Why we're building this

My wife Moran was diagnosed with a Grade 3 astrocytoma in 2024. IDH1-mutant — a brain tumor with a specific genetic fingerprint that has become the center of everything we do.

I'm a builder. I spent years in product and engineering. When Moran's diagnosis came, I did what builders do: I read everything, I mapped the problem, I looked for the gap. And I found one.

The IDH1 mutation causes her tumor to produce a molecule called 2-hydroxyglutarate — 2-HG. It does two things: it locks the tumor's cells in an aggressive state, and it suppresses the immune cells that would otherwise attack it. It's a metabolic trick the tumor runs to hide from the body's own defenses.

There's a drug for this. Vorasidenib, approved in 2024, blocks the mutant enzyme from making new 2-HG. Moran is on it. It's approved for grade 2 disease and is in a Phase 2 trial for grade 3 — a genuine advance, and we're grateful for it.

But grade 3–4 is a harder problem. At this stage the tumor doesn't lean on 2-HG alone; it has several ways to blind and disarm the immune system, so slowing 2-HG production is only part of the picture. And underneath that sits a deeper problem no drug on the market solves.

You cannot cut out or reach the whole tumor. By the time it's found, it has already spread as single cells centimeters into normal-looking brain — beyond anything a surgeon can remove, and too far for any locally delivered agent big enough to act on the tumor to physically travel. That's why it always comes back. The recurrence at the margin isn't a failure of effort; it's a fact of the biology.

There is exactly one thing in the body that can reach those scattered cells at the margin: the immune system. It goes everywhere blood and lymph go. So the gap I found wasn't a molecule to add or subtract — it was a strategy. Wake the immune system up inside the tumor, and let it carry the fight outward, to the places surgery and drugs can't reach.

So we decided to build one.

What we're building

Morca Bio is building a living therapy: engineered bacteria, delivered to the tumor, that ignite a controlled anti-tumor immune response right where the tumor is — and rely on the immune system to carry that response outward to the infiltrating margin.

The tumor's own 2-HG does three jobs for us. It targets the therapy to the tumor — a signal that only this kind of tumor produces. It acts as a leash — the bacteria are built to thrive where 2-HG marks the tumor and to shut down where it doesn't, keeping the therapy contained to where it's needed. And locally, right where the immune response is being lit, it helps lift the brake the tumor uses to hold immune cells off. One molecule, unique to this tumor, doing the targeting, the safety, and the local immune release at once.

Bacteria are a good vehicle for this because they're living, programmable factories: they can make and release more than one payload at a time. Immune activation is the lead — but the same vehicle can be built to do more, from direct tumor destruction to combining with other therapies. Bacteria are the tool we're using now, not the mission. The mission is the patients.

I want to be honest about where this is. It's early — a hypothesis we believe in and are testing rigorously, not a product anyone can get today. And the honest goal isn't a cure; no one has cured this disease. It's meaningful, potentially durable responses for a subset of patients — a real step beyond what today's standard of care can offer. That would be worth everything.

Why in the open

We're doing this in public. Every experiment is named before it runs. Every result is recorded — positive findings and kill criteria alike. The journal is the accountability structure.

We don't have decades. The urgency is personal, and it is real. Openness is how we hold ourselves to it.