The Food and Drug Administration’s decision to greenlight aducanumab (trade name Aduhelm) for Alzheimer’s disease has touched off an explosion of criticism and debate (see Part 1 of this series). Some researchers, however, consider the approval an overall positive development that the neurodegeneration field can build on as it seeks combination therapies that slow disease progression. For example, Ken Marek at the Institute for Neurodegenerative Disorders in New Haven, Connecticut, believes the aducanumab decision heralds the beginning of a new era in neurodegenerative disease research, with a focus on therapies that move biomarkers in Alzheimer's and related diseases and slow the march of the underlying pathology (STAT news). Marek leads the Parkinson’s Progression Markers Initiative, which studies biomarkers of PD.

  • Some Alzheimer’s researchers welcome aducanumab’s approval.
  • Across the board, stakeholders slam the drug’s price tag.
  • Will it cool interest in other therapeutic trials and observational studies?

Dawn of Disease Modification?
Some Alzheimer’s researchers, too, see the approval as a step toward disease-modifying therapies. They draw parallels with the history of drug development in other fields. “I think the FDA decision will benefit the AD field greatly, as did the approval of betaferon for the multiple sclerosis field in 1993. It will boost drug development and research in general,” Philip Scheltens at VU University, Amsterdam, wrote to Alzforum (full comment below). Bart De Strooper, who leads the U.K. Dementia Research Institute at UCL, compared the decision to the fast-tracking of the first drugs for AIDS, which had minimal clinical benefit. “This opened the way for further clinical experimentation and trials and brought the AIDS field in two decades to almost curative therapy,” De Strooper wrote.

Others drew a distinction between the messy approval process for aducanumab and its end result. “We all recognize the liabilities of the path to aducanumab approval, which I believe were more a function of trial execution than an intrinsic weakness of the agent or the biology behind it,” Dennis Selkoe at Brigham and Women’s Hospital wrote to Alzforum. “In my view, the strength of the biology and the clarity of aducanumab’s key biomarker endpoint overcame an imperfect clinical dataset,” Selkoe added (full comment below). Marwan Sabbagh, at the Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas, went further. “It was a transformative moment in the field. It’s the first step toward taking Alzheimer’s from a terminal to a chronic disease,” Sabbagh said.

Other stakeholders hailed the decision, as well. In addition to positive reaction from advocacy groups such as the Alzheimer’s Association and Us Against Alzheimer’s, the Global Alzheimer’s Platform commended the FDA for its stance, and the National Institutes of Health called the approval a milestone achievement. “The hope is greater than it’s ever been before that we’re going to find increasingly effective interventions,” NIA director Richard Hodes told Alzforum.

The Price Isn’t Right
Even those who agree with the FDA’s decision, however, take issue with Biogen’s planned price of $56,000 per patient per year. In a poll of biopharma executives, 75 percent considered this too high, given the drug’s uncertain efficacy and known safety risks. They warned that given the large number of retirement-age people who might qualify for treatment, aducanumab's cost would blow an enormous hole into the taxpayer-funded budgets of Medicare and the Veteran's Health Administration. A recent analysis by the Kaiser Family Foundation estimated aducanumab could cost Medicare $57 billion per year, roughly the same amount as all other hospital outpatient services combined.

The approval could also deepen inequity in the U.S. health care system, where the well-off typically receive better care. “We know there will be disparities in access because our health care system is riddled with them,” Emily Largent, University of Pennsylvania, Philadelphia, wrote to Alzforum (full comment below). Others fear that hope and desperation may prompt patients whose disease is too advanced for them to benefit from this treatment to spend their life savings on out-of-pocket aducanumab.

“This price is simply unacceptable. … We call on Biogen to change this,” the Alzheimer’s Association wrote in a June 12 statement

In a June 8 call with investors, Biogen CEO Michel Vounatsos defended the price, noting that aducanumab’s cost is about one-third that of cancer immunotherapies. He said the company is talking to private insurers such as Cigna about using value-based contracts, which set the price of a drug based on how well it performs, but gave no details on how that would work or what performance benchmarks might be used. He also promised not to raise the price for four years.

Meanwhile, Biogen’s chief financial officer Mike McDonnell estimated that U.S. sales of the antibody would ramp up over several years into the multibillion-dollar range. Mainstream and industry press likewise believe Biogen stands to rake in the cash (New York Times news; Endpoints newsSTAT news). 

Some predicted the antibody’s cost could spur renewed calls for drug pricing reform (Fierce Pharma news; STAT news). One senator has already called for Medicare to have the ability to negotiate cost, specifically citing aducanumab as an example of unjustifiable pricing (Endpoints news). A coalition representing employers and other health care purchasers is advocating for this as well.

