T cell exhaustion is a major barrier in cancer immunotherapy, where chronic antigen exposure in the tumor microenvironment drives loss of effector function and sustained inhibitory receptor expression. Checkpoint blockade has improved clinical outcomes, but many tumors remain unresponsive, highlighting the need to identify intrinsic regulators such as Cbl-b. As an E3 ubiquitin ligase, Cbl-b sets the threshold for TCR signaling, yet its precise role in the progression toward terminal T cell exhaustion remains unclear. Using an OT-I CD8⁺ T cell model driven by OVA stimulation, we examined how pharmacological Cbl-b inhibition influences exhaustion dynamics. In this model, exhaustion was characterized by increased TOX expression and reduced cytokine production. Cbl-b inhibition reversed these changes, restoring IFN-γ and IL-2 production and altering exhaustion-associated phenotypes across multiple stages of exhaustion. This effect was also observed under suppressive conditions generated by MC38 tumor-conditioned media. In vivo studies using MC38-bearing mice further showed that Cbl-b inhibition enhanced antitumor responses and altered the functional state of tumor-infiltrating lymphocytes. Together, these results suggest that targeting Cbl-b may limit progression toward terminal exhaustion and improve antitumor immunity.