# A Novel Therapeutic Peptide to Treat P. aeruginosa Infection in Cystic Fibrosis Patients

> **NIH NIH R43** · VIRTICI, LLC · 2020 · $158,832

## Abstract

Project Summary
Our objective is to develop 6K-F17 as an antimicrobial agent that can be prescribed with tobramycin for the
treatment of chronic, antibiotic-resistant Pseudomonas aeruginosa infection in cystic fibrosis (CF) patients. CF
affects over 70,000 people worldwide1. Even with the current array of antibiotics, 80-95% of CF patients will
ultimately succumb to respiratory failure brought on by chronic bacterial infections3. As a result, there is a
significant unmet need to develop new antimicrobials for chronic, antibiotic-resistant infections in CF patients.
CF is a genetic disease arising from mutations in the cystic fibrosis transmembrane conductance regulator
(CFTR) gene that encodes a chloride ion transporter4. Impaired trans-epithelial chloride transport leads to
dehydrated airway secretions and a lack of airway mucus clearance5, 6. As a result, individuals with CF are
prone to chronic, biofilm-based bacterial infections, bronchiectasis and respiratory failure6, 7In particular,
chronic infection with P. aeruginosa has been shown to lead to more rapid lung function decline, a lower quality
of life, and premature death8-11. Chronic infection with P. aeruginosa is particularly challenging to treat as this
strain continually adapts to environmental challenges, including the formation of a mucus-like biofilms. These
biofilms protect bacteria from natural host defense mechanisms and make them more resistant to small
molecule antibiotics 5, 12-18.
Progress toward developing treatments for biofilm infections has been made through the use of cationic
antimicrobial peptides (CAPs). CAPs are found naturally in a wide variety of organisms ranging from plants to
humans and constitute a major component of the innate immune system19-21. Importantly, these natural CAPs
kill bacteria by destroying their membranes – in effect ‘blowing up’ the bacteria by lodging and accumulating in
their membranes - rather than by targeting a specific bacterial protein or biochemical pathway. This
mechanism impedes the advent of bacterial resistance to CAPs. Recently, our team developed a novel
peptide, called 6K-F17, that can disrupt biofilms created by P. aeruginosa and kill the bacteria using a novel
mechanism of membrane association. Due to its unique mechanism of action, 6K-F17 synergizes with
antibiotics, such as tobramycin, to kill antibiotic-resistant strains of P. aeruginosa.
Building from this work, the objective of this proposal is to generate the optimal dose, pharmacokinetics and
toxicology profiles for 6K-F17 in mice. The specific aims are to: 1) produce sufficient amounts of 6K-F17 and
standardize analytical and potency assays; 2) determine the optimal effective dose of 6K-F17 to eliminate P.
aeruginosa infection in mice; and 3) establish a preliminary acute toxicology profile for 6K-F17 in normal mice.
Successful completion of these studies will advance an exciting antimicrobial agent for the treatment of
antibiotic-resistant P. aeruginosa, and potentia...

## Key facts

- **NIH application ID:** 9975726
- **Project number:** 5R43AI147773-02
- **Recipient organization:** VIRTICI, LLC
- **Principal Investigator:** Neil A Fanger
- **Activity code:** R43 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $158,832
- **Award type:** 5
- **Project period:** 2019-07-11 → 2021-10-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9975726

## Citation

> US National Institutes of Health, RePORTER application 9975726, A Novel Therapeutic Peptide to Treat P. aeruginosa Infection in Cystic Fibrosis Patients (5R43AI147773-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/9975726. Licensed CC0.

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