Novel Phosphorylation that Controls the Stability of Hypoxia-Inducible Factor 1 Alpha

This invention relates to a polyclonal antibody against a novel phosphorylation site that is known to be correlated with increased tumor growth. Specifically, the antibody targets a phosphorylation site on HIF-1α, which is controlled by PIM kinases. This invention can be used not only as a therapeutic against cancer but also potentially as a means for predicting responses to PIM kinase inhibitors during drug development as way to test the sensitivity to other PIM kinase inhibitors and anti-angiogenic drugs.

 

Background:
Anti-angiogenic therapy is a new and promising strategy for combatting solid cancers such as myeloma, leukemia, prostate and breast cancer. Angiogenesis is considered a hallmark indicator of tumorigenesis and is believed to be required for tumor growth and metastasis. HIF-1 is a master regulator gene involved in the cellular response to hypoxia. Activation of HIF-1 is dependent on HIF-1α and HIF-2α protein levels. Under hypoxic conditions, HIF-1α and HIF-2α protein levels rise due to phosphorylation by PIM kinases which become overexpressed under hypoxic conditions. This leads to further activation of HIF-1 and results in transcription of genes involved in tumorigenesis including angiogenesis.
 

In attempting to develop effective treatments against solid cancers, it has been shown that prolonged activation of HIF-1 is associated with greater resistance to anti-angiogenic agents. Thus, this invention is a promising approach because it is an antibody that targets the phosphorylation site on HIF-1α to prevent phosphorylation by PIM kinase, thus reducing HIF-1 master regulator activation and ultimately, decreasing resistance to anti-angiogenic drugs.

 

Applications:

  • Therapeutic
  • Combination therapy
  • Drug development/testing

 

Advantages:

  • Reduce resistance to and increase efficacy of anti-angiogenic drugs
  • Can be used to test the efficacy of PIM kinase inhibitors and anti-angiogenic drugs
Patent Information: