Objective: Cholangiocarcinoma (CCA) is a highly aggressive malignancy with limited therapeutic options and poor prognosis. Erianin has demonstrated broad-spectrum antitumor activity, yet its role in CCA and tumor immunity remains unclear. Methods: The cytotoxic and growth-inhibitory effects of erianin were evaluated in CCA cell lines and xenograft models. Apoptosis induction, mitochondrial dysfunction, and suppression of focal adhesion kinase (FAK) signaling were examined. The effects of erianin on cellular senescence, senescence-associated secretory phenotype (SASP) factor secretion, and senescent cell clearance were assessed. Pharmacological FAK inhibition was applied to validate the FAK-mediated cell growth and senolytic activity of erianin. The therapeutic efficacy of erianin alone or combined with anti-PD-L1 therapy was evaluated in senescent tumor-bearing mice. Results: Erianin exhibited significant cytotoxicity and induced mitochondrial apoptosis in CCA cells. Rather than inducing senescence, erianin eliminated senescent cells by promoting apoptosis and reduced SASP factor secretion. Erianin effectively inhibited FAK phosphorylation, and FAK blockade further enhanced its antiproliferative and senolytic activity. Moreover, erianin reprogrammed senescence-induced macrophage polarization from an M2- to an M1-like phenotype and increased antitumor immune cell infiltration within the tumor microenvironment. Importantly, erianin synergized with anti-PD-L1 therapy to achieve superior tumor control and prolonged survival in vivo. Conclusions: Erianin exerts potent antitumor effects in CCA by inhibiting FAK-mediated cell growth and senolytic activity, thereby enhancing antitumor immunity and immune checkpoint inhibitor efficacy. These findings identify erianin as a promising senolytic and immunotherapy adjuvant for CCA.