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This is a guest essay by Mitch Schneider, a writer in Israel.
You can also listen to the podcast version of this essay on Apple Podcasts, YouTube Music, YouTube, and Spotify.
The cruelest thing about ALS isn’t that it kills you. Plenty of diseases kill you. It’s that it takes you apart while you’re still sitting there watching it happen.
The mind usually stays. That’s the part most people don’t know.
In the majority of cases, the person is fully present, sharp, aware, remembering your name, and following every word, while the body switches off around them one muscle at a time. First a hand gets clumsy. Then an arm won’t lift. Then the legs go, then the voice, then the ability to swallow, and eventually the muscles it takes to breathe.
Two to five years is the usual span from first symptom to the end, and the person is awake for all of it.
Families who’ve lived it know the harder version: About half of patients show some change in thinking or behavior, and around one in seven meets the criteria for a form of dementia alongside the paralysis, though that second figure moves with how it’s defined. But for most, the person is entirely there.
Its full name is amyotrophic lateral sclerosis. You probably know it by the famous people it took, such as the baseball player Lou Gehrig and the physicist Stephen Hawking, who spent decades locked into a wheelchair and a computer-generated voice.
What’s happening underneath is that motor neurons are dying. Those are the nerve cells that carry the command from your brain down to your muscles, the wiring between the decision to lift your arm, and the arm lifting. The decision keeps getting made. The wire stops carrying it.
The first drug ever approved for ALS arrived in 1995. It’s called riluzole, and in the trials that got it approved it extended survival by about two to three months. In the biggest study, the median gain was 60 days. That was the best news the field had ever had.
The second drug, edaravone, didn’t arrive until 2017, and it helps slow the loss of function on some measures without clear evidence that it lets people live longer. Then there was Relyvrio, dreamed up by two Brown University students in a dorm room the year before the Ice Bucket Challenge, and the ALS Association put over $2 million behind it. When the mid-stage results came in positive, patients and advocates ran a campaign to get it to market fast, submitting more than 50,000 signatures to the U.S. Food and Drug Administration.
It worked. The drug was approved in the United States and Canada in 2022.
Then came the big confirming trial, the one with enough patients to give a clear answer. Relyvrio missed every goal it had been given, and the company pulled it off the market in 2024. The approval was formally withdrawn. Patients who’d been taking it, who’d fought to be allowed to take it, lost it.
So when the Ice Bucket Challenge poured roughly $115 million into the ALS Association in the summer of 2014, it wasn’t wasted. It funded real science. Some of that science became a drug that reached patients and then got recalled.
Part of the problem is that ALS isn’t one broken thing, but several at once. The motor neurons are dying for a tangle of reasons that seem to feed each other. There’s inflammation. There’s a strange buildup of iron. There’s a breakdown in how cells handle RNA, both the working copies of genetic instructions that tell a cell what to build and the smaller regulatory strands that decide how much of each instruction gets read.
Chase one of those with one drug and you’re trying to stop a house fire by closing a single window, while smoke pours through the other three.
In 2004, Avi Kremer was a captain in the IDF, a graduate of Technion (a public research university located in Haifa, Israel), and a project manager at Elbit Systems (military technology company and defense contractor), and he’d just been admitted to Harvard Business School.
He was diagnosed during his first semester. He was 29.
His classmate Nate Boaz laid out the choice years later: Go home to family and friends or fight back — and most of us would have gone home. Kremer stayed. He founded Prize4Life in 2006 and an Israeli sister organization, Pras-la’Chaim, in 2007, on a simple idea: If drug companies won’t chase a rare disease, put up cash prizes and let anyone in the world come try. He ran it for most of 12 years and put up two $1-million prizes.
Then in 2011 the disease found Shay Rishoni. He’d flown commercial airliners, served as a colonel in the IDF, guided treks around the world, and finished an Ironman race. He had an MBA, a wife, and two sons.
Within two years, he was completely paralyzed and on a ventilator, communicating through a computer that tracked his eyes. And from that chair he took over as CEO of Prize4Life. In 2015, he addressed a technology conference in Tel Aviv through the eye-tracking device, and the first thing the computerized voice said was, “Hi, my name is Shay Rishoni, I’m the CEO of Prize4life.” The room went quiet.
He also co-founded a company called EyeControl, building better communication technology for people in exactly his condition. He was constructing the thing he needed while he needed it.
In 2016, he met a biotech consultant named Alon Ben-Noon, who had never met an ALS patient before. Rishoni pushed him to use his resources and go find a treatment. He knew perfectly well that nothing then in development could arrive in time to save his own life.
Ben-Noon founded NeuroSense in 2017, working out of Herzliya, a coastal city just north of Tel Aviv. Rishoni died the following year.
Here’s the decision that makes this story different from 30 years of failures: If ALS is several problems at once, and if brand-new molecules keep dying in trials, then stop trying to invent the miracle. Go shopping instead. Comb through drugs that are already approved for other conditions, that doctors have prescribed safely for years, and look for a combination that hits several of the disease’s mechanisms together.
They landed on two drugs that have been sitting in pharmacies for decades. One is ciprofloxacin, a common antibiotic, the kind you get handed for a stubborn infection. The other is celecoxib, an anti-inflammatory sold to arthritis patients for years. Separately, neither has anything to do with ALS.
