FDA Panel Endorses New Alzheimer’s Drug After Accelerated Approval

• by Natasha Hobley

• Published June 26, 2023
• Pharma

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The newest Alzheimer’s drug is on its way for full regulatory approval after a U.S. Food and Drug Administration (FDA) advisory panel voted that the drug was beneficial in slowing cognitive decline. The drug is expected to be fully approved by July 6, 2023.¹

In clinical trials the drug, known as lecanemab, demonstrated a 27 percent slower decline in cognitive abilities by removing sticky plaques known as amyloids from the brain. Lecanemab will go by the brand name Leqembi and, according to the drug’s manufacturers Eisai and Biogen, it is the first drug to attempt to modify the course of the disease rather than treat the symptoms alone.

It is anticipated that once approved, Leqembi sales could exceed $1 billion in 2026 and reach $5.7 billion by 2030.¹

Serious Side Effects Noted in Drug Trials

Clinical trials have also revealed serious side effects in some patients that include brain swelling and bleeding, also known as microhemorrhages. These adverse events are known as “amyloid-related

imaging abnormalities” (ARIA), which don’t usually present symptoms but can be serious and even fatal.¹

Leqembi Recieves Accelerated Approval

In January 2023, the FDA approved Leqembi via an Accelerated Approval pathway, “under which the FDA may approve drugs for serious conditions when there is an unmet medical need” and a drug is shown to be reasonably likely to be clinically beneficial. Leqembi submitted its Phase 3 clinical trial, which monitored 856 patients with Alzheimer’s disease.

The treatment was initiated in patients who suffered from mild cognitive impairment or mild dementia with confirmed presence of amyloid beta pathology. According to the trials, patients who received the drug demonstrated statistically significant reduction in brain amyloid plaque from baseline to week 79 compared to the placebo group.²

Experts Doubt Leqembi’s Efficacy

Biogen is the same company behind the current most popular Alzheimer’s drug known as Aduhelm. But many experts are expressing doubts about Leqembi’s ability to be much better than Aduhelm.³

Assistant professor of neurology at Vanderbilt School of Medicine Matthew Schrag, MD, PhD says that the effects of Leqembi are modest and may not even be noticeable. He also stated that when looking only at the absolute difference between placebo and treated test subjects, the treatment really only improved patients’ condition by about 2.5 percent.³

Hypothesis Behind Alzheimer’s Cause May Stem From Fabricated Data

Like other Alzheimer’s drugs on the market, Leqembi will target the amyloid beta (Aβ) protein. However, last summer, an investigation led to questioning whether the data surrounding amyloid beta protein’s contribution to cognitive decline and Alzheimer’s was fabricated from the beginning.⁴

The original Aβ protein research was conducted in 2006 by neuroscientist Sulvain Lesné, PhD, MSci, of the University of Minnesota, Twin Cities. His work proposed that the Aβ protein caused dementia in rats and has been cited nearly 2,300 times. His work is aggressively promoted by the Alzheimer’s Association and the U.S. National Institutes of Health (NIH) has provided as much as $280 million in research funding based upon this theory.⁴

Last summer, a six-month investigation by award winning reporter Charles Piller published in Science broke news of claimed fabrications of Lesné’s work. Piller worked with Matthew Schrag, who has long criticized the approval of the Aβ targeting drug Aduhelm. Aduhelm was approved despite 10 of 11 FDA panel members voting against the approval due to Aβ drugs failing to demonstrate any benefit.⁴

In his investigative work, Piller found that after 15 years of publications, scientists have been unable to replicate Dr. Lesné’s findings, and few have been able to even detect the protein in human tissue. The investigation also found what appeared to be “shockingly blatant” examples of image tampering. Molecular biologist and forensic image consultant Elisabeth Bik, PhD said that the authors “appeared to have composed figures by piecing together parts of photos from different experiments. The obtained experimental results might not have been the desired results, and that data might have been changed to… better fit a hypothesis.”

Alzheimer Drugs Target Protein That May Not Be Cause of Disease

While both drugs target the Aβ protein, leqembi works by targeting a particularly toxic form of Aβ called protofibrils.³

Schrag, who has heavily researched the Aβ protein hypothesis, believes the hypothesis appears to be, if anything, a very small component of the disease process. “We need to have a big rethink of this disease,” he said “We need to have investment in these alternative pathways. We need to develop a much more intellectually diverse field and not punish people for not working on the leading hypothesis.”³

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