Abbott’s Humira, the 3rd-in-Class Drug That Toppled Lipitor as No. 1

4/16/12Follow @xconomy

Sometimes the biggest success stories in business never make it to the magazine covers. There’s no single Eureka moment, no surprise turning point, no redemption, no swashbuckling CEO delivering the goods. There’s just a team pursuing genius like Edison once said: through 1 percent inspiration and 99 percent perspiration.

Dull as it may sound, there is something remarkable in the Reuters report this week that Abbott Laboratories’ adalimumab (Humira), is on track to replace Pfizer’s atorvastatin (Lipitor) as the world’s top-selling pharmaceutical in 2012. You can easily read that sentence and conclude it’s just another sign that Big Pharma companies like Pfizer (NYSE: PFE) have failed to come up with innovative new drugs to replace their aging blockbusters that are losing patents.

There’s hard truth in that statement, but to dwell on that is to miss the big picture. It obscures the fact that Abbott (NYSE: ABT) has achieved something important by turning a biotech drug into the world’s best-selling pharmaceutical, with an estimated $9.3 billion in sales this year. This is no small thing, given that these products, made through gene-splicing techniques and manufactured inside living cells, are not as cheap and straightforward to mass-produce as chemically synthesized pills like Lipitor. Many of these biotech drugs have been able to hit precise biological targets in ways that conventional pills can’t, opening up new avenues for treating disease.

“It’s a bit of the changing of the guard that you’re seeing,” says Doug Williams, the executive vice president of R&D at Weston, MA-based Biogen Idec. “It’s brought about partly by the patent expirations of the drugs of the past. But there’s no question, biotech has established itself, and protein therapies are incredibly important additions to patient care. There’s no turning back.”

Humira, a drug for autoimmune diseases, will never be taken by millions of people like Lipitor, and it will never be a household name brand. It is expensive, but it provides a lot of bang for the buck, by helping very sick people feel healthy again and go back to their regular lives.

The story of this drug and the others in its class is one for the medical history books. But from a business perspective, it’s also fascinating that Abbott was able to climb its way to the top—not by blazing a completely new trail, but by doing methodical, consistent, disciplined work in maximizing a drug that could have languished as a third-in-class product.

Humira easily could have ended up being the third wheel of rheumatoid arthritis therapy. The drug was first approved by the FDA on Dec. 31, 2002, a little more than four years after the trailblazing drugs in its class hit the market. Those products, Johnson & Johnson’s infliximab (Remicade) and Amgen’s etanercept (Enbrel), were the first-generation drugs that showed scientists you could make a profound difference for rheumatoid arthritis patients if you could make targeted therapies that zeroed in on a marker called TNF-alpha. By doing that, you could soak up excess inflammatory molecules that were hammering the joints of patients.

They worked wonders for alleviating pain, swelling, and joint damage. Patients rhapsodized about these products in first-generation online chat rooms in the dotcom bubble era, stoking all kinds of demand.

While those drugs opened scientific eyes throughout their R&D journey in the 1990s, and started generating hundreds of millions in sales from virtually the moment they were introduced in 1998, some scientists in Boston and Cambridge, U.K. thought they could still innovate.

Bob Kamen, an entrepreneur-in-residence at Third Rock Ventures

Bob Kamen, now an executive-in-residence at Third Rock Ventures in Boston, recalls how the project then known as “D2E7″ was born through a collaboration between the BASF Bioresearch Center he led in Massachusetts, and a group at Cambridge Antibody Technologies in the U.K. The scientific idea was to see if they could develop an antibody drug candidate against the TNF target that was “fully human”—that is, didn’t use mouse DNA. By using only human DNA in the drug, it was supposed to help the treatment circumvent immune-system surveillance, and therefore avoid triggering immune-system reactions that might cause additional side effects.

There was one other key design feature, which many scientists didn’t fully appreciate at the time, but turned out to be a crucial advantage. The J&J drug had to be taken … Next Page »

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