ChemicalBook--->CAS DataBase List--->229971-81-7

229971-81-7

229971-81-7 Structure

229971-81-7 Structure
IdentificationBack Directory
[Name]

ADH 1
[CAS]

229971-81-7
[Synonyms]

ADH 1
Exherin
CS-2142
Exherin TFA
ADH-1 Exherin
Exherin (ADH-1)
L-Cysteinamide, N-acetyl-L-cysteinyl-L-histidyl-L-alanyl-L-valyl-, cyclic (1→5)-disulfide
[Molecular Formula]

C22H34N8O6S2
[MDL Number]

MFCD18251730
[MOL File]

229971-81-7.mol
[Molecular Weight]

570.69
Chemical PropertiesBack Directory
[Boiling point ]

1183.4±65.0 °C(Predicted)
[density ]

1.40±0.1 g/cm3(Predicted)
[storage temp. ]

Keep in dark place,Sealed in dry,Store in freezer, under -20°C
[solubility ]

DMSO:2.2(Max Conc. mg/mL);3.86(Max Conc. mM)
[form ]

A solid
[pka]

13.13±0.70(Predicted)
[color ]

White to off-white
[InChIKey]

FQVLRGLGWNWPSS-BXBUPLCLSA-N
[SMILES]

S1SC[C@@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](C1)C(=O)N)C(C)C)C)Cc2[nH]cnc2)NC(=O)C
Safety DataBack Directory
[WGK Germany ]

WGK 3
[Storage Class]

11 - Combustible Solids
Hazard InformationBack Directory
[Uses]

ADH-1, an N-cadherin antagonist, inhibits N-cadherin mediated cell adhesion.
[Biological Activity]

ADH-1 is an N-cadherin (CD325; NCAD) antagonist th at selectively inhibits NCAD-dependent neurite outgrowth (IC50 = 323 μM; PN1-2 r at cerebral neurons on monolayer of chick NCAD-expressing 3T3)while exhibiting no effect against integrin receptor-dependent neurite outgrowth. ADH-1 inhibits NCAD-mediated signaling events in cultures (0.2-2.5 mg/mL) and exhibits anti-tumor efficacy in vivo (50-100 mg/kg i.p. in rats and mice).
[in vivo]

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].
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].

[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. DOI:10.1002/ijc.23027
[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. DOI:10.1097/CAD.0b013e328020043e
[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 DOI:10.1097/SLA.0000000000000635
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