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GR 144053 trihydrochloride

CAS# 1215333-48-4

GR 144053 trihydrochloride

Catalog No. BCC6998----Order now to get a substantial discount!

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Chemical structure

GR 144053 trihydrochloride

3D structure

Chemical Properties of GR 144053 trihydrochloride

Cas No. 1215333-48-4 SDF Download SDF
PubChem ID 173613 Appearance Powder
Formula C18H28ClN5O2 M.Wt 381.9
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in water
Chemical Name 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]piperidin-1-yl]acetic acid;hydrochloride
SMILES C1CN(CCC1N2CCN(CC2)C3=CC=C(C=C3)C(=N)N)CC(=O)O.Cl
Standard InChIKey UFCPHZZPRPPDMC-UHFFFAOYSA-N
Standard InChI InChI=1S/C18H27N5O2.ClH/c19-18(20)14-1-3-15(4-2-14)22-9-11-23(12-10-22)16-5-7-21(8-6-16)13-17(24)25;/h1-4,16H,5-13H2,(H3,19,20)(H,24,25);1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of GR 144053 trihydrochloride

DescriptionA potent and selective platelet fibrinogen receptor glycoprotein IIb/IIIa (GpIIb/IIIa) antagonist (IC50 = 37 nM). Orally active and highly effective at inhibiting thrombus formation in vivo.

GR 144053 trihydrochloride Dilution Calculator

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GR 144053 trihydrochloride Molarity Calculator

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Preparing Stock Solutions of GR 144053 trihydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.6185 mL 13.0924 mL 26.1849 mL 52.3697 mL 65.4622 mL
5 mM 0.5237 mL 2.6185 mL 5.237 mL 10.4739 mL 13.0924 mL
10 mM 0.2618 mL 1.3092 mL 2.6185 mL 5.237 mL 6.5462 mL
50 mM 0.0524 mL 0.2618 mL 0.5237 mL 1.0474 mL 1.3092 mL
100 mM 0.0262 mL 0.1309 mL 0.2618 mL 0.5237 mL 0.6546 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on GR 144053 trihydrochloride

Comparative antiplatelet effects of aspirin, vapiprost and GR144053, a GPIIb/IIIa antagonist, with a special reference to the role of platelet microaggregates.[Pubmed:10455258]

Br J Pharmacol. 1999 Jul;127(5):1129-34.

Microthrombi produced have a potential to form larger thrombi, leading to vascular occlusions. Recently, a new device to easily detect microaggregates using laser-light scattering (LS) has been developed. We adopted this device to comparatively evaluate the inhibitory effects of aspirin (1,3 or 10 mg kg(-1)), vapiprost (0.3, 1 or 3 mg kg(-1)) or GR144053 (0.1, 0.3 or 1 mg kg(-1)) on ex vivo aggregation of hamster platelets in relation to their in vivo antithrombotic effects. A transluminal thrombus was produced in the hamster femoral artery by the photochemical reaction. Each compound was injected i.v. as a bolus 10 min prior to the reaction, showing a dose-dependent antithrombotic effect, i.e. they prolonged the time before the artery occluded. At that time cyclic flow reductions occurred more marked when aspirin or vapiprost was given. At the end of experiments, blood was collected to evaluate the platelet aggregation using both the new LS device and the conventional optical density (OD) method. Many more small aggregates were still formed when the highest dose of aspirin or vapiprost was used as compared with that of GR144053, although suppression of the platelet aggregation using the OD method, prolongation of the occlusion time and the bleeding time were quite similar. In conclusion, a GPIIb/IIIa antagonist markedly suppressed the microthrombi and reduced the cyclic flow reduction. This further indicates the importance of small aggregates as triggers of thrombosis and shows that prevention of their formation may result in improved vascular patency after thrombotic insult.

GR144053, a fibrinogen receptor antagonist, enhances the suppression of neointima formation by losartan, an angiotensin II receptor antagonist, in the injured carotid artery of hamster.[Pubmed:9480031]

Br J Pharmacol. 1997 Nov;122(6):1099-104.

1. The present study investigated the inhibitory effect of losartan, a type 1 angiotensin II (AT1) antagonist, and of combined treatment with losartan and GR144053, a fibrinogen receptor (GPIIb/IIIa) antagonist, on neointima formation subsequent to vascular injury in the hamster carotid artery. Vascular injury was achieved by a roughened-tip 2F catheter and the neointimal area was measured up to 2 weeks inducing the injury. 2. Compared to non-treated hamsters (intimal area (IA/internal elastic laminal area (IELA) ratio = 60.3 +/- 5.9%, n = 12), losartan dissolved in drinking water (1, 3 and 10 mg kg-1 per day, n = 8 each) reduced neointimal area dose-dependently, a significant decrease (IA/IELA = 39.7 +/- 5.6%) being attained with the highest dose when it was administered from 1 day before injury. However, neointima formation was not prevented even with the highest dose of losartan when the administration was started after injury. 3. When the administration of GR144053 (1.0 mg kg-1 per hour) via an implanted osmotic pump was started 30 min before the injury and continued for the next 2 weeks, no suppression of neointima formation was observed, although platelet aggregation evoked ex vivo by adenosine diphosphate (ADP) at the end of treatment period was efficiently inhibited. 4. In separate experiments in which 5-bromo-2-deoxy-Uridine (BrdU) was used to test smooth muscle cell (SMC) proliferation 1 and 7 days after injury, the ratio of SMC proliferation in the injured area was only slightly decreased by losartan when its administration was started after the injury, despite the marked reduction of SMC proliferation when treatment was started before the injury. Treatment with GR144053 as indicated above also significantly decreased the SMC proliferating index 1 day after the injury. 5. To examine the potential benefit of the coadministration of the GPIIb/IIIa antagonist with the AT1 receptor antagonist, GR144053 (1.0 mg kg-1 per hour) was combined with post-injury treatment with losartan (10 mg kg-1 per day). This markedly reduced the proliferation of SMCs and significantly decreased the neointimal area (IA/IELA = 31.2 +/- 4.6%) measured 2 weeks following the catheterization. 6. According to the results of a time-dependent study in which GR144053 was given in combination with post injury treatment with losartan for 1, 3, 7 or 14 days, neointima formation could be reduced by treatment with GR144053 for just 7 days. 7. In conclusion, GR144053, a fibrinogen receptor antagonist, enhanced the inhibitory effect of losartan, an AT1 receptor antagonist, on neointima formation in the damaged carotid artery of hamsters.

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