# Development of surfactant protein A-derived peptidomimetics for the treatment of asthma

> **NIH NIH R41** · RAESEDO, LLC · 2020 · $214,912

## Abstract

Current treatments for asthma, while reducing exacerbations in a subset of patients by focusing
on airway inflammation, do not eliminate them. There is no current innate immune modulator for
the treatment of asthma. Asthma exacerbations are a significant cause of morbidity and mortality
in asthma as they can lead to airway injury, lung function decline and death. The cause of an
exacerbation is often an infection in the setting of abnormal airway inflammation. The response
to infection is complex, involving both the innate and adaptive immune systems. Exacerbations in
more severe asthmatics are of particular concern, as health care costs and lost productivity
account for $21 billion/year in US annual health care expenditures. Thus, there is a critical need
to develop new therapies to be used in the treatment of inflammatory lung diseases including
asthma. The objective of this Phase I proposal is to develop new short peptide derivatives and
mimetics of the active region of surfactant protein-A (SP-A), a protein that regulates key innate
immune functions in the lung, and perform a drug screen that identifies those most active and
stable with similar efficacy as the full-length protein. SP-A-derived peptides do not occur naturally
and by synthetically produced analogs, we can create custom modifications with improved
pharmacokinetic properties and stability. We will use asthma as our test model where SP-A
peptide analogs modulate eosinophil and epithelial cell functions, key targets where cellular
mechanisms drive the allergic asthma phenotype. The rationale for this study is based on our
findings that the SP-A peptide reduces airway hyperresponsiveness (AHR), a fundamental
characteristic of asthma, in two different pre-clinical mouse models of asthma. We have strong
evidence to support that the mechanisms of protective action are due to 1) direct interaction with
eosinophils to induce apoptosis and promote their resolution from the airway and 2) direct
interaction with epithelial cells to inhibit mucin production. Therefore, our central hypothesis is
that through direct effects upon airway eosinophil and epithelial cells, SP-A-derived peptides
reduce airway inflammation and hyperresponsiveness associated with asthma. We propose to
test this hypothesis through two specific aims. In Aim 1 we will synthesize, engineer and optimize
peptides and structural mimetics derived from SP-A to identify a lead mimetic. In aim 2 we will
characterize the bioactivity of SP-A-derived peptides and mimetics at specific cellular targets to
identify a lead compound using a high throughput. Our company, RaeSedo LLC, was founded on
the principle that we can create custom modifications with improved pharmacokinetic properties
and stability for the development of this new class of asthma therapeutics.

## Key facts

- **NIH application ID:** 10019073
- **Project number:** 1R41HL152942-01
- **Recipient organization:** RAESEDO, LLC
- **Principal Investigator:** Scott Boitano
- **Activity code:** R41 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $214,912
- **Award type:** 1
- **Project period:** 2020-07-15 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10019073

## Citation

> US National Institutes of Health, RePORTER application 10019073, Development of surfactant protein A-derived peptidomimetics for the treatment of asthma (1R41HL152942-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10019073. Licensed CC0.

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