# Development of IFNA2-LNP01 for tumor lung metastases immunotherapy

> **NIH NIH R43** · CHEMEDIMMUNE, INC. · 2024 · $320,597

## Abstract

Project Summary
 Lung metastasis is the 2nd most common metastasis and accounts for 30% of all metastatic diseases in
human cancer patients. Patients with lung metastases have a very short survival time. For example, the 5-
year survival rate for colorectal cancer patients with lung metastases, if left untreated, is only 5%. Surgical
lung metastases resection (pulmonary metastasectomy) is a “curative” treatment for cancer patients with lung
metastases. For example, pulmonary metastasectomy increases the 5-year survival rate of colorectal cancer
patients with lung metastases from 50.3-66%. However, pulmonary metastasectomy is currently performed
only in a very small population of cancer patients with lung metastases due to the risk-related highly selective
criteria. For example, only 5% of colorectal cancer patients with lung metastases are treated with pulmonary
metastasectomy. A neoadjuvant therapy that can effectively reduce lung metastases number and/or size is
therefore expected to significantly increase the eligible patient population for this life-saving pulmonary
metastasectomy. ChemMedImmune Inc. is developing IFNA2-LNP001, a lipid nanoparticle-encapsulated
IFN2-encoding mini-plasmid DNA for treatment of patients with lung metastases. IFNA2-LNP01 will be
administered in the clinically neoadjuvant setting, where it activates the type I interferon (IFN-I) signaling
pathways in lung metastases to increase the expression of T cell chemokines CXCL9 and CXCL10, resulting
in enhanced T cell recruitment to the tumor site to reduce the size and number of lung metastases. A key
differentiating feature of IFNA2-LNP01 is its administration in the neoadjuvant setting, which is necessary to
give patients the best chance to fight their metastatic tumor ahead of other lines of therapies that can
negatively affect T cells. IFNA2-LNP01 is designed based on our recent published data showing that loss of
IFN-I expression and function is a major mechanism underlying lung metastases immune evasion and growth.
Two aims will be pursued in this project: 1) determine the efficacy of IFNA2-LNP01 in suppression of tumor
lung metastases in vivo; and 2) determine IFNA2-LNP01 biodistribution and toxicology in vivo. This project is
expected to generate sufficient efficacy and toxicology data for a Phase II IND-enabling study of IFNA2-
LNP01.

## Key facts

- **NIH application ID:** 10820250
- **Project number:** 1R43CA287611-01
- **Recipient organization:** CHEMEDIMMUNE, INC.
- **Principal Investigator:** Priscilla Simon Redd
- **Activity code:** R43 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $320,597
- **Award type:** 1
- **Project period:** 2024-05-01 → 2026-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10820250

## Citation

> US National Institutes of Health, RePORTER application 10820250, Development of IFNA2-LNP01 for tumor lung metastases immunotherapy (1R43CA287611-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10820250. Licensed CC0.

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