Why We Invested in Metri Bio 

A few years ago, one of the world’s foremost human geneticists told me what they’d found when they turned their attention to endometriosis. They had identified nearly every cancer-driver variant we know. None of them appeared to be oncogenic. The biology was dense, contradictory, and unlike anything they had encountered.

They had run away screaming. Their words, not mine.

That conversation changed the way I thought about this disease. Not because the science was confusing, though it was. But because of what it implied. If this person, with all their resources and expertise, didn’t feel confident they could make meaningful progress, then the number of people on earth who did could probably fit in a single room.

It was hard to square that with the scale of the problem. Endometriosis affects roughly one in ten women. Over 190 million people worldwide. And NIH funding for endometriosis research accounts for about 0.03% of the annual health budget. That is a gap too large to reconcile and for a long time I couldn’t articulate why it felt so familiar.

Then I placed it.

I spent nearly a decade working in rare disease before that conversation. My career was shaped by the legacy of Henri Termeer and what he built at Genzyme, a company that proved you could serve tiny patient populations and still build a great business. I watched the story of Milasen unfold: a drug designed and manufactured for a single child, which became a proof of concept that the impossible could be solved by improved cooperation, goodwill, and urgency. In rare disease you learn to recognize a particular feeling. An unstoppable force meeting an immovable object. The need is undeniable. The biology says no. And the solution, when it finally comes, arrives not through a lone genius but through an improbable coalition. The drugs that reach patients in rare disease are as much miracles of coordination as they are miracles of science.

And what happened next is instructive. Rare disease didn’t stay a backwater. It became a cornerstone of biotech and for years one of the largest and fastest-growing areas of therapeutic investment. The pattern was: impossible, then improbable, then inevitable.

I believed women’s health was approaching its own version of this transition. Endometriosis had all the hallmarks. Massive patient population with devastating quality-of-life impact. Virtually no disease-modifying treatment. Minimal research infrastructure. And a slowly building consensus that the status quo was indefensible. What was missing was the scientific breakthrough that could convert moral urgency into forward motion.

To understand why progress has stalled, you have to understand one thing about endometriosis that separates it from most diseases of comparable magnitude.

There is a well-worn playbook in drug development. You build a model of the disease, you use that model to identify the biological targets driving it, then you screen for molecules that hit those targets. This is how we got trastuzumab for breast cancer (target: HER2), vemurafenib for melanoma (BRAF), adalimumab for rheumatoid arthritis (TNF-alpha). Model, target, drug. It works.

For endometriosis, there is no model. There are no validated disease-modifying targets. There are no targeted therapeutics.

The reason is almost absurdly simple: mice don’t menstruate. Their endometrium doesn’t shed. The biology that defines endometriosis in humans just doesn’t exist in the standard lab animal. True menstruation turns out to be vanishingly rare in the animal kingdom. Only some primates, a handful of bat species, the elephant shrew, and the spiny mouse do it. Even the spiny mouse, which researchers have explored as a possible model organism, lacks the glandular depth and immune complexity of the human endometrium.

So the bottleneck is a quirk of comparative biology. Without a model, you can’t find targets. Without targets, you can’t develop drugs. Nearly 200 million patients, and the whole thing is stuck on the fact that the animals we use in labs didn’t evolve to shed their uterine lining.

This is the immovable object.

But the insight that endometriosis needed a new kind of model system wasn’t unique to us. Someone had figured this out years before and built her entire scientific career around solving it.

I met Ashley Abel when she was about halfway through her PhD at Yale. At the time, endometriosis was still just a thought in the back of my mind. Our core work at Pillar is finding extraordinary founders, and that was my first and overwhelming impression of Ashley. The energy and drive seem to radiate off of her. You feel it the moment she walks into a room.

And then you look at what she’d actually been doing, and it becomes hard to reconcile with the calendar. Alongside her PhD, Ashley had won competitive NIH grants, founded Yale’s Women in Biotech initiative, built a STEM program for unhoused women and youth in Seattle, and published in some of the most competitive journals in biology. At some point I started to wonder whether she had a twin she wasn’t telling me about.

But what stopped me cold was the science. In the Sozen lab at Yale, Ashley and her colleagues in the lab had achieved what nobody else had been able to build: a human model system for endometrial disease. A 3D platform that integrates the right cell types, reproduces the complex tissue architecture, and generates functional readouts relevant to drug discovery. The Sozen lab’s previous organoid work had been recognized as Nature Method of the Year in 2023. Ashley had taken that foundation and pointed it directly at endometriosis.

I’ve helped start several companies over the years, and I’ve noticed they all share one thing: an absurd amount of serendipity. The right person working on the right problem at the right time, finding the right collaborator in a way nobody planned. I’ve come to look for it. It’s not something you can manufacture. But when you see it, you know. I had spent years circling endometriosis as one of the most important unsolved problems in medicine. Ashley had spent years building the tool that could crack it open. And we’d found each other almost by accident.

While she finished her PhD, we used nights and weekends to build the bones of what would eventually become Metri Bio: the first company to pioneer a human model system for endometriosis and go after the world’s first disease-modifying drug targets. Ashley co-founded the company alongside Berna Sozen, who serves as SAB Chair, and Kathy Potts, Gameto’s first scientist, who joined the company as COO. Late last year, the company raised an oversubscribed $5 million pre-seed to transfer the platform from Yale, scale it for high-throughput screening, and start the target and drug discovery that this field has been waiting decades for.

It’s worth pausing on what this means. For the first time, there is a platform capable of modeling endometrial disease in a way that supports real drug discovery. The bottleneck was never the demand. It was never the willpower or the funding appetite. It was the model. And now we have one.

I think the rare disease parallel is more than a metaphor. It’s a prediction. Rare disease taught us that when science finally unlocks, capital follows, talent follows, and the entire ecosystem reorganizes around the opportunity. Women’s health is at the very beginning of that arc. Endometriosis is where science is breaking through first.

There is more to say about where this goes, and more to share about the broader vision we are building at Pillar in women’s health. For now, I’ll just say this: I’ve learned to trust the pattern. When the unstoppable force finally meets the immovable object, something has to give. And this time, it’s the object.