The SARS-CoV-2 KP.2 variant, a descendant of JN.1 with mutations S:R346T and S:F456L, is rapidly spreading globally as of April 2024. This variant has three mutations in the spike (S) protein compared to JN.1, including two new substitutions. The relative effective reproduction number (Re) of KP.2 is 1.22-1.32 times higher than that of JN.1 in the USA, UK, and Canada, suggesting higher viral fitness and potential dominance worldwide. By early April 2024, KP.2 had reached 20% prevalence in the UK. However, KP.2 shows significantly lower infectivity (10.5-fold) compared to JN.1 in pseudovirus assays. Neutralization assays revealed that KP.2 is more resistant to sera from vaccinated individuals, particularly those vaccinated with monovalent XBB.1.5 vaccine, with neutralization titers 3.1- and 1.8-fold lower than those against JN.1. These findings indicate that KP.2's increased immune resistance may contribute to its higher Re compared to previous variants. The study used genome surveillance data and a Bayesian model to estimate Re. The research highlights the importance of monitoring KP.2's virological properties and immune evasion capabilities. The study was supported by various grants and the authors declare potential conflicts of interest.The SARS-CoV-2 KP.2 variant, a descendant of JN.1 with mutations S:R346T and S:F456L, is rapidly spreading globally as of April 2024. This variant has three mutations in the spike (S) protein compared to JN.1, including two new substitutions. The relative effective reproduction number (Re) of KP.2 is 1.22-1.32 times higher than that of JN.1 in the USA, UK, and Canada, suggesting higher viral fitness and potential dominance worldwide. By early April 2024, KP.2 had reached 20% prevalence in the UK. However, KP.2 shows significantly lower infectivity (10.5-fold) compared to JN.1 in pseudovirus assays. Neutralization assays revealed that KP.2 is more resistant to sera from vaccinated individuals, particularly those vaccinated with monovalent XBB.1.5 vaccine, with neutralization titers 3.1- and 1.8-fold lower than those against JN.1. These findings indicate that KP.2's increased immune resistance may contribute to its higher Re compared to previous variants. The study used genome surveillance data and a Bayesian model to estimate Re. The research highlights the importance of monitoring KP.2's virological properties and immune evasion capabilities. The study was supported by various grants and the authors declare potential conflicts of interest.