Sobering fact: Pharma's drug pipeline is producing half the number of truly new medications it turned out a decade ago. 2008 is likely to see between 24 and 29 new molecular entities launch worldwide, according to IMS Health. Compare that with 1997, when IMS counted 52 new compounds for sale. Output has dwindled steadily for 10 years. There is no uptick in sight.
"Every piece of data suggests that research is not a core competency of Big Pharma," says Barbara Ryan, a managing director and pharmaceutical analyst at Deutsche Bank. "Something will have to change. The big companies may have to learn to outsource more research and figure out how to maintain access to it."
As discouraging as the numbers look, some great products are moving through clinical trials. From fresh insights into the beta-amyloid pathway, which offer the tantalizing prospect of preventing Alzheimer's disease, to a host of new antibacterials set to battle that scourge of hospitals, MRSA, the industry is tackling some of the nation's major health challenges. Here's a look at 61 new drugs that our experts from Wall Street to university teaching hospitals find most exciting.You Must Remember This . . .
Alzheimer's: Prevention and Management
Flurizan, a gamma secretase modulator, interferes with the manufacture of "amyloid precursor protein," the parent protein of amyloid. With Flurizan, gamma secretase produces less of the most-toxic variety of soluble amyloid and more of a less-toxic sort, Cummings explains. Flurizan's efficacy data is expected in early 2008.
Bapineuzumab, a humanized monoclonal antibody, is infused intravenously to remove plaque—as well as the toxic intermediate—from the brain, Cummings said. PBT2, a chelator or metal-protein attenuating compound, is currently in a Phase II trial in Sweden. According to Cummings, the drug is designed to inhibit the aggregation of amyloid before it becomes toxic. Researchers theorize that accumulation of metals in the brain converts beta-amyloid into an enzyme that catalyzes production of hydrogen peroxide and damages brain cells.
The hope, Cummings says, is that one of these drugs makes it possible to intervene early in the onset of the disease, retard the development of soluble amyloid, and thereby prevent the memory loss and dementia. The recent failure of Neurochem's Alzhemed to show drug–placebo differences in a Phase III trial was a disappointment, Cummings admits, but not a reason to give up on the beta-amyloid pathway. The company is continuing to evaluate the treatment.
Dimebon, a symptomatic agent in the same family as Forest's Namenda (memantine), is a cholinesterase inhibitor and NMDA receptor antagonist that inhibits mitochondrial pore formation. It raised hopes by exceeding goals in a Phase II trial in Russia. "At 12 months, the difference between drug and placebo on some measures was larger than at six months," Cummings said. "That's what one would expect with a disease-modifying compound."