Z-(3S)-1,2,3,4-tetrahydroisoquinolene-3-carboxylic acid
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Z-(3S)-1,2,3,4-tetrahydroisoquinolene-3-carboxylic acid

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Category
CBZ-Amino Acids
Catalog number
BAT-005739
CAS number
79261-58-8
Molecular Formula
C18H17NO4
Molecular Weight
311.34
Z-(3S)-1,2,3,4-tetrahydroisoquinolene-3-carboxylic acid
IUPAC Name
(3S)-2-phenylmethoxycarbonyl-3,4-dihydro-1H-isoquinoline-3-carboxylic acid
Synonyms
Z-Tic-OH
Appearance
White to off-white powder
Purity
≥ 98% (HPLC)
Density
1.309g/cm3
Melting Point
137-141 °C
Boiling Point
522.5ºC at 760 mmHg
Storage
Store at 2-8°C
InChI
InChI=1S/C18H17NO4/c20-17(21)16-10-14-8-4-5-9-15(14)11-19(16)18(22)23-12-13-6-2-1-3-7-13/h1-9,16H,10-12H2,(H,20,21)/t16-/m0/s1
InChI Key
YWVQGUBCAUFBCP-INIZCTEOSA-N
Canonical SMILES
C1C(N(CC2=CC=CC=C21)C(=O)OCC3=CC=CC=C3)C(=O)O
1. Homologous desensitization of human platelet thromboxane A2/prostaglandin H2 receptors
A K Okwu, M E Ullian, P V Halushka J Pharmacol Exp Ther. 1992 Jul;262(1):238-45.
Desensitization of platelet thromboxane (TX)A2/prostaglandin (PG)H2 receptors was induced by incubating platelet-rich plasma with the stable PGH2 analog 11 alpha,9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid (U46619) (1 microM). Iloprost, a stable prostacyclin analog, was included in the incubation to prevent platelet activation. The TXA2 mimetic, [1S-1 alpha,2 beta(5Z), 3 alpha(1E,3S*), 4 alpha)]-7-[3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo - [2.2.1]heptan-2-yl]-5-heptenoic acid (I-BOP), was used to induce platelet aggregation, shape change and increases in intracellular free calcium. The EC50 values for I-BOP-induced rise in intracellular free calcium (control = 10.2 +/- 1.5 nM; desensitized = 79.4 +/- 22.4 nM, n = 6, P less than .05), aggregation (control = 15.8 +/- 2.4 nM; desensitized = 51.7 +/- 11.9 nM; P less than .05, n = 5) and shape change (control = 172 +/- 37 pM; desensitized = 350 +/- 60 pM; P less than .05, n = 7) were increased by the preincubation with U46619. Aggregation responses to thrombin and the calcium ionophore, ionomycin, were unaltered by the preincubation with U46619. Equilibrium binding studies at pH 7.4 revealed a decrease in the number of binding sites for the receptor antagonist 9,11-dimethylmethano-11,12- methano-16(3-iodo-4-hydroxyphenyl)-13,14-dihydro-13-aza-15 alpha beta-omega- tetranor-TXA2 [125I]PTA-OH) (control = 3246 +/- 509 sites/platelet, desensitized = 2198 +/- 324 sites/platelet, n = 6, P less than .05) without a change in affinity.(ABSTRACT TRUNCATED AT 250 WORDS)
2. Differential effect of pH on thromboxane A2/prostaglandin H2 receptor agonist and antagonist binding in human platelets
P R Mayeux, T A Morinelli, T C Williams, E S Hazard, D E Mais, J E Oatis, D A Baron, P V Halushka J Biol Chem. 1991 Jul 25;266(21):13752-8.
