Two Careers,
One Programme.

Some of the most important things at BioFund look nothing like announcements when they happen. They look like two scientists on a call, agreeing that something is worth trying. This September, one of those calls became a programme.

BioFund's Cell Therapy Research is the long arc: three cycles of seven years. Within it, each Cell Therapy Development Programme runs for three years, and we have just started the first — BF-CT01, which brings together our first molecule and natural killer cells. I want to say a little about what that means. Mostly, though, I want to write about where it came from, because that is the part I find most moving.

Thirty-six years in Szeged.

Róbert Katona — Robi, to everyone who works with him — has spent thirty-six years engineering cell lines — since 1989, and counting. It is exacting, unglamorous work: persuading living cells to be stable, reproducible, and willing to do what you need of them, week after week, year after year. Very little of it ever makes a headline. All of it is load-bearing.

Our first molecule exists because of that work. The cell engineering came first, and the molecule was made possible by it. That is the part of the story that is easiest to skip, and I would like us never to skip it.

Over the years, Robi and his team in Szeged have built a whole library of engineered cell lines, including caninized lines for our animal health work. Each one is a small monument to patience.

His lab is also where much of BioFund's collaboration begins. When a researcher in California asks what we can bring to the table, the answer very often starts in Szeged — with a cell line that already exists, made by someone who knows exactly how it behaves. That is a rare thing to be able to offer, and it is Robi's to offer.

Thirty years in Guelph.

Jim Petrik has spent more than thirty years studying the tumor microenvironment — the neighborhood a tumor builds around itself. The blood vessels it recruits, the signals it sends, the ways it persuades the body's defenses to stand down. If the cancer cell is the house, the microenvironment is the street, the gate, and the guard dog.

It is also where many promising therapies quietly fail. They reach the tumor and find the door locked from the inside.

Once the molecule existed, Jim was the person who could take it into preclinical studies and ask it the hard questions. He has been doing exactly that, as a Tier 1 Canada Research Chair — and, in whatever hours remain, as a volunteer fire chief. At the Ontario Veterinary College, six to eight thousand animal cancer patients walk through the doors every year. That is where One Problem stops being a paper and becomes a waiting room.

Why natural killer cells.

Natural killer cells are among the body's first responders. Unlike the T cells that most cell therapies have been built on, they need no prior training to recognize a stressed or abnormal cell and destroy it. In principle, they can also be given more safely from one person to another, which matters enormously if a therapy is ever to become affordable rather than bespoke.

Their weakness is precisely the terrain Jim has spent his career mapping. Tumors are very good at switching them off.

BF-CT01 brings those cells and the molecule together. It is work you can only do properly if both halves live in the same family: the craft to make and hold the cells, and a deep understanding of the ground they have to cross. The founding hypothesis has already been confirmed. What lies ahead is development — three years of it, starting with the year in front of us.

A story about collaboration.

When I describe BF-CT01 to people, I find myself talking less about cells and more about people. Two scientists, in two countries, each spent more than three decades on questions much of the field considered specialist. Neither was working toward this programme. Neither could have built it alone. Nearly seventy years of work, done separately, turned out to fit together.

Nobody designed this programme from the top. Two careers made it possible, and a family was patient enough to notice.

In my last note I wrote that a published result is easy to read, and that decades of craft behind it are much harder to reproduce. This is what I meant. You can publish a protocol. You cannot publish Robi's hands, or Jim's instinct for what a tumor will do next.

It is also why the conversations Neeki has opened in California now have somewhere concrete to go. A researcher at UCLA or USC who wants to test an idea about immune cells and the tumor microenvironment no longer has to be asked to imagine what BioFund might become. They can be shown what it already is.

Built for the long clock.

Cell therapy is slow. Cells have to be made, banked, tested, and made again. Each step takes months, and some of the most valuable results are the ones that send you back to the beginning.

Cell Therapy Research runs on the long clock: three cycles of seven years. Each development programme is a step along it, measured in three years rather than twenty-one. A fund with a ten-year life would ask when this becomes a company. We ask something simpler, of BF-CT01 and of every programme after it: is this further along than it was? That is the only question the long clock needs answered, and we can afford to keep asking it for as long as it takes.

This is exactly the kind of work BioFund was built to carry — and exactly the kind that gets abandoned elsewhere the moment money grows nervous.

For Ron.

This note is written for the LUA Focus Summit, which carries Ron's legacy, and it feels right that it does.

Ron never let anything slide. He would have read this, smiled, and found the one question nobody else in the room was willing to ask. I suspect it would have been about time — how much of it this will take, and whether we have the nerve for it. He taught us the answer himself: most impossible things are a matter of time and nerve. We have the time. We are working on the nerve.

“You guys make sure to cure cancer.”Ron Sege, 1957 – 2025

Two careers. One programme. Twenty-one years on the clock. We're on it.