The story is three thousand years old. The mechanism is new.
The Greeks spent ten years trying to take Troy. They tried ladders, battering rams, and siege engines. The walls held. Then they built a horse, hid soldiers inside, and let the Trojans wheel it through the gates themselves.
Once inside, the soldiers opened the city from within.
This is the architecture of an Immune-Tag Conjugate.
Why the walls hold
For three decades, oncology has tried to storm the walls of solid tumors. Each generation of immunotherapy has been a bigger weapon than the last.
Checkpoint inhibitors release the brakes on the immune system. CAR-T cells are engineered from scratch outside the body and infused back in. Antibody-drug conjugates deliver chemotherapy payloads directly to the surface of cancer cells.
All three work, in some patients, some of the time. All three cap at 25 to 50 percent response. And all three ride a single tumor marker — a flag on the wall — that 40 to 50 percent of tumors learn to drop under treatment.
The wall doesn't fall. The flag comes down.
A different question
What if the problem isn't the size of the weapon?
The immune system is already capable of destroying tumor cells. It does this constantly. Every adult carries decades of trained T-cell memory against pathogens they have encountered or been vaccinated against — BCG. CMV. Epstein-Barr. Influenza. COVID. The training is already complete. The army is already in the city.
The problem has never been firepower. It has been recognition.
Solid tumors don't look foreign. They look like the body's own tissue, with a few subtle modifications. The immune system walks past them every day.
The Trojan Horse approach asks a different question: what if we could make a tumor cell look like an infected cell?
Bind. Tag. Kill.
An Immune-Tag Conjugate is a small, modular recombinant protein with two jobs.
The first job is to find the right cell. A binding arm — built on the same antibody scaffold regulators already understand and patients already tolerate — docks onto a surface marker. For our lead program ORION™, that marker is HER2, the most studied target in oncology.
The second job is to deliver something to that cell that does not belong there. A fragment of a pathogen the patient's immune system already knows. A signal peptide tag derived from BCG, CMV, or another well-trained antigen. The fragment is presented on the tumor cell's surface, where it is now indistinguishable from a fragment of an active infection.
The horse has arrived at the gate. The soldiers are emerging.
What happens next happens entirely inside the patient. Pathogen-primed memory T-cells — the ones built by a vaccination decades ago — recognize the cell as infected and destroy it. Polyclonal. Picomolar sensitivity. Multiple T-cell populations, not just one.
The city opens itself from within.
Why this changes the geometry
The Trojan Horse approach is not a bigger weapon. It is a different physics.
It redirects immunity that was already trained, by infections and vaccinations the patient has already had, against cells that previously looked invisible. The training cost was paid years ago. The army was already in place. We just gave it a target it recognizes.
This is why epitope spreading keeps the system working after the original marker is gone. This is why a tumor that has learned to evade an ADC has not learned to evade a virus it has never met. This is why the response is polyclonal — many T-cell populations recognizing many fragments of the tag — rather than a single brittle line of attack.
The walls of solid tumors have held for thirty years against the weapons we built to break them.
We are not building a bigger weapon. We are building a better disguise.
The city has always had its own defenders. It just needed to be told where to look.