There’s a hard-nosed advantage here on top of the poetry: A brand-new molecule has to prove from scratch that it’s even safe to put in a human body, which takes years and kills most candidates before anyone learns whether they work. Those drugs have cleared that bar. The doses are mapped and the risks are documented, which isn’t the same as saying either drug is harmless. For a disease that moves this fast, that head start is close to everything.
NeuroSense combined the two into a single slow-release pill and called it PrimeC. In the company’s own careful words, it’s designed to target several key mechanisms that contribute to neuron degeneration, inflammation, iron accumulation, and impaired RNA regulation, with the potential to inhibit disease progression.
A mid-stage trial called PARADIGM enrolled 68 people with ALS across Canada, Italy, and Israel — two-thirds of them on PrimeC and the rest on placebo — for six months. Neither the patients nor their doctors knew who was getting which. Most people in both groups were already taking riluzole, so PrimeC was being tested on top of the existing standard of care rather than against it.
Start with the hardest number: By the company’s own reckoning of its long-term follow-up data, the gap in median survival between the two groups came out to roughly 15 months. That’s the company’s own look at a small study rather than a number a regulator has signed off on, so it isn’t a fair one-to-one against the approvals that came before. Put it next to a disease whose first approved drug bought 60 days anyway.
Then, in June 2026, the trial met its main scientific goal.
There’s a protein called TDP-43. In a healthy nerve cell, it does a housekeeping job in the cell’s control center. In ALS, it goes wrong and clumps where it doesn’t belong, and pathologists find that signature in 97 percent of ALS cases.
Now, the usual way to measure whether an ALS drug is working is a 48-point checklist called the ALSFRS-R, which scores what a patient can still do, from walking to speaking to breathing. That’s measuring the damage from outside, like judging a fire by how much of the house has burned. Measuring TDP-43 is more like reading the temperature inside the walls.
PrimeC lowered it. The company reports a statistically significant reduction against placebo at six months, at p=0.0421. A p-value is the statistician’s estimate of how likely a result like this would turn up by chance alone. Under 0.05 counts as significant by convention, and 0.0421 clears that line without much room to spare.
It reports a deeper effect at 18 months, though by then there was no placebo group left to measure against. Nearly everyone who finished the first six months rolled into an extension where all of them got the drug, so the later comparison is between patients who were on PrimeC the whole time and patients who started six months late.
On the older checklist measure, counting only the patients who completed the six-month trial exactly as prescribed, function declined about 37 percent more slowly than on placebo.
PrimeC is investigational. It isn’t approved in the United States, Israel, or anywhere else; no patient can get a prescription for it; and everything above comes from a study of 68 people.
In November 2025, the U.S. Food and Drug Administration cleared NeuroSense to run its pivotal Phase 3 trial, called PARAGON, designed for 300 patients over 12 months. Clearance means permission to run the test. It is not a judgment that the drug works.
Meanwhile, the company is targeting December 2026 to file for approval in Canada, based on the mid-stage evidence. If Health Canada accepts the filing, and if the review goes the company’s way, and if the Phase 3 confirms what the smaller trial suggested, then there’s a treatment.
You may have already noticed that filing before the confirming trial reads out is close to what happened with Relyvrio. That’s a fair thing to sit with. The ALS Association, which pushed hard for that early approval and watched it collapse, still stands by the decision, because patients told the U.S. Food and Drug Administration plainly that they’d rather take the risk than wait.
For 30 years, the smartest people working on this disease kept reaching for something new: a designed molecule or a breakthrough compound, the miracle that was always one trial away.
It took a company in Israel, founded because one man couldn’t stop thinking about another man who was vanishing in front of him, to try the humbler thing. Two ordinary pills, each of them approved for something else decades ago, aimed together at a disease that has beaten everything thrown at it one piece at a time.
Maybe the big trial bears it out. Maybe it doesn’t. Nobody in Herzliya is promising you the ending before it’s earned, but look at what happened here.
A 29-year-old Israeli got a death sentence at Harvard University and built an institution instead of going home. A paralyzed colonel ran that institution through his eyes, built communication technology for people who couldn’t speak, and spent his last working years recruiting a healthy stranger into a fight he knew he would lose before it was won.
Alon Ben-Noon brought the early laboratory results to Shay Rishoni personally, and describes him as visibly excited by what he saw. He died a few months later. Avi Kremer was still alive 22 years past a diagnosis that gives most people two to five.
Inspiring, well-written, timely article. One hopes the same determination, commitment and focus will lead to a cure for other deadly neurological diseases, such as glioblastoma.
With the six scientific revolutions in our hands (RNA science, immuno-oncology, AI/ML; cancer neuroscience; biomarkers-liquid biopsy; advanced neuroimaging), we can figure it out. The best is yet to be!
I lost a dear cousin to MDS and I wish to God that this possible cure could have been there for him in his time. I pray that it will prove to be the answer, and I'm very proud that it's an Israeli group that found it. The world that is anti-Semitic and anti-israel will benefit from this and other life saving procedures that Jewish scientists have already discovered.