GPR17 receptor modulators and their therapeutic implications: review of recent patents

ABSTRACT

Introduction: The GPR17 receptor, phylogenetically related to both purinergic P2Y and CysLT receptors, is mainly expressed in the CNS and, in general, in organs that can typically undergo ischemic damage. This receptor is involved in various pathologies including stroke, brain and spinal cord trauma, multiple sclerosis and in all diseases characterized by neuronal and myelin dysfunction. Therefore, there is a strong needed to identify molecules capable of binding specifically to GPR17 receptors.

Areas covered: The review provides a summary of patents, published between 2009 and 2018, on chemicals and biologics and their clinical use. In this work, information is reported about the representative structures and biological activity of recently developed GPR17 receptor ligands.

Expert opinion: The GPR17 receptor is an enigmatic receptor and an interesting therapeutic target in a variety of brain disorders and demyelinating diseases such as multiple sclerosis, stroke, schizophrenia, and depression. The modulation of this receptor could also be potentially useful in obesity treatment. Unfortunately, so far, there are no compounds under investigation in clinical trials but many researchers and companies are investing in the discovery of future potential GPR17 receptor drugs.

KEYWORDS:

• GPR17 receptor
• leukotrienes
• nucleotides
• oligodendrocytes myelination
• patent

Article highlights

• GPR17 receptor is a promising target to cure neurodegenerative diseases.

• The come to light of new molecule classes able to interact with GPR17 receptor opened a new perspective in the pharmacotherapy, in particular for multiple sclerosis.

• Unfortunately, until now, no clinical trial is started with the new GPR17 receptor ligands.

• Until now only academia is focused on the discovery of new ligands for GPR17 receptor.

This box summarizes key points contained in the article.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.