ADH-1trifluoroacetate是选择性和竞争性的N-钙粘蛋白拮抗剂，具有潜在抗肿瘤和抗血管生成活性。
CAS：1135237-88-5
分子式：C24H35F3N8O8S2
分子量：684.71
纯度：98%
存储：Store at -20°C

Background:

ADH-1 trifluoroacetate is an N-cadherin antagonist, which inhibits N-cadherin mediated cell adhesion.

ADH-1 (0.2 mg/mL) blocks collagen I-mediated changes in pancreatic cancer cells, and is highly effective at preventing cell motility that is induced by expression of N-cadherin. ADH-1 (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner[1].

ADH-1 (50 mg/kg) significantly prevents tumor growth and metastasis in a mouse model for pancreatic cancer. ADH-1 prevents tumor cell invasion and metastasis in an orthotopic model for pancreatic cancer using N-cadherin overexpressing BxPC-3 cells[1]. ADH-1, at the dosages evaluated, does not display either antiangiogenic activity in a rat aortic ring assay or antitumor potential in a PC3 subcutaneous xenograft tumor model[2]. ADH-1 (10 mL/kg, i.p.) augmentation of melanoma tumor growth is overcome through its ability to make regionally infused melphalan more effective. ADH-1 mediated augmentation of melanoma tumor growth is not altered by regionally infused temozolomide. In A375, but not DM443 xenografts, ADH-1 treatment increases phosphorylation of AKT at serine 473. ADH-1 slightly diminishes N-cadherin expression in both xenografts[3].

[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7. [2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8. [3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77