On a Tuesday morning in April 2026, somewhere on the EGFR-driven oncology service of a teaching hospital, a nurse pushed a clear bag of antibody onto an IV pole. The drug, EPI-326, didn't go looking for a kinase pocket to plug, the way EGFR drugs have for twenty years. It found a cell-surface protein, gripped it, dragged it to a nearby receptor that knows how to take out the trash, and let the cell's lysosome do the rest. The patient was the first in the world to receive it. The press release went out the next week. The bag, by then, was in biohazard.
EpiBiologics is the four-year-old San Mateo biotech behind that bag. It is small - about 47 people - and quiet by the standards of an industry that loves its press conferences. But by January 2026 it had raised $280 million in cumulative funding, including a $107 million Series B co-led by GV and Johnson & Johnson Innovation, an unusual pairing that says more about the company's thesis than any deck ever could.
The Idea, Roughly
Targeted protein degradation - the field of drugs that don't inhibit proteins but delete them - grew up inside the cell. PROTACs and molecular glues recruit the cell's intracellular trash service, the proteasome, to grind down bad proteins. Wonderful, except it leaves out the proteins that don't live inside the cell. Membrane proteins. Soluble proteins. The growth factors that whisper to cancer cells. By most counts, that's roughly 40% of the proteome, and small molecules can't reach it.
EpiBiologics builds bispecific antibodies that walk those outside proteins to a different trash service - the lysosome - using a catalog of more than 270 internalizing receptors that vary by tissue. The platform is called EpiTAC. One arm binds the protein you want gone. The other arm grabs a receptor that knows how to bring things inside and dispose of them. The receptor is the address. The address is what makes this tissue-selective. The address is the whole game.
From a Few Lab Benches
The company started in February 2022 in a small incubator in San Carlos, with one office and a handful of lab benches. Two scientists from Jim Wells' lab at UCSF moved in with a license to platform IP and a list of receptors that looked interesting. Wells, the academic founder, is a name biochemists recognize: a chemist who spent decades inventing antibody tools that other companies later turned into drugs. Phage display libraries. Engineered proteases. The boring-sounding infrastructure that most of biotech now treats as plumbing.
By March 2023, EpiBiologics emerged from stealth with $50 million in Series A funding co-led by Mubadala Capital and Polaris Partners, with Vivo Capital and GV joining. It had not yet announced a clinical candidate. It mostly had a thesis and a wet lab.
Pipeline
EpiBiologics, in stages
EPI-326 - lead bispecific antibody, degrades wild-type and mutant EGFR. Currently in a global Phase 1 trial in NSCLC and HNSCC.
What EPI-326 Actually Does
EGFR is the workhorse of lung cancer biology. Tarceva. Iressa. Tagrisso. Three generations of small-molecule inhibitors have plugged its kinase domain, and three generations of resistance mutations have eventually outflanked them. EpiBiologics' answer is to not plug it at all. EPI-326 grabs every form of EGFR - wild-type, mutant, oncogenic, the resistant kind, the freshly mutated kind no one has named yet - and routes the whole protein into the lysosome. No protein, no signal. The trick is selectivity: the second arm of the bispecific targets a receptor enriched in tumor tissue, so healthy skin and gut, which also express EGFR and have suffered for decades under EGFR drugs, are largely spared.
Whether it works in patients is a question the Phase 1 trial will answer. Phase 1s often disappoint. Some don't. EpiBiologics has been disciplined about pacing - one clinical candidate, deep preclinical work, a second molecule following behind.
Funding
Investors include GV, Johnson & Johnson Innovation, Novartis Venture Fund, Mubadala Capital, Polaris Partners, and Vivo Capital.
People
EpiBiologics' executive bench is unusually senior for a clinical-stage company of its size. Ann Lee-Karlon, who spent 18 years at Genentech overseeing project leadership for more than 80 drug development teams and was COO of Altos Labs, runs the company as President and CEO. The 2025 hiring round brought in Chief Medical Officer Eric Humke, who came from IGM Biosciences and Genentech with over two decades of oncology development experience, and CFO Aaron Mishel. Shyra Gardai serves as Chief Scientific Officer.
What Makes It Unusual
270+ Receptors
Most degrader companies use one or two internalizing receptors. EpiBiologics built a catalog. The catalog is the moat.
Tissue-by-Tissue
Choose a receptor that's enriched in tumor or autoimmune tissue. Healthy organs barely notice.
Bispecific Antibodies
Familiar manufacturing. Familiar pharmacokinetics. Unfamiliar mechanism.
The Outside Proteome
Membrane and secreted proteins - roughly 40% of human proteins - have been hard to drug. EpiTAC reaches them.
EPI-326 in Patients
One bispecific that degrades all clinically relevant EGFR variants. First dose was April 2026.
Wells Lab, UCSF
The platform IP is exclusively licensed from the lab that helped invent modern antibody engineering.
Latest Updates
- April 2026 - First patient dosed in the EPI-326 global Phase 1 trial for EGFR-driven solid tumors.
- January 2026 - $107M Series B co-led by GV and Johnson & Johnson Innovation closes.
- 2025 - Eric Humke (CMO) and Aaron Mishel (CFO) join the executive team.
- November 2024 - Disease-selective extracellular degradation data presented at multiple scientific meetings.
- March 2023 - Emerges from stealth with $50M Series A.
The Return
Back at the teaching hospital, the bag was empty by lunchtime. What was inside it had not invented the lysosome. It had not invented the bispecific antibody. It had not even invented the idea of degrading proteins instead of blocking them. EpiBiologics' contribution was quieter than that. It built a catalog of cellular addresses - 270 and counting - and learned to deliver to the right one. The patient went home that afternoon. The drug went to work. The receptor on the surface of the tumor cell pulled EGFR inside, the lysosome did what lysosomes do, and somewhere in San Mateo, 47 people watched, again, to see whether the idea they had been pursuing since 2022 in a few small lab benches was the one that finally worked.