Mathew Maurer, MD, is the Arnold and Arlene Goldstein Professor of Cardiology at Columbia University Irving Medical Center, Vagelos College of Physicians & Surgeons.

Mathew Maurer, M.D.

I-124 evuzamitide positron emission tomography (PET)/computed tomography (CT) scans are highly sensitive and specific for detecting cardiac amyloidosis, according to results from the REVEAL study.

I-124 Evuzamitide PET/CT Highly Sensitive, Specific in Amyloid Detection

Heart Failure Society of America (HFSA) Annual Scientific Meeting 2026

 in Phoenix, Arizona, by Mathew Maurer, MD, the Arnold and Arlene Goldstein Professor of Cardiology at Columbia University Irving Medical Center, Vagelos College of Physicians & Surgeons.

“We think that this could be a very useful way to not only diagnose amyloid but diagnose it in a more sensitive and potentially more specific manner than currently available imaging,” Maurer told 

 in an exclusive interview. “And, importantly, at a time when the patient doesn’t have advanced cardiac amyloid, when drug therapy is most effective.”

REVEAL was a phase 3, open-label, multicenter study of I-124 evuzamitide as an imaging agent to diagnose cardiac amyloidosis. Patients were eligible for enrollment if they were suspected of having cardiac amyloidosis and were or would be undergoing a diagnostic evaluation for cardiac amyloidosis, among other criteria. Patients were excluded if they had an already established diagnosis of cardiac amyloidosis, were receiving therapy for amyloid transthyretin (ATTR) cardiac amyloidosis at enrollment, or had a myocardial infarction within 3 months of screening, among other criteria.

Patients were administered a single dose of I-124 evuzamitide, which was administered intravenously. This was followed by oral potassium iodide for 3 days and a safety follow-up of 5 +/-2 and 30 +/- 5 days, at which point clinicians conducted safety blood tests. Standard-of-care tests were then undertaken up to day 60. The trial’s primary endpoint was the sensitivity and specificity of PET/CT images based on visual scan interpretation versus adjudicated diagnosis. The secondary endpoint was sensitivity and specificity by amyloid subtype.

After taking PET/CT scans, the resulting images were de-identified and interpreted by 3 physicians with extensive experience, looking for the visual presence or absence of I-124 evuzamitide uptake. The standard-of-care diagnostic evaluations were interpreted by 3 amyloid expert physicians to determine diagnosis of cardiac amyloidosis based on current guideline recommendations. Both groups were blind to clinical data.

A total of 195 patients were ultimately enrolled in the trial, of whom 170 received evuzamitide. Among these 170 patients, average NT-proBNP was 471 ng/L, while average LV wall thickness was 13 mm and LV ejection fraction was 57%. Additionally, 54 patients were confirmed to have ATTR, 21 had amyloid light-chain (AL), and 93 had no cardiac amyloidosis.

Maurer and colleagues ultimately recorded an overall sensitivity of 93.5% (95% CI, 85.5-97.9; 

 <.0001) and a specificity of 86% (95% CI, 77.3-92.3; 

 <.0001) with I-124 evuzamitide. The negative prediction value was 94.1% (95% CI, 86.8-98.1) and the positive prediction value was 84.7%. Sensitivity was comparable among patients with ATTR (96.3%, 52 of 54) and AL (95.2%, 20 of 21). Additionally, evuzamitide PET outperformed bone scintigraphy in early ATTR, primarily in early, low-burden ATTR; 44% of PET-detected adjudicated ATTR had low natriuretic peptides or normal wall thickness, and 8 patients who were equivocal or negative on bone scintigraphy were detected by evuzamitide PET.

Ultimately, Maurer and colleagues concluded that these data reflect evuzamitide PET scanning’s capacity to streamline 

 amyloid evaluation and to identify early ATTR currently missed by imaging. While Maurer cites a handful of limitations inherent in the study’s structure, he is optimistic about the potential of this novel scanning technology.

