Z-N-Me-L-norleucine
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Z-N-Me-L-norleucine

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Category
CBZ-Amino Acids
Catalog number
BAT-005785
CAS number
225386-32-3
Molecular Formula
C15H21NO4
Molecular Weight
279.34
Z-N-Me-L-norleucine
IUPAC Name
(2S)-2-[methyl(phenylmethoxycarbonyl)amino]hexanoic acid
Synonyms
Z-N-Me-L-Nle-OH; Z-N-Me-L-2-aminohexanoic acid
Appearance
White powder
Purity
≥ 98% (HPLC)
Melting Point
37-41 °C
Storage
Store at 2-8°C
InChI
InChI=1S/C15H21NO4/c1-3-4-10-13(14(17)18)16(2)15(19)20-11-12-8-6-5-7-9-12/h5-9,13H,3-4,10-11H2,1-2H3,(H,17,18)/t13-/m0/s1
InChI Key
ZRIGUBDEWMLBRB-ZDUSSCGKSA-N
Canonical SMILES
CCCCC(C(=O)O)N(C)C(=O)OCC1=CC=CC=C1
1. Enhanced endothelin ET(B) receptor down-regulation in human tumor cells
J Drimal, J Drimal Jr, D Drimal Eur J Pharmacol. 2000 May 12;396(1):19-22. doi: 10.1016/s0014-2999(00)00198-9.
The characteristics of specific binding of human [125I]Tyr(13)-endothelin-(1-21), [125I]-Tyr(13)-Suc-[Glu(9),Ala(11, 15)]-endothelin-(8-21), ([125I]IRL-1620) and endothelin ET(A) receptor antagonist [125I]Tyr(3)-(N-[(hexahydro-1H-azepin-1-yl)carbonyl]-L-Leu]-1Me )-D-Trp ([125I]PD151242) (number of sites and their affinity) and proliferation responses to exogenous endothelin receptor agonists (endothelin-1 and the endothelin ET(B) receptor-selective, truncated N-acetyl-[Ala(11,15)]-endothelin-(6-21) analogue BQ3020) were determined in cultured human fibroblasts and in tumorigenic HeLa cells. The cells were pre-incubated with equimolar concentrations of human endothelin-1 or its truncated analogue BQ3020. After pre-incubation (2 h), both peptides induced down-regulation of surface-membrane endothelin-1 receptors. This process was specific for endothelin ET(B) receptors and was much more intensive in tumorigenic cells. BQ3020, acting mostly through its C-terminus, induced nearly maximal endothelin ET(B) receptor down-regulation in HeLa cells. Staurosporine, a wide spectrum protein kinase inhibitor, significantly reduced, and N-[N-[N-[2, 6-dimethyl-1piperidinyl)carbonyl]-4-Me-L-Leu]-1-(methoxycarbonyl)- D-t ryptophanyl]-D-norleucine (BQ788), an endothelin ET(B) receptor antagonist, attenuated the down-regulation of endothelin receptors induced by endothelin receptor agonists. The down-regulation of endothelin ET(B) receptors was prevented by pre-incubation of the cells with the lysosomal enzyme blocker chloroquine. The endothelin-1-induced cell proliferation was attenuated by pre-incubation of the cells with the non-selective endothelin receptor antagonist Ac-D-10,11-dihydro-5H-dibenzo[a,d] cycloheptene-glycine-3,3-D-diphenyl-Ala-Leu-Asp-Ile-Ile-Trp (PD142893) and it was only partially reduced by the endothelin ET(A) receptor-selective endothelin antagonist PD151242.
2. Context-independent, temperature-dependent helical propensities for amino acid residues
Robert J Moreau, Christian R Schubert, Khaled A Nasr, Marianna Török, Justin S Miller, Robert J Kennedy, Daniel S Kemp J Am Chem Soc. 2009 Sep 16;131(36):13107-16. doi: 10.1021/ja904271k.
Assigned from data sets measured in water at 2, 25, and 60 degrees C containing (13)C=O NMR chemical shifts and [theta](222) ellipticities, helical propensities are reported for the 20 genetically coded amino acids, as well as for norvaline and norleucine. These have been introduced by chemical synthesis at central sites within length-optimized, spaced, solubilized Ala(19) hosts. The resulting polyalanine-derived, quantitative propensity sets express for each residue its temperature-dependent but context-independent tendency to forego a coil state and join a preexisting helical conformation. At 2 degrees C their rank ordering is: P << G < H < C, T, N < S < Y, F, W < V, D < K < Q < I < R, M < L < E < A; at 60 degrees C the rank becomes: H, P < G < C < R, K < T, Y, F < N, V < S < Q < W, D < I, M < E < A < L. The DeltaDeltaG values, kcal/mol, relative to alanine, for the cluster T, N, S, Y, F, W, V, D, Q, imply that at 2 degrees C all are strong breakers: DeltaDeltaG(mean) = +0.63 +/- 0.11, but at 60 degrees C their breaking tendencies are dramatically attenuated and converge toward the mean: DeltaDeltaG(mean) = +0.25 +/- 0.07. Accurate modeling of helix-rich proteins found in thermophiles, mesophiles, and organisms that flourish near 0 degrees C thus requires appropriately matched propensity sets. Comparisons are offered between the temperature-dependent propensity assignments of this study and those previously assigned by the Scheraga group; the special problems that attend propensity assignments for charged residues are illustrated by lysine guest data; and comparisons of errors in helicity assignments from shifts and ellipticity data show that the former provide superior precision and accuracy.
3. Endothelin-1-induced in vitro cerebral venoconstriction is mediated by endothelin ETA receptors
N Fernandez, L Monge, A L Garcia-Villalon, J L Garcia, B Gomez, G Dieguez Eur J Pharmacol. 1995 Dec 29;294(2-3):483-90. doi: 10.1016/0014-2999(95)00577-3.
The in vitro effects of endothelin-1 on cerebral veins were studied using cylindrical segments, 5 mm long, from dog pial veins. Isometric responses to endothelin-1 (10(-12)-10(-7) M) and to the endothelin ET(B) receptor agonist, IRL 1620 (Suc-[Glu9,Ala11,15]endothelin-1-(8-21), 10(-12) -10(-7) M), were recorded in veins under control conditions and pretreated with the endothelin ET(A) receptor antagonist, BQ-123 (cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp), 10(-8) -10(-5) M), and the endothelin ETB receptor antagonist, BQ-788 (N-[N-[N-[(2,6-dimethyl-1-piperidinyl)carbonyl]-4-methyl-L-leucyl]-1-(me thoxycarbonyl)-D-tryptophyl]-D-norleucine monosodium, 10(-6) and 10(-5) M). The response to endothelin-1 was also recorded in veins pretreated with the nitric oxide synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M), or the cyclooxygenase inhibitor, meclofenamate (10(-5) M), and in veins without endothelium or placed in medium without Ca2+ but with EDTA (0.1 mM). In control veins, endothelin-1 produced a concentration-dependent contraction (EC50 = 2.0 x 10(-10) M; maximal contraction = 113 +/- 6 mg) and IRL 1620 induced no effects or a small contraction only with high concentrations (10(-8) - 10(-6) M) (EC50 = 1.5 x 10 (-8) M; maximal contraction = 9 +/- 3 mg). BQ-123 shifted the response to endothelin-1 to the right in a parallel, concentration-dependent way, whereas BQ-788, L-NAME or meclofenamate did not modify the response to endothelin-1. Compared with the control, veins in a medium without Ca2+ had similar EC50 values, but a lower maximal contraction induced by endothelin-1 (57 +/- 10 mg, P < 0.05), and veins without endothelium exhibited similar EC50 values. Thus, endothelin-1 produces marked cerebral venoconstriction that could be mainly mediated by activation of endothelin ETA receptors, may be dependent on extracellular Ca2+, and may be independent of endothelium, nitric oxide and prostanoids.
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