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Unsurprisingly, inactivating variants of these receptors have been implicated in a spectrum of reproductive phenotypes, including failure to undergo puberty, and infertility. Clinical induction of puberty in patients harbouring such variants is possible, but restoration of fertility is not always a realisable outcome, particularly for those patients suffering from primary hypogonadism. Thus, novel pharmaceuticals and\/or a fundamental change in approach to treating these patients are required. The increasing wealth of data describing the effects of coding\u2010region genetic variants on GPCR function has highlighted that the majority appear to be dysfunctional as a result of misfolding of the encoded receptor protein, which, in turn, results in impaired receptor trafficking through the secretory pathway to the cell surface. As such, these intracellularly retained receptors may be amenable to \u2018rescue\u2019 using a pharmacological chaperone (PC)\u2010based approach. PCs are small, cell permeant molecules hypothesised to interact with misfolded intracellularly retained proteins, stabilising their folding and promoting their trafficking through the secretory pathway. In support of the use of this approach as a viable therapeutic option, it has been observed that many rescued variant GPCRs retain at least a degree of functionality when \u2018rescued\u2019 to the cell surface. In this review, we examine the GPCR PC research landscape, focussing on the rescue of inactivating variant GPCRs with important roles in the HPG axis, and describe what is known regarding the mechanisms by which PCs restore trafficking and function. We also discuss some of the merits and obstacles associated with taking this approach forward into a clinical setting.<\/jats:p>","DOI":"10.1111\/jne.13418","type":"journal-article","created":{"date-parts":[[2024,6,9]],"date-time":"2024-06-09T20:49:55Z","timestamp":1717966195000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Restoring function to inactivating G protein\u2010coupled receptor variants in the hypothalamic\u2013pituitary\u2013gonadal axis\n                    <sup>1<\/sup>"],"prefix":"10.1111","volume":"36","author":[{"given":"Tarryn","family":"Radomsky","sequence":"first","affiliation":[{"name":"Centre for Neuroendocrinology, Department of Immunology, Faculty of Health Sciences University of Pretoria  Pretoria South Africa"},{"name":"Department of Physiology, Faculty of Health Sciences University of Pretoria  Pretoria South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ross 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