In my last post, I wrote about BCMA CAR-T therapy — one of two treatments I’ve been tracking closely as someone who has been using a wheelchair outdoors since 2019.
This post is about the other treatment – an anti-ETX monoclonal antibody called AST-001. It has the potential to offer a much cleaner safety profile than BCMA CAR-T.
Timothy Vartanian was my neurologist. He and Rick Rudick founded Astoria Biologica, a company developing an antibody therapy for MS that neutralizes epsilon toxin (ETX), a byproduct of infection by the C. perfringens (CP) bacteria. The hypothesis: a bacterial toxin created from a bacteria you ingest from food, water, or the environment, crosses into your brain, damages the myelin sheath directly, and which then triggers the immune response that current MS drugs work so hard to suppress. If that’s right, then every drug I’ve ever taken — every drug almost every MS patient has ever taken — addresses only the effects of the bacteria, not the cause.
Tim’s team has demonstrated a causal relationship between ETX and the pathogenesis of MS. CP is widespread: it is found in meat, in the environment, and anywhere you find hoofed animal products. The bacterium is particularly associated with horses and sheep — animals central to the nomadic cultures of the Caucasus and Central Asian steppe. MS is believed to have originated roughly 5,000 years ago, when people bedded down with their herds. However, when people moved indoors, their immune systems overreacted to the bacteria, causing an extreme reaction.
For most people, CP infection causes no lasting harm. But in patients with the ‘right’ genetic susceptibility, infection produces ETX as a byproduct, which crosses the blood–brain barrier and triggers the cascade of events we recognize as MS.
ETX produced by the infection damages myelin, which stimulates the immune system to attack the brain. In that setting, ETX leads to brain inflammation. Currently, scientists do not understand why some have healthy controls have low levels of toxin in the gut. One possibility is that these people do not have the genetic predisposition for autoimmune brain inflammation. However, more research will have to be done to draw a conclusion.
I saw Tim about a year before he died. He told me that Mavenclad— which I had just completed year 2 in June 2025 — was sometimes called “Lemtrada lite.” Lemtrada is currently the MS drug with the highest efficacy, but also the one with one of the highest serious side effect profiles. In February 2026, I was hospitalized with urinary sepsis and later treated with Linezolid for VRE — a drug-resistant infection that requiresis one of the last-resort antibiotics to treat. So I know frm experience what it means to have your immune system tamped down by MS drugs year after year.
I told Tim once that UTIs would do me in before the MS did. Because the results of CAR-T are so promising, I would be tempted to join a clinical trial. At the same time, I think the wiser MS patient who has been on several immune modifying DMT’s might choose to wait for the approval of an anti-ETX monoclonal antibody rather than heading in for the chemo destruction, followed by a rebuild of their immune system required by BCMA CAR-T theraoy. Although I’ve never been a wise MS patient; at 64, I may have acquired the wisdom – the wariness, really – that comes from having taken every likely MS DMT.
The Question Nobody Was Asking
Yinghua Ma, Tim’s colleague who worked in his lab for twenty-four years, wrote a tribute to him after he died on October 25, 2025. He described the question that animated the last decade of Tim’s scientific life.
While the entire field of MS research was focused on autoimmunity — the immune system attacking the myelin sheath — Tim asked a different question: What starts it? He was convinced that autoimmunity was a consequence, not a cause. There had to be a first trigger. An environmental factor. Something that came before the immune response.
That conviction launched a decade-long quest that led to Tim’s defining discovery: a link between epsilon toxin, a byproduct of CP infection and MS. He spent the last years of his life working on something different.
AST-001: Not Another Immune Suppressant
Astoria Biologica — co-founded by Tim Vartanian and Rick Rudick, and others from Weill Cornell and Rockefeller University – has developed a monoclonal antibody they named AST-001. It neutralizes ETX directly.
It does not deplete your B cells. It does not suppress your T cells. It does not require chemotherapy. It targets the toxin itself — the thing that, if the hypothesis is correct, initiates the cascade that destroys myelin and ultimately disables people like me.
So let me say clearly: AST-001 has not been tested in humans yet. Everything I have described is preclinical, and first-in-human trials are not expected to begin until 2027, with safety and early efficacy data anticipated in 2028.
This potential drug is more compelling than any other MS drug I’ve researched, and the fundamental premise — that you could neutralize the trigger rather than suppress the response — matters to someone who has been on immune-suppressing therapy for fifteen years and spent time in the hospital because of it.
What Epsilon Toxin Is, and Why It Matters
CP is a bacterium found in soil, farm runoff, marine sediment, and the gut microbiomes of animals and humans. Certain strains produce epsilon toxin — a pore-forming toxin that can cross the blood–brain barrier, bind to the CNS microvasculature, and cause demyelination.
The research from Tim’s lab and his collaborators — published in peer-reviewed journals including PLOS Pathogens and the Journal of Clinical Investigation — has produced a substantial body of preclinical evidence:
A Disclosure
Through my nonprofit, the Mind Brain Foundation, we continue to fund research at Weill Cornell. Jennifer Linden, one of Astoria’s founders, is an affiliated researcher there. Ian Green, my partner and co-founder of the Mind Brain Foundation, and I have invested in Astoria Biologica, and I hope to be among the first patients in their clinical trials, if AST-001 gets there.
Our investment was an act of faith in a man — in Tim, and in the decade he and his colleagues devoted themselves to a question the rest of the field isn’t asking. We believe so strongly in his work and in his legacy to his patients and colleagues that we want to continue to be part of whatever comes next with this drug. I am convinced that he did not leave us all sitting here with nothing.
Please weigh everything I’ve written here with that in mind.
