Precision Immuno-Oncology

Turning coldtumors hot.

Ignitio Therapeutics develops precision medicines that reignite the immune system inside solid tumors. Our therapeutics deplete the suppressor cells that keep a tumor immunologically cold — exposing the tumor to attack by the immune system.

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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.

01

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.

02

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.

03

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
Platform

Engineered for the clinic.

Both programs are built on the same precision-engineered bispecific antibody design — 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

AND-gate logic for exquisite target selectivity

Each arm of our bispecific binds its marker weakly on its own. Only when both markers are present — as they are on a tumor's suppressor cells — do the two arms grip together, binding roughly 1,000× more tightly.

This avidity-driven "AND-gate" concentrates activity inside the tumor and minimizes effects on healthy tissue.

Affinity versus avidity binding curve: a monovalent arm with weak affinity (Kd ~1 uM) versus bivalent avidity binding with an apparent Kd ~1 nM, about a 1000-fold difference

A clinically validated, highly developable format

Our bispecifics are built on a clinically validated format — a proven knobs-into-holes Fc for reliable chain pairing, with a streamlined single-chain design engineered for manufacturability from the very first step. The architecture assembles only as the intended heterodimer, virtually eliminating homodimer by-products — and the yield loss and purification difficulties they create. It expresses at high titer, purifies cleanly in a few steps, formulates at high concentration for subcutaneous delivery, and has shown clean safety and pharmacokinetics in non-human primates.

6–11 g/LHigh titers from stable CHO clones — among the highest reported for a bispecific
100%SEC purity from a streamlined two-step purification, with no detectable homodimers
200 mg/mLHigh solubility and low viscosity — supports subcutaneous delivery
1-stepSingle-CH1 design enables one-step purification of clean, correctly paired molecules
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-EnablingPhase I/II
MDSC Program
MechanismTumor-selective MDSC depleter using the same "AND-gate" precision (bispecific antibody)
IndicationBroad solid tumors · mono & combination
DiscoveryPreclinicalIND-EnablingPhase I/II
Evidence

IG1013: What the preclinical data show.

Across mouse tumor models, the approach selectively cleared tumor suppressor cells, drove durable responses, and amplified existing immunotherapies.

Preclinical data · mouse tumor models · representative

Selective depletion inside the tumor

At every dose and timepoint, treatment sharply reduced suppressor (Treg) cells inside the tumor — while the Tregs circulating in the blood were largely spared. The effect is selective to the tumor.

Tumor Tregs fell sharply at every dose, while blood Tregs stayed near normal.
Tumor vs. blood Treg levels
Suppressor (Treg) cells as a fraction of immune cells, by timepoint
Bar charts of regulatory T cell levels in tumor versus blood across three timepoints; tumor Tregs are sharply reduced at every dose while blood Tregs are largely unchanged

Potent and durable responses

Treated animals achieved complete, lasting tumor regression. When survivors were later re-challenged with tumor cells, they rejected them — a hallmark of protective immune memory.

These responses came from IG1013 alone — strong potential as a monotherapy.
Tumor growth & re-challenge
Single dose IG1013 vs. vehicle; survivors re-challenged with tumor
Tumor-growth curves: vehicle-treated tumors grow rapidly while IG1013-treated tumors stay flat at baseline, including after a later tumor re-challenge — indicating durable immune memory

Amplifies existing immunotherapies

Combined with a checkpoint inhibitor, the approach produced deeper, more durable tumor control than either agent alone — pointing to broad potential alongside today's immuno-oncology therapies.

Combination outperformed either single agent across the study.
Tumor growth · individual animals
Four treatment groups; each line is one animal
Four-panel tumor-growth small multiples: control and anti-PD-1 tumors grow, IG1013 partially controls growth, and the IG1013 plus anti-PD-1 combination keeps nearly all tumors flat
Get in touch

Turning cold tumors hot.

We welcome conversations with partners, collaborators, and investors who share our urgency in reaching patients with hard-to-treat solid tumors.

info@ignitiotx.com www.ignitiotx.com