| Description | ADH-1 (Exherin) is an N-cadherin antagonist, inhibits N-cadherin mediated cell adhesion with potential antineoplastic and antiangiogenic activities. |
| In vitro | Exherin (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. Exherin (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner[1]. |
| In vivo | Exherin (50 mg/kg) significantly prevents tumor growth and metastasis in a mouse model for pancreatic cancer. Exherin prevents tumor cell invasion and metastasis in an orthotopic model for pancreatic cancer using N-cadherin overexpressing BxPC-3 cells[1]. Exherin, 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]. Exherin (10 mL/kg, i.p.) augmentation of melanoma tumor growth is overcome through its ability to make regionally infused melphalan more effective. Exherin mediated augmentation of melanoma tumor growth is not altered by regionally infused temozolomide. In A375, but not DM443 xenografts, Exherin treatment increases phosphorylation of AKT at serine 473. Exherin slightly diminishes N-cadherin expression in both xenografts[3]. |
| Synonyms | Exherin |
| molecular weight | 570.69 |
| Molecular formula | C22H34N8O6S2 |
| CAS | 229971-81-7 |
| Storage | keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| Solubility | DMSO: 10 mM |
| References | 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. 4. Jiang D, Christ S, Correa-Gallegos D, et al. Injury triggers fascia fibroblast collective cell migration to drive scar formation through N-cadherin[J]. Nature communications. 2020, 11(1): 1-13. |
| Citations | 1. Jiang D, Christ S, Correa-Gallegos D, et al. Injury triggers fascia fibroblast collective cell migration to drive scar formation through N-cadherin. Nature communications. 2020 Nov 6;11(1):5653. doi: 10.1038/s41467-020-19425-1. |