Pfizer, which is one of those companies, announced late Monday that the drug, bapineuzumab, did not improve either cognition or daily functioning of patients compared to a placebo in the Phase 3 trial.

The company did not provide detailed results, saying they would be presented at a medical meeting in September. But one of the principal investigators in the study, Dr. Reisa Sperling, said in an interview that there was no sign of any effect.

“There was absolutely no evidence at all of a clinical benefit of treatment on either of the primary measures, one cognitive and one functional,” said Dr. Sperling, director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital in Boston.

To be sure, most doctors and Wall Street analysts had been expecting the drug not to succeed, since an earlier phase 2 trial had not shown a statistically significant effect.

Moreover, the patients in the new trial — 1,100 Americans with mild to moderate disease — all had a gene called ApoE4, which raises the risk a person will get Alzheimer’s disease and can make the disease worse. Based on the phase 2 data, bapineuzumab has a somewhat better chance of working in patients who do not have that gene.

There are three other trials still under way, one involving patients with the gene and two in patients without. Results from one of the trials of noncarriers are expected within weeks. About half of Alzheimer’s patients have the gene.

Bapineuzumab is being developed jointly by Pfizer and Johnson & Johnson. Elan, an Irish pharmaceutical company, also has a financial stake in the drug.

The drug is a monoclonal antibody designed to bind to beta-amyloid, a protein that has toxic effects in the brain and is believed by many scientists to be a cause of Alzheimer’s.

Eli Lilly & Company is also developing an antibody against beta amyloid, which it calls solanezumab. Clinical trial results are expected in the coming weeks.

Bapineuzumab is the latest of several drugs aimed at clearing beta amyloid or preventing its formation that have failed to work in clinical trials. The failures have raised questions about whether beta amyloid really is the culprit behind Alzheimer’s disease.

But some experts say the drugs are being tried too late in the course of the disease and would be best used to prevent the formation of amyloid plaque rather than to try to destroy it after it has formed.

“All these symptomatic trials are 25 years too late,” said Dr. Samuel Gandy, director of the Center for Cognitive Health at the Mount Sinai School of Medicine in Manhattan, explaining that plaque begins to build as much as 25 years before Alzeheimer’s symptoms appear. “I’m not terribly surprised and I’m not discouraged” by the results of the bapineuzumab trial, he said.

Trials aimed at preventing Alzheimer’s, using imaging and other tests to detect plaque before cognitive symptoms are evident, are starting to get under way.

Existing drugs for Alzheimer’s can treat the symptoms for a while but do not affect the underlying mechanism of the disease. If bapineuzumab or solanezumab succeed, they could garner billions of dollars in sales each year.

While success would probably have push up the stocks of the drug’s manufacturers, the failure, since it is expected, might not hurt the stocks much.

Pfizer shares fell about 1 percent after hours and those of Johnson and Johnson barely moved. But shares of Elan, a far smaller company with more to gain or lose from bapineuzumab, fell nearly 19 percent after hours to $11.