

Bristol Myers Squibb just dropped five years of follow-up data for Camzyos at ESC Congress 2026, and the results held up across the board. Nearly every patient hit their target, most became asymptomatic, and a billion-dollar drug just got a lot harder to argue against.
Imagine buying a car and the dealership says, "We've only tested this engine for six months." You'd probably want more road time before committing. That's essentially what doctors face when prescribing a new heart drug: short clinical trials show promise, but nobody knows what happens years down the road.
Bristol Myers Squibb just answered that question for Camzyos, its blockbuster heart medication. At ESC Congress 2026, the company dropped five years of follow-up data on patients with obstructive hypertrophic cardiomyopathy (oHCM), a condition where the heart muscle gets abnormally thick and blocks blood flow. The results? The drug kept working. No ugly surprises hiding in the fine print.
That matters more than you might think.
To understand the data, you need a quick primer on the disease. In oHCM, the heart muscle bulks up like an overzealous gym rat, squeezing the outflow tract (the exit ramp where blood leaves the heart). Patients feel short of breath, fatigued, and sometimes faint. Before Camzyos, the main options were beta-blockers, calcium channel blockers, and eventually surgery to physically shave down the extra muscle.
Camzyos works differently. It's a cardiac myosin inhibitor, which means it dials down the force of heart muscle contractions at the molecular level. Think of it like turning down the volume on a speaker that's cranked too loud. The heart still beats, but it stops squeezing so hard that it blocks its own plumbing.
When the FDA approved it in 2022, the pivotal trial (EXPLORER-HCM) only had 30 weeks of data. Impressive, but cardiologists prescribing a lifelong drug understandably wanted more mileage on the clock.
Now they have it.
At 252 weeks (nearly five years), the results paint a clear picture of durability. Resting pressure gradients in the heart's outflow tract dropped by 38.7 mmHg, while the more demanding Valsalva measurement (where patients bear down to stress the system) fell by .

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Put differently: almost every single patient got better. A staggering 97.4% of patients reached the target threshold that cardiologists consider a successful response. That's not a marginal improvement; it's near-universal.
The functional improvements tracked alongside those hemodynamic wins. About 70% of patients improved by at least one NYHA class (the standard grading system for heart failure symptoms, ranging from I to IV). And 59.2% became asymptomatic, meaning they went from feeling limited by their condition to feeling essentially normal.
For context, in the original 30-week trial, 65% of patients on Camzyos improved by at least one NYHA class versus 31% on placebo. The five-year data show those gains didn't fade. They held.
Long-term data isn't just about proving a drug keeps working. It's about proving it doesn't slowly poison you. This is where Camzyos had a lingering concern: because the drug weakens heart contractions on purpose, there's always been a worry that it might weaken them too much over time.
The five-year data showed that LVEF (the percentage of blood the heart pumps out with each beat) remained within the normal range, and no new safety signals emerged beyond what was already known from the original study.
Still, LVEF trends are worth watching. It's the kind of metric that keeps cardiologists vigilant with monitoring, even if it hasn't translated into clinical problems yet.
These aren't just academic results for Bristol Myers Squibb. They're fuel for a commercial rocket ship that's already airborne.
Camzyos pulled in $1.068 billion in 2025 revenue, a 77% jump from $602 million in 2024. International sales grew by more than 200%. And the momentum hasn't slowed: Q1 2026 sales hit $314 million, nearly double the $159 million from the same quarter a year earlier.
Five-year durability data is the kind of evidence that makes doctors more comfortable prescribing, insurance companies more willing to cover, and patients more likely to stay on therapy. BMS is clearly banking on this ESC presentation to shift the conversation from "novel drug option" to "standard of care."
Camzyos isn't the only cardiac myosin inhibitor in the game. Aficamten, developed by Cytokinetics, is knocking on the door with some compelling advantages.
In the MAPLE-HCM trial, aficamten beat metoprolol (a standard beta-blocker) head-to-head on exercise capacity, positioning it as a potential first-line therapy rather than a second- or third-line add-on. Reviews also describe aficamten as having a wider therapeutic window, faster dose titration, and a less burdensome drug interaction profile.
If Camzyos is the Toyota Camry of cardiac myosin inhibitors (reliable, first to market, proven track record), aficamten is trying to be the Tesla: newer, potentially more convenient, and aiming to leapfrog straight to the front of the treatment algorithm.
Camzyos's five-year data is a powerful counter-punch. No competitor can match that kind of long-term evidence yet. But the competitive window won't stay open forever.
The 2024 AHA/ACC guidelines already carved out a role for cardiac myosin inhibitors before invasive surgery in appropriate patients. That was a big deal, because it shifted oHCM treatment from a "try pills, then cut" paradigm to one where targeted pharmacology could potentially replace the scalpel.
Five years of durability data strengthens that argument considerably. If patients are still responding at year five with no new safety concerns, the case for trying Camzyos before sending someone to a surgical suite gets much harder to argue against.
BMS is also presenting adolescent data and real-world cohorts at ESC 2026, which could widen the addressable market further. The company has framed this as the largest body of worldwide evidence for any cardiac myosin inhibitor, a claim that's tough to dispute right now.
This ESC presentation won't cause a stock price earthquake. It's incremental, not transformative. But in medicine, incremental proof of durability is exactly how drugs graduate from "interesting option" to "obvious choice."
For the roughly 200,000 Americans with symptomatic oHCM, the message is simple: the first drug designed specifically for their condition works, it keeps working, and five years later, the side effects look manageable. That's not revolutionary news. It's something better: it's reassuring news. And in cardiology, reassurance is worth its weight in gold.
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