A Rabbit Anti-pT1989 ATR Monoclonal Antibody for Use in Immunoassays


Ataxia telangiectasia mutated and Rad3 Related (ATR) protein kinase is essential for regulating DNA damage checkpoints during the cell cycle. ATR, is phosphorylated at threonine 1989 site (T1989) in response to DNA damage and ATR activation leads to activation of downstream substrates, signaling cascades and cell cycle arrest. ATR is a potential target for anticancer therapeutics to induce cancer cell death by inhibiting cell cycle arrest pathways in response to chemotherapeutics.

Researchers at the National Cancer Institute (NCI) have developed a monoclonal antibody against ATR. The invention antibody specifically binds to the phosphorylated threonine 1989 position. The antibody can be used in immunoassays to detect ATR in a sample, to determine the inhibitory activity of ATR agents, and to measure the effectiveness of an ATR modulator agent or ATR inhibitor as therapeutics. 



Potential Commercial Applications: Competitive Advantages:

• Improved method to detect a rare, genetic disease that is debilitating and often life-shortening. 
• Antibody for detection of pATR-T1989 in biological samples, including biopsies. 
• Antibody for determination of activation of ATR by phosphorylation of T1989 by DNA damaging agents or genotoxic chemotherapeutic agents.
• Antibody for measuring ATR activation, inhibition or modulation.

 

• Antibody works in Western Blot on crude lysates and in IFA.
• Antibody works for standard processed preclinical and clinical samples.
• Antibody staining pattern specificity can be demonstrated with available blocking phosphopeptides. 



Development Stage:
Pre-clinical (in vivo)

Inventors:

James Doroshow (NCI)  ➽ more inventions...

Ralph Parchment (NCI)  ➽ more inventions...

Thomas Pfister ()  ➽ more inventions...

Allison Marrero ()  ➽ more inventions...


Intellectual Property:

Collaboration Opportunity:

Licensing only


Licensing Contact:
John Hewes, Ph.D.
Email: John.Hewes@nih.gov
Phone: 240-276-5515

OTT Reference No: E-001-2014
Updated: Oct 23, 2017