Cyclin-dependent kinase 8 (CDK8) belongs to the transcription-related CDK family. It has been reported to play a significant role in regulating fundamental cellular processes, including proliferation, survival, differentiation. Achondroplasia (ACH), the most common form of genetic dwarfism, occurs at a frequency of approximately 1 in 20,000 in humans. Over 98% of ACH cases result from a glycine-to-arginine substitution (G380R) in the fibroblast growth factor receptor 3 (FGFR3) gene, which leads to the constitutive activation of the FGFR3 signaling pathway. This leads to abnormal chondrogenesis due to the overactivation of the signal transducer and activator of transcription (STAT) and the mitogen-activated protein kinase (MAPK) pathways. Vosoritide, the first precision drug approved for ACH treatment in children, antagonizes the MAPK pathway. Here, we demonstrate that the CDK8 kinase inhibitor KY-065 rescues impaired chondrogenesis and stunted long bone growth in an ACH mouse model expressing a mouse Fgfr3 harboring a G380R mutation under the Col2a1 promoter (Fgfr3Ach mouse). CDK8 expression and the phosphorylation of STAT1ser727 were elevated in Fgfr3Ach mouse chondrocytes. KY-065 reversed the suppression of chondrogenesis induced by the Fgfr3Ach mutation. Interestingly, KY-065 selectively blocked the CDK8- STAT1ser727 axis without affecting MAPK activation. Additionally, daily subcutaneous injection of KY-065 from three to 30 days of age significantly increased long bone length in Fgfr3Ach mice. Moreover, KY-065 administration to Fgfr3Ach mice increased the thickness of growth plate cartilage and hypertrophic chondrocyte area in the distal femur epiphysis, thereby improving growth plate cytoarchitecture. Our findings suggest that the CDK8 in chondrocytes as a potential therapeutic target for ACH and KY-065 as a promising candidate drug treatment for ACH.