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Hypothalamic dysfunction from paternally imprinted gene deletions is the main pathogenesis of PWS and is characterized by short stature, infantile hypotonia, hypothalamic hypogonadism, excessive appetite, and progressive obesity [1,2]

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untreated heterozygous mice (Hz, igf-1 (+/-)) and Hz (igf-1 (+/-)) mice treated with low doses of IGF-1 for 10 days (Hz + IGF-1)

Ipraglifozin has a five-membered ring structure with low selectivity for SGLT-2 and was first approved in Japan in 2014