ADH-1 trifluoroacetate (Exherin trifluoroacetate) is a cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis.

在胰腺癌细胞中，Exherin (0.2 mg/mL) 阻断了胶原蛋白I介导的变化且在阻止由N-cadherin表达引发的细胞移动性方面表现出高度效力。Exherin (0-1.0 mg/mL) 以N-cadherin依赖的方式剂量依赖性地诱导细胞凋亡。

在小鼠胰腺癌模型中，ADH-1 (50 mg/kg) 显著抑制肿瘤生长和转移[1]。在大鼠主动脉环实验或PC3皮下异种移植瘤模型的抗肿瘤潜力评估中，ADH-1 未显示出抗血管生成活性[2]。ADH-1 介导的黑色素瘤肿瘤生长增强作用不会因局部输注替莫唑胺而改变。在A375异种移植瘤中，ADH-1 可增加AKT在丝氨酸473位点的磷酸化，但在DM443异种移植瘤中则无此效应。ADH-1 在两种异种移植瘤中都略微降低N-钙黏蛋白表达[3]。

Exherin is prepared in PBS.Animals are anesthetized, and 40 μL of a single cell suspension containing 50,000 cells is injected into the pancreas. Mice are randomized into treatment groups 10 days after surgery. For treatment, mice are injected intraperitoneally once per day with Exherin at 50 mg/kg in 100 μL PBS (×1 per day, ×5 per week for 4 weeks). For in vivo bioluminescence, D-Luciferin is administered by intraperitoneal injection. Data are acquired 20 min after injection using the IVIS system. Tumor growth is monitored every 10 days from day 10 to day 50 after surgery. Luciferase activity is quantified using the IVIS system. Two months after surgery, the mice are killed, and the pancreas, liver, lung, and disseminated nodules are harvested, fixed in 10% buffered formalin, and embedded in paraffin. Serial 5-μM sections are cut, mounted on slides, and stained with H&E using standard procedures.