While current antidepressants tackle depressive symptoms, they often fall short in addressing cognitive deficits associated with depression. Expanding upon our previous study on HBK-10, a multimodal compound targeting 5-HT1A receptors and demonstrating antidepressant-like properties, we now aim to investigate its procognitive potential and the underlaying mechanisms.First, we evaluated the influence of HBK-10 on ß-arrestin recruitment using CHO-K1 cells expressing the 5-HT1Areceptor. Subsequently, we conducted the Morris water maze test, employing the NMDA receptor antagonist MK-801 to induce memory impairments in mice. Following the behavioral test, we collected mouse hippocampi and prefrontal cortex tissues to assess the levels of signaling proteins using ELISA.HBK-10 selectively inhibited ß-arrestin recruitment after binding to the 5-HT1A receptor. In the Morris water maze, it effectively reversed spatial memory deficits by reducing latency to find the platform on days 5 and 6 at all doses. Notably, on the last day of the experiment, animals previously treated with HBK-10 at a dose of 2.5 mg/kg exhibited a significant reversal of cognitive impairments. Additionally, HBK-10 upregulated BDNF levels in both the hippocampus and prefrontal cortex of mice administered with a dose of 2.5 mg/kg.Our study reveals HBK-10's functional selectivity at the 5-HT1A receptor, specifically in ß-arrestin recruitment, and demonstrates its procognitive potential, possibly mediated through BDNF upregulation. With dual properties of antidepressant-like and memory enhancement, HBK-10 emerges as a promising drug candidate for depression treatment.This study was financed by the National Science Centre, Poland (grant number 2021/05/X/NZ7/00719) and Jagiellonian University Medical College (grant number N42/DBS/000329).