Celera Corporation (NASDAQ:CRA) today announced that the United States Patent and Trademark Office has issued United States Patent 7,799,530 relating to methods of determining heart attack risk by detecting the KIF6 gene variant and reduction of such increased risk by statin therapy. The KIF6 gene encodes a kinesin, a member of a family of proteins involved in microtubule-mediated intracellular transport. Previous research has shown that this variant of the KIF6 gene is associated with up to a 55% increased risk of primary and recurrent coronary heart disease (CHD) events in the placebo arms of pravastatin clinical trials, and that this increased risk was significantly reduced with statin therapy.
“This patent is an important component of our intellectual property portfolio covering cardiovascular genetics, and we believe that Celera's growing patent estate should provide our products and services with long-term market protection.”
"We're pleased with the issuance of this patent on the KIF6 gene variant's association with increased risk for heart attack, and the reduction of this risk by statin therapy," said Kathy Ordoñez, Chief Executive Officer of Celera. "This patent is an important component of our intellectual property portfolio covering cardiovascular genetics, and we believe that Celera's growing patent estate should provide our products and services with long-term market protection."
The association between KIF6 and event reduction during pravastatin (Pravachol®) therapy has been demonstrated previously in three prospective, placebo-controlled randomized clinical trials on the prevention of CHD events: the secondary prevention Cholesterol and Recurrent Events (CARE) study; the primary prevention West of Scotland Coronary Prevention Study (WOSCOPS); and the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) study. Additionally, a genetic study of PROVE IT-TIMI 22 reported that in patients who experienced an acute coronary syndrome (ACS), high-dose atorvastatin (Lipitor®), compared with standard dose pravastatin, was significantly more effective at reducing CHD events in KIF6 carriers than in noncarriers. To date, the benefits of statin therapy for KIF6 carriers has only been demonstrated with atorvastatin and pravastatin therapy.
The KIF6 gene variant was previously reported to predict risk of CHD in other prospective studies. This gene variant was associated with increased risk of CHD in Caucasian and African American participants of the Atherosclerosis Risk in Communities (ARIC) study (a study of 12,556 middle aged Americans), and with increased risk for myocardial infarction (MI) in both the Cardiovascular Health Study (a study of 4,552 Americans, aged 65 or older), and the Women's Health Study (a study of 25,283 women older than 45 years without a previous history of CHD). Thus, this KIF6 gene variant has been associated with CHD risk in studies including a total of approximately 55,000 people.
The increased risk of CHD events observed in KIF6 carriers has been shown to be independent of other well-known CHD risk factors, including smoking, hypertension, cholesterol level, age and sex, further supporting the conclusion that the KIF6 gene variant is an independent predictor of risk for CHD. To date, the benefits of statin therapy for KIF6 carriers has only been studied with atorvastatin and pravastatin therapy.
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