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Kisspeptin-10

The story

It was found twice, for two completely different reasons. In 1996 a group in Hershey, Pennsylvania identified a gene that stopped melanoma cells spreading without stopping them growing, and named it KiSS-1 after the town's chocolate. Then in 2001 Tetsuya Ohtaki and colleagues at Takeda in Tsukuba, Japan worked out what the gene actually made: a 54 amino acid amidated peptide they isolated from human placenta, the natural partner of an orphan receptor, which they named metastin for its ability to block invasion and lung spread. Two years later the second discovery arrived from the opposite direction. Nicolas de Roux in Paris and Stephanie Seminara in Boston, working on families whose children never entered puberty, independently found that the fault was a broken GPR54, the receptor for that same peptide. A cancer suppressor turned out to be the master switch for human reproduction. Imperial College London then carried it into people: Waljit Dhillo's group mapped its effects across men and women, compared the ten and 54 residue forms head to head, used it as a gentler trigger for egg maturation in fertility treatment, and in 2023 showed it changing sexual and emotional brain processing in men with low desire. In 2026 the same group solved the timing problem, holding the axis raised for twelve days with intermittent dosing under the skin. Chinese work has since taken it somewhere else entirely, showing kisspeptin-10 acting on GPR54 in bone-dissolving osteoclasts to prevent bone loss, and Russian groups at Perm have followed its role in the immune tolerance that lets a pregnancy survive.

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