Bane or Boon for Alzheimer’s Drug Research?
Many researchers fear the aducanumab approval will complicate their efforts to evaluate better Alzheimer’s drugs. One concern is that patients may prefer to take an approved medication rather than roll the dice on one still in development, especially given that they might end up on placebo. “Once aducanumab becomes commonly available, it’s going to become really hard to recruit for mild cognitive impairment trials,” Sabbagh predicted.

Some worry that participants in ongoing AD trials might drop out to go on aducanumab instead. Researchers at Eli Lilly, who are developing donanemab, among other investigational medicines for AD, did not respond to a request for comment. Roche scientists, meanwhile, expressed confidence in their program. “We are not changing our scientific approach for the pivotal trials of gantenerumab in AD,” Rachelle Doody of Roche wrote to Alzforum. “We're working closely with our investigator network to address any questions they or trial participants may have about continuing in our studies,” she added (full comment below).

Others think the field will adapt. “Finishing current trials will no doubt be more challenging with Aduhelm on the market, but other fields have faced this problem and moved on to add multiple new agents over time,” Selkoe wrote.

A related concern is that the aducanumab approval might lead funding agencies to favor anti-amyloid drugs at the expense of other approaches. The NIH, at least, has no plans to change course. “Right now, the large majority of Phase 1 and 2 [AD] trials are against non-amyloid targets, and this will certainly continue,” Hodes told Alzforum (see Alzforum Therapeutics listing of such trials). Hodes also sees no imperative to change trial designs to compare new drugs against aducanumab as a positive control, given that the antibody has not shown a definitive effect on symptoms.

De Strooper sees ample opportunity in aducanumab’s approval. It will open the door for studies that define the antibody’s benefit in different patient populations and test its efficacy in combination with other drugs. “Alzheimer’s disease and dementia are complicated disorders, and it is unlikely that one simple hypothesis and one golden bullet will explain and treat all,” he wrote.

Many believe this approval will encourage further investment in AD drug research. “History has shown us that approval of the first drug in a new category invigorates the field, increases investments in new treatments, and encourages greater innovation,” wrote Maria Carrillo of the Alzheimer’s Association in a statement. There are already signs of renewed investor interest, with pharma companies reporting a deluge of calls (Fierce Biotech news; related news). In part, investors are lured by the prospect of gaining approval more easily with amyloid reduction data alone.

Retired neurologist Daniel Gibbs of the Oregon Health and Science University, Portland, compared aducanumab to tacrine, the first acetylcholinesterase inhibitor to go on the market in 1993. Tacrine’s efficacy was controversial at the time (Relman, 1991). It was also toxic to the liver and was soon supplanted by other drugs in its class. “Aducanumab may be the tacrine of today: the first drug of its class with likely effectiveness, but it will almost certainly be joined and possibly replaced by other, more effective drugs in the future,” Gibbs suggested.

Selkoe summed up the situation this way: “We have taken a sizeable, albeit controversial, step in the direction of actual disease modification. There’s no going back.”—Madolyn Bowman Rogers

Comments

  1. Overall, the FDA decision is a good thing for patients, the field, and the industry/investment community. I believe this for two reasons:

    1. The accelerated approval acknowledges the severity, fatality, and lack of treatment of Alzheimer’s, placing AD in the same category as cancer. It silences those who still think AD is just a normal part of aging and constitutes a myth.
    2. The FDA approval is for lowering amyloid, i.e., interfering in the disease process, recognizing that this has not led to convincing clinical benefit yet, but is expected to do so over the longer term.  

    To counter the criticism of not finding an effect on the CDR consistently in the two trials, aside from the trials being interrupted and far from perfect, I would say that it is quite unrealistic to find such an effect if treatment is started 10-15 years after onset of disease and using insensitive clinical measures such as the CDR. Comparing a quantitative measure such as amyloid-lowering on PET with qualitative measures such as clinical interviews is like comparing apples and oranges. We need much more sensitive and meaningful outcome measures to recognize the effect of disease modification.

    I think the FDA decision will benefit the field greatly, as did the approval of betaferon for the multiple sclerosis field in 1993. It will boost drug development and research in general. Aducanumab is not the definitive answer for many reasons, but it is the beginning of the development of a range of better drugs for our patients.

    Whether this decision will make recruiting for other trials more difficult has to be seen on a case-by-case basis. I am not convinced Aduhelm will be considered the standard of care for all patients. Whether a trial arm with Aduhelm is needed or required for future trials will depend on the trial design, drug, target, and phase. For context, placebo-controlled trials without a donepezil arm are still possible, as well. I do hope the general audience will be inspired and invigorated to take part in clinical trials developing better or different (in many aspects) drugs for AD.

