broad potential as cancer therapeutics.

Advantages:
-Potent anticancer agents
-Designed to be metabolically stable

Potential Applications:
-AML therapeutic
-Treatment for multiple cancers

Related Publication:
Identification of new FLT3 inhibitors that potently inhibit AML cell lines, via an azo cllick-it/staple-it approach. ACS Medicinal Chemistry Letters.
Aug 15, 2017
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Feb 21, 2017
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United States
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Aug 15, 2016
Provisional-Patent
United States
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