What is ALS, and why does it matter?
ALS, or amyotrophic lateral sclerosis, is a brutal disease. It eats away at the nerve cells that control your muscles-until you can’t move, speak, swallow, or breathe on your own. There’s no cure. No magic fix. And most people live only 3 to 5 years after symptoms start. That’s why even a small extension of life-just a few months-feels like a lifeline.
It’s not just about weakness. It’s about losing the ability to hold your child’s hand, to laugh without choking, to turn over in bed. The brain still works. The mind is clear. But the body? It’s slowly shutting down, one muscle at a time. That’s what makes ALS so terrifying-and why any treatment that slows it down, even a little, becomes essential.
Riluzole: The first real weapon against ALS
In 1995, after decades of failed experiments and dead ends, the FDA approved riluzole. It was the first drug ever shown to make a measurable difference in ALS. For the next 22 years, it was the only option. Today, other drugs exist-but riluzole is still the most widely prescribed treatment worldwide.
Riluzole doesn’t reverse damage. It doesn’t bring back lost strength. But it does something rare in ALS: it buys time. Clinical trials showed it reduces the risk of death or needing a breathing tube by about 35% over 18 months. That translates to roughly 2 to 3 extra months of life on average. Sounds small? In a disease where most people don’t make it past two years, those months mean birthdays, holidays, final conversations. One patient told me, "I got to see my granddaughter graduate. That was worth the nausea."
How does riluzole actually work?
The science behind riluzole is messy. Even after 30 years of research, scientists still don’t fully understand how it works. But they know it targets glutamate-the brain’s most common excitatory chemical.
In ALS, too much glutamate builds up around motor neurons. It’s like a constant scream that overstimulates and kills the cells. Riluzole steps in by:
- Blocking the release of glutamate from nerve endings
- Reducing the activity of sodium channels that trigger glutamate release
- Interfering with glutamate’s effects on NMDA receptors
It’s not a perfect fix. Other drugs tried to do the same thing and failed. That’s why researchers think riluzole might have other, hidden effects-maybe on inflammation, energy use in neurons, or cell survival pathways. We don’t know yet. But it works, even if we can’t fully explain why.
Dosing, forms, and what to expect
Riluzole comes in three forms:
- Tablets (Rilutek): 50mg, taken twice daily
- Oral suspension (Tiglutik): Liquid form for people who have trouble swallowing
- Oral thin film (Exservan): Dissolves on the tongue-no water needed
The standard dose is 100mg per day: two 50mg tablets, one in the morning and one at night. You don’t take it all at once. The body clears it in 7 to 15 hours, so twice-daily dosing keeps levels steady.
It’s absorbed at about 60% efficiency. That means if you take a 50mg tablet, only about 30mg actually gets into your bloodstream. That’s why timing matters. Take it with food if you get nauseous. Skip the coffee-caffeine can interfere with how your body processes it.
Side effects: The price of extra time
Most people tolerate riluzole, but not without cost. The most common side effects are:
- Nausea (25% of users)
- Diarrhea (15%)
- Fatigue (20%)
- Elevated liver enzymes (12%)
Liver damage is the biggest concern. That’s why doctors require blood tests before you start-and monthly for the first three months. If your liver enzymes spike, you stop. No exceptions. One patient on Reddit wrote: "After 9 months, my liver was fried. I had to quit. Felt like I lost my only shot."
Eight percent of people stop taking it because side effects are too much. But 62% of patients in one survey kept going-even with nausea, fatigue, and monthly blood draws-because they believed it was helping. "I’d rather be sick and alive than healthy and gone," said a woman in her 50s who’s been on it for 4 years.
Real-world results: Does it actually work?
Here’s the tricky part. In clinical trials, riluzole showed clear survival benefits. But in the real world? Results are mixed. Some studies show 6 to 19 extra months. Others show no difference at all.
Why? Because ALS isn’t one disease. It moves differently in every person. Some decline fast. Others crawl. Some have genetic forms. Some start with speech problems. Others lose arm strength first. Riluzole might help one person more than another-and we still don’t know why.
Still, major medical groups stand by it. The American Academy of Neurology gives it a Level A recommendation-the strongest possible-based on multiple high-quality studies. It’s not a miracle. But it’s the best we’ve had for decades.
Riluzole vs. newer ALS drugs
Since 2017, two other drugs have joined the fight: edaravone and tofersen.
Edaravone (Radicava) is an antioxidant that reduces oxidative stress. It’s given as an IV infusion or oral suspension. It doesn’t extend life, but it slows functional decline in some patients-especially early-stage ones. It’s expensive and requires frequent clinic visits.
Tofersen (Qalsody) is a gene therapy for the 2% of ALS patients with SOD1 mutations. It’s injected into the spinal fluid. It’s targeted, powerful, and only works for a tiny group.
Riluzole? It works for everyone. No genetic testing needed. No infusions. Just a pill. That’s why, despite newer options, it’s still the first drug most neurologists prescribe.
Who should take riluzole? Who shouldn’t?
If you’ve been diagnosed with ALS, riluzole is almost always recommended-unless you have severe liver disease. If your liver is already damaged, riluzole can make it worse. No exceptions.
It’s not for people with kidney problems? Actually, it is. Kidney function doesn’t affect how riluzole is processed. Only the liver does.
Drug interactions matter too. Riluzole can raise the levels of theophylline (used for asthma), which can be dangerous. Caffeine can slow its breakdown, making side effects worse. Always tell your doctor what else you’re taking-even over-the-counter stuff.
And yes, it’s expensive. Even after patents expired, brand-name versions still cost $500-$800 a month in the U.S. Generic versions are cheaper, but access is still a problem in low-income countries. Only 15-20% of ALS patients there can afford it without help.
What’s next for riluzole?
Researchers aren’t giving up on it. New formulations are making it easier to take. The thin film version (Exservan) causes 30% less nausea than tablets. That’s huge for people who are already struggling to eat.
There’s also a trial right now in Michigan testing riluzole combined with sodium phenylbutyrate. Early results suggest it might protect neurons better than riluzole alone. If it works, we could see combination therapies become standard.
And while gene therapies like tofersen are exciting, they only help a small slice of patients. Riluzole? It’s the baseline. The foundation. For the next decade, it’s likely to remain the first step in ALS treatment-no matter what else comes next.
Final thoughts: A modest drug, a massive impact
Riluzole isn’t glamorous. It doesn’t cure ALS. It doesn’t restore movement. It doesn’t even make everyone feel better. But it’s the only drug that’s ever given people with ALS a real shot at more time.
Three months might not sound like much. But for a parent, it’s one more Christmas. For a spouse, it’s one more morning coffee together. For a patient, it’s the chance to say goodbye properly.
In a world where ALS steals everything, riluzole gives back a little. And sometimes, that’s enough.
