Fig. 3.

AHT-102 demonstrates significant antitumor efficacy in mouse models of gastric cancer (GC). a Tumor growth inhibition in humanized PBMC immune system mice subcutaneously implanted with human gastric cancer NUGC4-CLDN18.2 cells. AHT-102 was administered intravenously once daily (3 days on, followed by 3 days off for each cycle) for 4 cycles (mean ± SD, n = 10). **p < 0.01 compared with the vehicle control group. b Statistical analysis of tumor weights harvested at the end of the study (PG-D21). AHT-102 exhibited dose-dependent inhibition of tumor weight, reaching a maximum inhibition of 51% in the 1.0-mg/kg group (mean ± SD, n = 10). **p < 0.01 compared with the vehicle group. c Representative photograph of the harvested tumors from the vehicle and AHT-102 treatment groups (0.1, 0.3, and 1.0 mg/kg) at the end of the experiment (PG-D21). d Body weight changes across all groups during the study period. A downward trend in body weight was observed in all cohorts as time progressed, attributed to PBMC-induced graft-versus-host disease (GvHD) (mean ± SD, n = 10). No statistically significant differences were observed between the AHT-102 treated groups and the vehicle group (p > 0.05). PBMC peripheral blood mononuclear cell