The antibody came first. The company built itself around what the antibody might do.
That's the story Immutrin is telling as it steps into public view with £65 million in Series A financing—roughly $87 million—led by Frazier Life Sciences. The Cambridge-based biotech, which formally announced its existence in late March, is betting on a mechanism that has humbled others: not just blocking the toxic protein deposits that strangle heart muscle in ATTR cardiomyopathy, but pulling them out by the roots.
It's an approach anchored in decades of antibody science, Nobel pedigree included. And it arrives at a moment when the broader amyloidosis field is suddenly crowded with approved drugs—none of which do quite what Immutrin hopes to accomplish.
The Problem With Stopping What's Already There
ATTR cardiomyopathy is progressive and, left untreated, fatal. Misfolded transthyretin protein accumulates as rigid amyloid fibrils in cardiac tissue, stiffening the heart until it can no longer pump effectively. For years, treatment options were sparse. That changed recently. BridgeBio's acoramidis secured FDA approval in November 2024, with European clearance following in February 2025. Alnylam's vutrisiran, an RNA interference therapy, won U.S. approval for ATTR-CM in March 2025. Ionis and AstraZeneca are deep into a large outcomes trial for eplontersen, an antisense drug.
All of those work upstream: they stabilize the protein or silence its production, preventing new deposits. What they don't do is clear what's already embedded in tissue.
Immutrin's lead antibody candidate is engineered to bind selectively to amyloid fibrils already laid down in the heart and recruit the immune system to dismantle them. In theory. Whether that translates from bench to bedside is the open question—one that $87 million is now funding.
The company plans to push its candidate through proof-of-concept trials in ATTR-CM patients, though it hasn't disclosed IND timing or provided trial registry details. Incorporated back in September 2019, Immutrin has been operating quietly out of Cambridge Innovation Capital's offices on Station Road, refining its approach before surfacing.
Nobel Laureates and Board Veterans
Immutrin didn't lack for scientific firepower at the outset. Co-founder Sir Gregory Winter shared the 2018 Nobel Prize in Chemistry for pioneering phage display of antibodies—a technique that revolutionized how researchers identify therapeutic candidates. He's joined by Prof Sir Mark Pepys, who founded the UK National Amyloidosis Centre at University College London, and Prof Daniel Christ, who leads antibody therapeutics at the Garvan Institute in Sydney.
All three have spent careers working at the intersection of antibody engineering and amyloid biology, which gives Immutrin's platform a certain gravitas. Perhaps more than the founders might have anticipated when they first began collaborating.
CEO Mihriban Tuna brings industry-tested credentials: she was previously CSO at Adaptate Biotherapeutics before Takeda acquired it, and held senior roles at F-star and Domantis (later bought by GSK). Sef Kurstjens, the board chair, most recently ran Bright Peak Therapeutics and served as chief medical officer at Astellas, Allergan, and Urovant.
The syndicate backing the Series A includes F-Prime Capital, Qiming Venture Partners, SR One, and founding investors Cambridge Innovation Capital and Cambridge Enterprise Ventures. Parkwalk also appears on the company's investor roster. Three new board members arrived with the financing: James N. Topper from Frazier, Nihal Sinha from F-Prime, and Alex Sinclair-Wilson from Qiming, joining Tuna, Kurstjens, and Michael Anstey from Cambridge Innovation Capital.
A Mechanism That's Proven Stubborn
Amyloid clearance sounds elegant. Executing it has been anything but.
Novo Nordisk is testing coramitug, another antibody depleter, in a Phase 2 signal-detection study that's been enrolling since 2024. Prothena discontinued birtamimab—its own antibody candidate—in May of last year after a Phase 3 trial in a different form of amyloidosis missed its endpoints. The approach works in mice. Human hearts, as usual, are less cooperative.
What's changed the calculus somewhat is diagnostics. Better access to nuclear cardiology imaging has accelerated ATTR-CM detection, expanding the pool of patients who might benefit from treatment—assuming treatment works. Market forecasters, with their typical blend of optimism and spreadsheet confidence, have sized the broader amyloidosis therapeutics space at north of $6 billion within a decade.
That estimate comes with all the usual hedges and assumptions baked in. What's less debatable is that the field has matured quickly, and investors are paying attention.
The Wait Begins
Immutrin now has runway. Whether it can translate protein science honed over decades into a therapy that actually depletes amyloid in living patients—safely, measurably, durably—remains the test. The antibody engineering is sophisticated. The biology is unforgiving.
Clearing what's already accumulated, rather than simply preventing more accumulation, would represent a genuine advance. But it's a harder problem than it looks, and others have stumbled. The capital is committed. The science is ready.
Now comes the part where the antibody has to work in people.
