The post-ADC era begins with a smarter payload

Abion is transitioning from a single-asset biotech into a platform oncology company. Our iRAC platform delivers a proprietary IFN-β mutein directly into the tumor microenvironment — replacing cytotoxic payload with immune-biologic payload logic.

iRAC interferon-β antibody

iRAC — interferon-β antibody conjugate — is not a chemically conjugated ADC. The antibody points it at the tumor; the proprietary IFN-β mutein kills directly and activates the local immune system with the long-term memory.

Targeting module

Redirectable Immune Engine

One immune engine, redirected across tumors. Trop-2 is the first targeting module; the platform is engineered to accept EGFR, HER2, CLDN3, and more. You name the cancer. We tailor the warhead.

Proprietary IFN-β mutein

Direct tumor killing + immune activation.

Proprietary IFN-β Mutein:Anti-tumor PotencyWithout Peripheral Toxicity

Most clinical-stage ADCs have shown severe toxicities; wild-type IFN based variants add hematologic toxicity. Our mutein re-tunes receptor engagement instead: muted at blood pH, active in acidic tumor environment.

Three pillars, one integrated mechanism

Direct killing

IFNAR–driven JAK–STAT arrest and TRAIL/Fas death signaling.

Tumor selectivity

A pH-tuned mutein that binds tighter in acidic tumor tissue — preserving the tumor.

Immune activation

Dendritic-cell maturation, myeloid remodeling, antigen presentation, and cytotoxic CD8 T-cell activity with durable memory.

Direct killing

Payload-grade potency, broad across tumors. IFN-β lands in the low-picomolar range. TROP2 abundance draws iRAC in. Low pH switches it on. Two independent gates — target density and tumor acidity — confine activity to the tumor microenvironment.

In-vivo efficacy

Each engine carries efficacy on its own. In immune-deficient models the direct arm regresses even Trop-2-low tumors. The immune arm alone sufficiently controls tumors with a clean dose response — and monotherapy outperformed an approved ADC–checkpoint combination.

Cold → Hot,and durable

The tumor turns hot — then remembers. While the exhaustion-like phenotype stays low.

Immune activation

A second engine the ADCs don't have. Type I interferon engages a second, immune-mediated killing mechanism beyond direct tumor-cell cytotoxicity.

Redrawing the limits of cancer therapy

It survives the resistance that stops ADCs.

Barrier 1 — Chemotherapy resistance

Barrier 2 — Antibody resistance

Barrier 3 — ADC resistance

Looking for a partner in precision oncology?

We are building a Korea-originated global oncology model — combining Abion´s discovery engine with partners platform-commercialization, CMC, and global BD capabilities.

Contact our BD team