# Melanocortin Receptor Selective Ligands

> **NIH NIH R01** · UNIVERSITY OF MINNESOTA · 2022 · $648,763

## Abstract

Obesity (body mass index, BMI >30) afflicts millions of people in the United States and
other countries, and is a major risk factor for heart disease, type II diabetes mellitus,
stroke, hypertension, and morbidity. The G-protein coupled melanocortin-3 receptor
(MC3R) is expressed in the central nervous system (brain) and is part of the
melanocortin pathway involved in the regulation of energy homeostasis. The specific role
of the MC3R in the regulation of obesity has not been clearly defined due to a lack of
receptor specific ligands and a complex metabolic phenotype of the MC3R knockout
mouse. This project is focused upon the discovery of MC3R selective molecular probes
(peptide and small molecules), in vitro lead candidate selection, and use of wild type and
knockout mice for further molecule lead selection. The working hypothesis of this project
is that the MC3R is directly involved in the regulation of food intake, satiety, and
energy/metabolic homeostasis. It is anticipated that MC3R ligands have the potential to
become therapeutic ligands for obesity related diseases that bypass the human
melanocortin-4 receptor (MC4R) agonist associated side effects of male erectile activity
and hypertension.

## Key facts

- **NIH application ID:** 10430233
- **Project number:** 5R01DK124504-02
- **Recipient organization:** UNIVERSITY OF MINNESOTA
- **Principal Investigator:** Marc Giulianotti
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $648,763
- **Award type:** 5
- **Project period:** 2021-07-01 → 2025-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10430233

## Citation

> US National Institutes of Health, RePORTER application 10430233, Melanocortin Receptor Selective Ligands (5R01DK124504-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10430233. Licensed CC0.

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