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ADH-1

Catalog No. T2637 CAS 229971-81-7

Synonyms: Exherin

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

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ADH-1, CAS 229971-81-7

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2 mg	5 days	$ 52.00

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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].
Kinase Assay	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.

Synonyms	Exherin
Molecular Weight	570.69
Formula	C22H34N8O6S2
CAS No.	229971-81-7

Storage

keep away from moisture

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 10 mM

References and Literature

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.

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Keywords

ADH-1 229971-81-7 Metabolism Dehydrogenase ADH 1 Inhibitor ADH1 Exherin inhibit inhibitor

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