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Amgen Looks to Biomarkers to Boost Its Batting Average in Developing New Drugs

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About 17 percent of patients with normal KRAS genes had tumors shrink after they took the drug, while none of those with mutated KRAS genes saw that benefit, according to research published in March in the Journal of Clinical Oncology. About 43 percent of patients have the mutated KRAS, and suddenly looked like they should avoid the drug, which is high-priced, and causes a significant rash as a side effect.

European regulators, who initially balked at the company’s application when the tumor shrinkage rate was about half that good when spread across the whole population, agreed with the company’s analysis. The EU approved the medicine in December for patients with the normal KRAS genes. U.K-based DsX makes a test that can determine a patient’s KRAS status, Patterson says.

The FDA hasn’t yet accepted the same subpopulation analysis in the U.S., preferring to wait for results from more trials, Patterson says. But the evidence is mounting for KRAS, particularly since Vectibix’s competitor, Erbitux, was shown to offer a similar type of benefit for patients with normal KRAS genes, according to a presentation in June at the American Society of Clinical Oncology.

What does it mean for Amgen as a company? Like a lot of people, I wonder if the company is really keen on finding out when its drug doesn’t work for more than 40 percent of patients, and that it therefore shouldn’t be given to them. It’s possible that by narrowing the pool of customers, but raising the overall odds of success among those who do take it, Amgen could sell even more of the drug. After all, Genentech’s breast cancer treatment, Herceptin, which is approved for about one-fourth of breast cancer patients with a certain gene mutation, still generated $1.3 billion in U.S. sales last year.

“We want our drug given to the patients who are most likely to benefit,” Patterson says.

The biomarker project has yielded some other valuable information. One small-molecule drug in development, which Patterson didn’t name, was supposed to block two different receptors on cells. An early-stage human study went fine, with no adverse events. However, when the team looked at biomarkers in samples, it found that the drug completely blocked one receptor as planned, but only partially blocked another—and was likely to fail in further clinical trials. It saved at least a year’s work and several million dollars, Patterson says. “It was a clean kill decision,” he says.

The method has also worked in the opposite direction, by pumping new life into a drug that researchers thought was probably a dud. A drug for metabolic diseases was thought to require twice-daily dosing, at possibly more than 100 milligrams, making it inconvenient for patients and costly to manufacture, Patterson says. After studying samples, company scientists found it was blocking its target enzyme much more efficiently than expected, and could be dosed once-daily at about 1 milligram, which is what is being tested in a Phase II trial, Patterson says.

The effort may not solve all of Amgen’s well-publicized woes with its top-selling anemia drugs, Aranesp and Epogen. But if nothing else, as Patterson says, the biomarker teams in Seattle and Cambridge will help give the corporate bosses some more confidence that the company’s R&D resources aren’t being thrown around in quite as big a crapshoot as in the past.

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