The effects of changes in pH on the binding of agonists and antagonists to the human platelet thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptor were determined. Competition binding studies were performed with the TXA2/PGH2 mimetic [1S-1 alpha,2 beta (5Z), 3 alpha(1E,3R*),4 alpha)]-7-[3-(3-hydroxy-4'-iodophenoxy)-1-buteny) 7-oxabicyclo-[2.2.1]-heptan-2-yl]-5-heptenoic acid ([125I]BOP). The pH optimum for binding of [125I] BOP to washed human platelets was broad with a range of pH 4-6 in contrast to that of the TXA2/PGH2 receptor antagonist 9,11-dimethyl-methano-11,12-methano-16-(3-iodo-4-hydroxyl)-13-aza-15 alpha,beta-omega-tetranorthromboxane A2 ([125I]PTA-OH) which was 7.4. Scatchard analysis of [125I]BOP binding in washed platelets at pH 7.4, 6.0, and 5.0 revealed an increase in affinity (Kd = 1.16 +/- 0.06, 0.64 +/- 0.09, and 0.48 +/- 0.05 nM, respectively) and an increase in the number of receptors (Bmax = 2807 +/- 415, 5397 +/- 636, and 7265 +/- 753 sites/platelet, respectively). The potency of I-BOP to induce shape change in washed platelets at pH 6.0 was also significantly increased from an EC50 value of 0.34 +/- 0.016 nM at pH 7.4 to 0.174 +/- 0.014 nM at pH 6.0 (n = 6, p less than 0.05). In contrast, the EC50 value for thrombin was unaffected by the change in pH. In competition binding studies with [125I]BOP, the affinity of the agonists U46619 and ONO11113 were increased at pH 6.0 compared to 7.4. In contrast, the affinity of the TXA2/PGH2 receptor antagonists I-PTA-OH, SQ29548, and L657925 were either decreased or unchanged at pH 6.0 compared to 7.4. Diethyl pyrocarbonate and N-bromosuccinimide, reagents used to modify histidine residues, reversed the increase in affinity of [125I]BOP at pH 6.0 to values equivalent to those at pH 7.4. In solubilized platelet membranes, the effects of NBS were blocked by coincubation with the TXA2/PGH2 mimetic U46619. The results suggest that agonist and antagonist binding characteristics are different for the TXA2/PGH2 receptor and that histidine residue(s) may play an important role in the binding of TXA2/PGH2 ligands to the receptor.
3. Inhibition of ligand binding to thromboxane A2/prostaglandin H2 receptors by diethylpyrocarbonate. Protection by receptor ligands and reversal by hydroxylamine
K Schrör, K Davis-Bruno, P V Halushka Biochem Pharmacol. 1995 Mar 30;49(7):921-7. doi: 10.1016/0006-2952(95)00015-r.
The potential of histidines to modulate the binding of agonists and antagonists to human platelet thromboxane A2 (TXA2) receptors was investigated. TXA2 receptors were purified from crude platelet membranes via affinity and wheat germ lectin chromatography. Radioligand binding studies were conducted using the TXA2, mimetic [125I]BOP (I-BOP (I-BOP = [1S-(1 alpha,2 beta(5Z),3 alpha(1E, 3R*),4 alpha)]-7-[3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)7-oxabicyclo- [2.2.1]heptan-2-yl]-5-heptenoic acid) and the TXA2 receptor antagonist [125I]SAP (I-SAP = 7-[(1R,2S,3S,5R)-6,6-dimethyl-3-(4-iodobenzene- sulfonylamino)-bicyclo-[3.1.1]hept-2-yl]-(5Z)-heptenoic acid). The histidine modifying reagent diethyl-pyrocarbonate (DEPC) produced a concentration (30-100 microM) dependent inhibition of binding of both [125I]BOP and [125I]SAP. DEPC treatment significantly (P < 0.05, N = 6) decreased the affinity of the receptor for [125I]SAP (Kd = 2.4 +/- 0.4 and 5.4 +/- 0.4 nM, control and DEPC, respectively) without significantly decreasing the Bmax. The effects of DEPC were reversed by hydroxylamine. The inhibition of [125I]BOP and [125I]SAP binding produced by DEPC was reduced significantly by prior incubation of the purified receptors with the TXA2 receptor agonist U-46619 or the TXA2 receptor antagonist SQ 29548. The results strongly support the notion that one or more histidines reside in a domain that can modulate ligand binding to the TXA2 receptor.
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