Lactate metabolism plays a central role in the metabolic reprogramming of tumors and is critically implicated in the progression, metastasis, and therapy resistance of pancreatic cancer. Beyond being a glycolytic byproduct, lactate functions as a key signaling molecule that regulates tumor proliferation, invasion, immune escape, and drug tolerance. Recent advances have identified lactate dehydrogenase A (LDHA) and monocarboxylate transporters (MCTs) as promising therapeutic targets in pancreatic cancer. Preclinical studies suggest that disrupting lactate metabolism can suppress tumor growth and remodel the immunosuppressive tumor microenvironment. Moreover, lactate-associated biomarkers show potential in enhancing the diagnosis and prognosis of pancreatic cancer. Despite these advances, current lactate-targeted therapies are limited by poor specificity, suboptimal safety, and pharmacological instability. This review outlines the mechanistic underpinnings of lactate metabolism in pancreatic cancer, highlights emerging therapeutic targets and strategies, and discusses the potential of integrating lactate-targeted approaches with immunotherapy to improve clinical outcomes.