Ignitio Therapeutics — Turning Cold Tumors Hot

The Challenge

Why some tumors stay cold.

Solid tumors don't just hide from the immune system — they actively shut it down. Two cell types do most of the suppressing: regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs).

Tregs are the immune system's peacekeepers, normally maintaining balance and preventing the body from attacking itself — a role recognized by the 2025 Nobel Prize in Physiology or Medicine. MDSCs are immature myeloid cells that accumulate in cancer. Inside the tumor, both are hijacked to build a deeply suppressive microenvironment — a "cold" tumor that quiets the immune response and blunts even the most advanced immunotherapies.

High levels of either population are consistently linked to poor prognosis and resistance to treatment — and tumors differ in which suppressor dominates. To make a cold tumor respond, that suppressor has to be removed — precisely.

The science of Tregs was awarded the 2025 Nobel Prize in Physiology or Medicine — underscoring how central these suppressive cells are to immunity, and to cancer.

Fluorescence micrograph of a breast tumor microenvironment — tumor-cell nests in cyan surrounded by dense green stroma

National Cancer Institute

Inside a "cold" tumor — suppressive cells (red) infiltrate the tumor-cell nests (cyan), driving the immunosuppressive microenvironment that keeps the tumor cold.

Our Approach

A precision spark to ignite immune attack.

Different tumors are held cold by different suppressor cells. Each Ignitio antibody selectively clears one of them — Tregs or MDSCs — wherever it dominates the tumor, while sparing the body's healthy immune balance. The result: the immune system reawakens exactly where it's needed.

Tumor-selective depletion

Each program acts only where two distinct markers are co-expressed on its target suppressor cell — a molecular "AND-gate" that concentrates depletion inside the tumor and minimizes the risk of systemic autoimmunity.

A dual mechanism

Our lead Treg program does more than deplete suppressive cells — it also delivers checkpoint activation that helps re-energize the immune response. Two complementary mechanisms working together to flip a cold tumor hot.

Matched to the tumor

Tumors differ in which suppressor cell dominates. With a program for each, the right medicine can be matched to a tumor's biology — used alone or alongside immuno-oncology therapies such as PD-1 / PD-L1 inhibitors.

Marker A

on suppressive cell

Marker B

on suppressive cell

→

Precise depletion — tumor only

Pipeline

Two programs, one precision mechanism.

The same "AND-gate" logic that powers our lead Treg program extends to a second program against another driver of tumor immunosuppression — MDSCs — giving a medicine matched to each suppressor phenotype. Our lead candidate is advancing through IND-enabling preclinical studies.

Program

Mechanism

Indication

Stage

IG1013

MechanismDual-mechanism, tumor-selective Treg depleter (bispecific antibody)

IndicationBroad solid tumors · mono & combination

DiscoveryPreclinicalIND-EnablingINDPhase 1

MDSC Program

MechanismTumor-selective MDSC depleter using the same "AND-gate" precision (bispecific antibody)

IndicationBroad solid tumors · mono & combination

DiscoveryPreclinicalIND-EnablingINDPhase 1

Platform

Engineered for the clinic.

Both programs are built on the same precision-engineered bispecific antibody — two targeting arms in a single molecule, with activity gated to fire only where both tumor markers appear together.

That shared foundation lets us turn differentiated biology into real, developable medicines — and to point the same "AND-gate" logic at new drivers of immunosuppression across the tumor microenvironment.

2-in-1Bispecific design — two targeting arms in a single antibody

AND·gateActivity gated to where both tumor markers appear together

mAb-likeDesigned for standard antibody manufacturing and stability

ModularOne AND-gate engine powering both programs

Turning coldtumors hot.