ADH-1 (Exherin) is an N-cadherin antagonist, inhibits N-cadherin mediated cell adhesion with potential antineoplastic and antiangiogenic activities.

ADH-1 (0.2 mg/mL) 阻断胰腺癌细胞中 I 型胶原引发的变化，并且在阻止 N-cadherin 表达诱导的细胞运动方面表现出高效性。ADH-1 (0, 0.1, 0.2, 0.5 和 1.0 mg/mL) 以剂量依赖和 N-cadherin 依赖的方式诱导细胞凋亡[1]。

ADH-1 (50 mg/kg) 显著阻止了小鼠胰腺癌模型的肿瘤生长和转移。在使用过表达N-cadherin的BxPC-3细胞的胰腺癌原位模型中，ADH-1防止了肿瘤细胞的侵袭和转移[1]。在所评估的剂量下，ADH-1既没有在大鼠主动脉环实验中显示出抗血管生成活性，也没有在PC3皮下异种移植肿瘤模型中显示出抗肿瘤潜力[2]。ADH-1 (10 mL/kg, i.p.) 增强了黑色素瘤肿瘤生长，但通过提高局部灌注的梅尔菲兰的效果被克服。区域性灌注的替莫唑胺并不改变ADH-1对黑色素瘤肿瘤生长的增强作用。在A375（但非DM443）异种移植瘤中，ADH-1处理增加了丝氨酸473位点AKT的磷酸化，同时略微降低了两种异种移植瘤中的N-cadherin表达[3]。

Kinase Activity Assays: The effect of VX-509 on JAK3 activity is assessed by measuring the residual kinase activity of the recombinantly expressed JAK3 kinase domain using a radiometric assay. The final concentrations of the components in the assay are as follows: 100 mM HEPES (pH 7.5), 10 mM MgCl2, 1 mM dithiothreitol (DTT), 0.01% BSA, 0.25 nM JAK3, 0.25 mg/ml polyE4Y, and 5 μM 33P-γ-ATP (200 μCi/μMol). A 10 mM stock solution of VX-509 is prepared in DMSO, from which additional dilutions are prepared. A substrate mixture (100 mM HEPES, 10 mM MgCl2, 0.5 mg/ml polyE4Y, and 10 μM 33P-γ-ATP) is added and mixed with VX-509 stock solution. The reaction is initiated by the addition of an enzyme mixture [100 mM HEPES (pH 7.5), 10 mM MgCl2, 2 mM DTT, 0.02% BSA, 0.5 nM JAK3]. After 15 minutes, the reaction was quenched with 20% trichloroacetic acid (TCA). The quenched reaction was transferred to the GF/B filter plates and washed three times with 5% TCA. Following the addition of Ultimate Gold scintillant (50 μl), the samples were counted in a Packard TopCount gamma counter (PerkinElmer). In this procedure, the radioactivity trapped is a measure of the residual JAK3 kinase activity. From the activity versus concentration of VX-509 titration curve, the Ki value was determined by fitting the data to an equation for competitive tight binding inhibition kinetics using Prism software.