    Compared to the scenario that the FDA had not approved Aduhelm, the future looks a lot brighter now. Of course we as a community have to work out many things: cost, monitoring, patient selection, etc. In that sense, I found the label profoundly inadequate—way too broad—and potentially harmful to patients, the field, and the drug as well. I do hope the EMA will follow the FDA, but will put some effort in restricting the use to a specific population of patients and setting bars for those who want to use this drug.

  2. First and foremost, the FDA’s approval of aducanumab is a signal event for our patients and their families. For the first time, they have an option that may offer modification of the disease in the brain and some slowing of cognitive decline over time in some patients. We all recognize the liabilities of the path to aducanumab approval, which I believe were more a function of trial execution than an intrinsic weakness of the agent or the biology behind it.

    Overwhelming evidence from genetics, cell and animal modeling, biomarker analyses, and other clinical trials all support the conclusions that Aβ accumulation in brain regions serving memory and cognition is a bad thing and that its removal should slow disease. This is what the FDA relied on in reaching their conclusion: that amyloid removal is—and increasingly will be—salutary for slowing decline. In my view, the strength of the biology and the clarity of aducanumab’s key biomarker endpoint overcame an imperfect clinical data set.

    The advent of a first, partial treatment for Alzheimer patients is likely to accelerate numerous further approaches to treating—and especially preventing—the disease, not just via amyloid-lowering but also by targeting tau, inflammation, and other pathogenic events. Finishing current trials will no doubt be more challenging with Aduhelm on the market, but other fields have faced this problem and moved on to add multiple new agents over time. Multiple sclerosis is a compelling example, moving from early, less-than-ideal agents to far more efficacious drugs, now numbering more than a dozen.

    Although thoughtful experts in Alzheimer’s disease and others are deeply disappointed by the decision and concerned about the complexity of administering this agent to many patients (including the management of ARIA), this is a challenge we all have been hoping to have for a long time. Hard work, resourcefulness, and dedication to our patients will likely move us toward feasible treatment plans. We have taken a sizeable, albeit controversial, step in the direction of actual disease modification. There’s no going back.

  3. Given the high price of the drug, we’ll have to see whether—and if so, for whom—insurers cover aducanumab. If they don’t cover it, there will be disparities in access as wealthier patients are able to pay out of pocket and others go without. Even if insurers do cover aducanumab, there will be disparities in access due to out-of-pocket costs that are burdensome or even prohibitive for some individuals. Here, we have to think about the co-payments and co-insurance associated with the infusions but also with the scans and office visits that will be needed.

    Looking beyond the financial aspects, we know there will be disparities in access because our health care system is riddled with them. So many patients go undiagnosed at present. There aren’t enough memory-care specialists to see the patients we have now. It’s simply harder for some patients than others to go into a clinic to get a monthly infusion due to structural barriers. The list goes on.  

    We also need to acknowledge that Alzheimer’s research has a persistent problem with recruiting representative samples. The number of minority individuals enrolled in the aducanumab trials was incredibly small, and now we have access concerns as the drug is approved. Disparities are simply rippling through the system. 

  4. This approval further energizes efforts to better diagnose, and improve outcomes for, people with Alzheimer’s, their families, and society at large. Ongoing research into potential new treatments for AD is critical to meeting the diverse needs of people affected by AD, and to making impactful progress for this community.

    At Roche, we have remained steadfast in our commitment to our ongoing research and studies of investigational medicines for different targets, types, and stages of Alzheimer’s, as well as delivering tests to detect, diagnose, and monitor the disease. This includes our late-stage investigational medicine, gantenerumab, a subcutaneously administered anti-Aβ antibody being evaluated in people with early AD in two global Phase 3 studies. We expect data from these studies in 2022. 

    We are not changing our scientific approach for the pivotal trials of gantenerumab in AD. We are grateful for the ongoing commitment of investigators and participants, and we’re working closely with our investigator network to address any questions they, or trial participants, may have about continuing in our studies.

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References

News Citations

  1. Aducanumab Approval Sparks Backlash

Paper Citations

  1. Tacrine as a treatment for Alzheimer's dementia: editor's note. An interim report from the FDA. A response from Summers et al. N Engl J Med. 1991 Jan 31;324(5):349-52. PubMed.

Other Citations

  1. Alzforum Therapeutics

External Citations

  1. STAT news
  2. commended 
  3. called
  4. analysis
  5. June 12 statement
  6. New York Times news
  7. Endpoints news
  8. STAT news
  9. Fierce Pharma news
  10. STAT news
  11. Endpoints news
  12. advocating
  13. Fierce Biotech news
  14. related news

Further Reading