Review
Version 1
Preserved in Portico This version is not peer-reviewed
Melanocortin 1 Receptor (MC1R): Potentials as Therapeutic Targets
†
Y Mun and W Kim equally contributed to this work
Version 1
: Received: 22 May 2023 / Approved: 23 May 2023 / Online: 23 May 2023 (04:16:14 CEST)
A peer-reviewed article of this Preprint also exists.
Mun, Y.; Kim, W.; Shin, D. Melanocortin 1 Receptor (MC1R): Pharmacological and Therapeutic Aspects. Int. J. Mol. Sci. 2023, 24, 12152. Mun, Y.; Kim, W.; Shin, D. Melanocortin 1 Receptor (MC1R): Pharmacological and Therapeutic Aspects. Int. J. Mol. Sci. 2023, 24, 12152.
Abstract
Melanocortins play crucial roles in regulating the stress response, inflammation, and skin pigmentation. In this review, we focus on the melanocortin 1 receptor (MC1R), a G protein-coupled receptor primarily known for regulating skin pigmentation and exhibiting anti-inflammatory effects. First, we provide an overview of the structure, signaling pathways, and related diseases of MC1R. Next, we discuss the potential therapeutic use of synthetic peptides and small molecule modulators of MC1R, highlighting the development of various drugs that enhance stability through amino acid sequence modifications and small molecule drugs to overcome limitations associated with peptide characteristics. Notably, MC1R-targeted drugs have applications beyond skin pigmentation-related diseases, which predominantly affect MC1R in melanocytes. These drugs can also be useful in treating inflammatory diseases with MC1R expression present in various cells. Our review underscores the potential of MC1R-targeted drugs to treat a wide range of diseases and encourages further research in this area.
Keywords
Melanocortin; receptor; peptide; modulator; disease
Subject
Chemistry and Materials Science, Medicinal Chemistry
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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