On the 2nd December, the next article was published by the japonese team leaded by Prof. Matsushita: “Meclozine promotes longitudinal skeletal growth in transgenic mice with achondroplasia carrying a gain-of-function mutation in the FGFR3 gene”
This team used the drug repositioning strategy entifying an FDA-approved drug that could suppressed abnormally activated FGFR3 signaling in ACH. This article was published precisely one year ago.
This year, this team examined the feasibility of meclozine administration in clinical settings, investigating the effects of meclozine on ACH model mice carrying the heterozygous Fgfr3ach transgene.
Increased longitudinal bone growth in Fgfr3ach mice (mice with achondroplasia) by oral administration of meclozine in a growth period indicates potential clinical feasibility of meclozine for the improvement of short stature in ACH.
Next step: clinical trial?