Oncology

FROM ANTIGEN SIGNAL TO DECISION-GRADE IN VIVO EVIDENCE

Oncology programs can fail when activity is not focused enough on the tumor to drive durable responses, or when off-target effectslimit dosing and feasibility. The gap is an approach that focuses cytotoxicactivation on tumor-specific antigens using a standardized engineered platform,supported by decision-grade in vivo evidence in aggressive solid-tumor settings.

Lunai closes that gap with an oncology program built around engineered immune-cell platforms configured to the tumor context. One componentis DCCT, a Dendritic Cell Combination Therapy that uses standardized engineered antigen-presenting cells and tunes specificity through tumor antigen loading.For patients, the goal is to help the immune system recognize the tumor more precisely and keep it controlled for longer.

OUR ONCOLOGY PROGRAM

Standardization:

An engineered dendritic-cellplatform designed for translation-ready manufacturing path and reproducibility.

Specificity by configuration:

Tumor antigen loading to focusimmune activation on tumor-specific signals, without changing the engineered platform.

Decision-grade evidence

Functional ex vivo cytotoxicity readouts and in vivo efficacy testing in humanized modelsto support go/no-go and translation planning.

OURONCOLOGY PROGRAM

Cancer immunotherapy requires antigen presentation that converts tumor signal into a cytotoxic response. Some cell therapies rely on selecting and genetically engineering effector cells, which can complicate scale-up and increase product variability. When target antigens are not tumor-restricted, systemic immune toxicities can limit tolerability and dosing. DCCT instead uses engineered antigen-presenting cells to prime endogenous effector cells via tumor antigen loading, standardizing the engineered platform while tuning specificity to tumor-specific antigens.

WHAT IT IS:

DCCT is a Dendritic Cell Combination Therapy built from allogeneic CD34+ hematopoietic stem cell (HSC)-derived dendritic cells (DCs) engineered to express CD40L, CD93, andCXCL13, configured via tumor antigen loading.

WHAT WE DID:

We developed a clinicallycompliant lentiviral vector encoding codon-optimized CD40L, CD93, and CXCL13under an EF1α promoter, then transduced CD34+ HSCs and differentiated them intoengineered DCs for head-to-head benchmarking versus the first-generation research construct.
We loaded engineered DCs with tumor antigen and evaluated antigen-dependent activation ex vivo by measuring T-cell proliferation, interferon gamma (IFN-γ) secretion, and CD8+T-cell cytotoxicity.
We tested engineered DCs configured by tumor antigen loading in humanized mouse models of pancreatic tumors, including primary and late-stage metastatic disease, and tracked tumor burden.

OUTCOMES:

In head-to-head testing, 6-fold greater CD40L expression than the first-generation research construct, with 2% lower toxicity; 4.5-fold greater CD40L secretion and 2.2-fold greater CXCL13 secretion.
Robust T-cell proliferation in up to 20% of T cells and up to 4-fold greater IFN-γ secretion versus controls,with higher activation in the antigen-loaded condition than the non-antigen loaded condition and evidence of antigen-specific cytotoxicity by CD8+ T cells.
Complete regression of primary pancreatic tumors and metastases in the tested humanized mouse models, with prolonged survival reported in treated mice.

IMPACT:

A clinically compliant vector design suitable for investigational new drug (IND) enabling work while preserving immune-activating function in engineered DCs.
An antigen-dependent functional gate for selecting tumor-specific antigen inputs and advancing configurations into in vivo studies.
Decision-grade in vivo evidence supporting advancement toward IND-enabling studies and licensing discussions for a standardized engineered DC platform configured by tumor antigen loading.

ONCOLOGY PROGRAM