# A novel monoclonal antibody-based anti-NK cell anti-inflammatory strategy for treating autoimmune and checkpoint inhibitor induced myocarditis

> **NIH NIH R43** · INFLAMMA THERAPEUTICS, LLC · 2021 · $308,650

## Abstract

Summary
The Problem: Despite current therapies, the prognosis of various forms of acute and chronic inflammation
of the heart (myocarditis) remains poor. Immune reactions that attack a patient’s own tissues (autoimmune
disease) is one major cause of myocarditis. Additionally, one of the complications of immune checkpoint
inhibitors (ICI), which attack cancer cells though activation of inflammation, is myocarditis.
Innovation:
Inflammation involves multiple molecules and multiple redundant pathways. The anti-inflammatory monoclonal
antibodies (mAbs) forming the basis of treatment of inflammation-related diseases target a single molecule and
a single inflammatory pathway. Therapeutic efficacy is thereby limited. NK cells are major orchestrators of
multiple inflammatory pathways. Inflamma Therapeutics (IFT) therefore developed a novel mAb—IFT100—that
depletes NK cells. By inhibiting NK cells IFT100 inhibits multiple inflammatory pathways.
As proof-of-concept of the efficacy of an NK cell depleting strategy, we demonstrated that an anti-NK cell mAb
that depletes mouse NK cells improves myocardial function in mice with acute heart attacks or with chronic
heart failure. IFT therefore decided to develop an anti-human NK cell mAb—IFT100—to serve as an
immunosuppressive therapeutic agent to treat inflammation-exacerbated human disease. IFT found that IFT
101 binds to and depletes human NK cells. IFT100 was sequenced and patents submitted.
The AIMS of the current proposal, using IFT100:
Aim 1: Determine the dose response for in-vivo NK cell depletion in mice.
Aim 2: Determine the impact of NK cell depletion on the prevention of Experimental Autoimmune Myocarditis.
Aim 3: Determine the impact of NK cell depletion on the prevention of Experimental Autoimmune Myocarditis
with or without the burden of ICI treatment.
Aim 4: Humanize our mAb.
In this project we will be validating the ability of our specific mAb (IFT100) to improve autoimmune-induced and
ICI-induced myocarditis. Importantly, however, we believe IFT100 will also be effective for improving
outcomes in many other diseases that are worsened by excessive inflammation. These include
myocardial dysfunction in patients with chronic heart failure, with cardiogenic shock, and with acute MI.
Another important additional therapeutic target for IFT100 is the massive inflammatory response responsible
for most of the deaths seen in Covid-19. Each of these conditions has no current effective therapy and, as
such, constitute conditions for which there are major unmet therapeutic needs.

## Key facts

- **NIH application ID:** 10258059
- **Project number:** 1R43HL158344-01
- **Recipient organization:** INFLAMMA THERAPEUTICS, LLC
- **Principal Investigator:** Dror Luger
- **Activity code:** R43 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $308,650
- **Award type:** 1
- **Project period:** 2021-04-15 → 2022-04-14

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10258059

## Citation

> US National Institutes of Health, RePORTER application 10258059, A novel monoclonal antibody-based anti-NK cell anti-inflammatory strategy for treating autoimmune and checkpoint inhibitor induced myocarditis (1R43HL158344-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10258059. Licensed CC0.

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