“We’re at a tipping point here where we can identify amyloid early,” Maurer said. “Amyloid is not pathologically normal, so it’s never normal to have amyloid in an organ, and as a result, we’ve been talking about earlier diagnosis for years, if not decades. This particular scanning technique could provide a real opportunity to improve outcomes for patients.”

Editors’ Note: Maurer reports disclosures with Alnylam, AstraZeneca, Bridge Bio, Ionis, Novo Nordisk, Pfizer, and others.

Maurer M, Masri A, Ezzeddine O, et al. 124I-Evuzamitide Amyloid-Targeted PET/CT: Detection of Early Cardiac Amyloidosis in a Prospective Multicenter Phase 3 Study Cohort. Presented at the Heart Failure Society of America (HFSA) Annual Scientific Meeting 2026, Phoenix, AZ. October 9-12, 2026.

Sharmila Dorbala, Brigham and Women’s Hospital. REVEAL - Research With I-124 EVuzamitide to Elucidate Cardiac AmyLoidosis (REVEAL). ClinicalTrials.gov Identifier: NCT06788535. Updated April 30, 2026. Accessed October 16, 2026. 

https://clinicaltrials.gov/study/NCT06788535?term=NCT06788535&rank=1

Videos

Mathew Maurer, MD, discusses the results of the phase 3 REVEAL study, which highlighted this novel scanning technology’s capacity for identifying amyloidosis early.

In an interview with Rare Disease Report, Mathew Maurer, MD, Arnold and Arlene Professor of Cardiology at Columbia University, explained the standard of care and current management tactics for individuals with hATTR Amyloidosis.

The standard treatment, or I should say management for this condition, is very different than what we hope treatment will be. Currently we manage the condition and the manifestations by treating the symptoms of, if you will, heart failure. We encourage patients to stay physically active, avoid smoking, adhere to a relatively low sodium diet, assuming they have a clinical syndrome a heart failure which means they’re swollen and full of water, and we also encourage self-management skills. For instance, weigh yourself on a daily basis because when you have some dietary indiscretion, eat a little extra salt, you can gain a lot of fluid pretty quickly and that can really exacerbate your baseline symptom—make you have much shorter breath. Those are kind of management strategies&mdash;none of them are treating the underlying condition. 

However, we’ve learned a great deal about this particular disease. We’ve learned that this protein 

, which is a small protein with only 127 amino acids. It fits together with 3 identical 

 proteins to make a 4-leaf clover, and the disease is mediated by the fact that when the protein falls apart or misfolds, the pieces get stuck in the heart.

So, there are actually 3 emerging treatment strategies. The first for cardiac amyloid is what’s called 

 stabilization. These are small oral drugs that fit in-between the leaves of the protein and actually keep the protein together, so called stabilizing it, the theory being that if the protein does not fall apart, you will slow down the progression or ideally halt the progression of the disease. There are several compounds that have been investigate in this area, one called diflunisal, which is a non-steroidal anti-inflammatory agent that’s available by prescription.

Then more recently there’s a drug called tafamidis, which recently reported in a large Phase 3 trial that they met their primary endpoint, which means the drug was reportedly successful, and we’re anxious to learn more. So that’s one of the first standard therapies that will come for 

The second strategy is what’s called silencing in which drugs usually administered by intravenous or by subcutaneous, underneath the skin injection, can amazingly go to the liver, go to the liver cells, and tell them, “

don’t make the protein anymore. Continue to do everything else you do but silence the production of that particular protein.” These aren’t pie-in-the sky ideas, these drugs exist, and they’ve been tested. They’ve mainly been tested in patients who have mutations in the 

 gene that causes a neuropathy, problems in the nerves not a cardiomyopathy, but they have been shown in recently conducted Phase 3 trials to be very effective. We have a lot of hope for those agents to be to patients with 

The final emerging idea at this point, which is really early in its infancy, is the idea of using what we would call monoclonal antibodies to target the amyloid that already exists inside the heart and try to activate the immune system and allow it, if you will, like pac-man to chew up and eliminate the amyloid that already exists. Those are the 3 strategies currently in development for the treatment of the problem.  

Mathew Maurer, M.D.

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