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TP508 Sale

目录号 : GC34255

TP508是由23个氨基酸残基构成的多肽,它代表了人凝血素的第508-530位氨基酸序列,被认为是高亲和性受体与凝血素的结合域。

TP508 Chemical Structure

Cas No.:121341-81-9

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1mg
¥1,071.00
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5mg
¥4,284.00
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Sample solution is provided at 25 µL, 10mM.

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实验参考方法

Animal experiment:

Mice: One hour after irradiation, mice are placed in a restrainer and intravenously (i.v.) injected through the tail vein with a single dose of TP508 in 100 μL sterile saline or 100 μL sterile saline alone. After 24 h, the mice are euthanized by CO2 inhalation and thoracic aortas are isolated from TP508- or saline-alone treated mice and transferred to culture dishes containing cold sterile EBM. The periaortic fibro-adipose tissue is removed under a dissecting microscope and aortas are rinsed with cold EBM and cut transversely to create 1 mm aortic rings (appr 10 per aorta). Aortic rings are cut, opened, and the inner endothelial surface is placed directly on Matrigel matrix-coated 24-well plates. Aortic explants are cultured in a 5% CO2 atmosphere at 37°C in EGM containing 5% FBS and SingleQuots endothelial growth factors. Endothelial cell sprouting is monitored daily by inverted phase contrast microscopy and images are captured using SPOT RT camera and advanced imaging software at 40× and 100× magnification.

References:

[1]. Olszewska-Pazdrak B, et al. Nuclear Countermeasure Activity of TP508 Linked to Restoration of Endothelial Function and Acceleration of DNA Repair. Radiat Res. 2016 Aug;186(2):162-74.
[2]. Olszewska-Pazdrak B, et al. Systemic administration of thrombin peptide TP508 enhances VEGF-stimulated angiogenesis and attenuates effects of chronic hypoxia. J Vasc Res. 2013;50(3):186-9
[3]. Chu LM, et al. Effect of thrombin fragment (TP508) on myocardial ischemia reperfusion injury in a model of type 1 diabetes mellitus. Circulation. 2010 Sep 14;122(11 Suppl):S162-9.
[4]. Tsopanoglou NE, et al. On the mode of action of thrombin-induced angiogenesis: thrombin peptide, TP508, mediates effects in endothelial cells via alphavbeta3 integrin. Thromb Haemost. 2004 Oct;92(4):846-57.

产品描述

TP508 is a 23 amino acid synthetic peptide representing residues 508-530 of human prothrombin which is identified as a potential receptor-binding domain based on competition for high-affinity thrombin binding to fibroblasts.

TP508 treatment reverses radiation effects on NO signaling, restores tube formation and accelerates the repair of radiation-induced DSB in irradiated human endothelial cells[1]. TP508 injection increases responsiveness of endothelial cells from aortic explants to VEGF-stimulated angiogenesis in vitro. TP508 stimulation does not significantly affect the VEGF mRNA levels in normoxic or hypoxic cells[2]. TP508 acts as an antagonist for the effects of thrombin. TP508 peptide inhibits these thrombin-induced effects through a RGD and αvβ3-related mechanism[4].

TP508 (500 μg) in sham-irradiated animals significantly increases the amount of endothelial cell sprouting from aortic explants. TP508 significantly increases the sprouting in sham-irradiated and irradiated animals, more than doubling the amount of sprouting in explants from animals at all exposure doses. TP508 (10 mg/kg) given 24 h after 8.5 Gy gamma irradiation significantly increases 30-day survival in mice, from 26.7 to 73.3%[1]. TP508 injection increases endothelial sprouting and potentiates VEGF-stimulated angiogenesis[2]. In type I diabetic swine, TP508 (1 mg/kg, infusion) reduces infarct size after IR[3].

[1]. Olszewska-Pazdrak B, et al. Nuclear Countermeasure Activity of TP508 Linked to Restoration of Endothelial Function and Acceleration of DNA Repair. Radiat Res. 2016 Aug;186(2):162-74. [2]. Olszewska-Pazdrak B, et al. Systemic administration of thrombin peptide TP508 enhances VEGF-stimulated angiogenesis and attenuates effects of chronic hypoxia. J Vasc Res. 2013;50(3):186-9 [3]. Chu LM, et al. Effect of thrombin fragment (TP508) on myocardial ischemia reperfusion injury in a model of type 1 diabetes mellitus. Circulation. 2010 Sep 14;122(11 Suppl):S162-9. [4]. Tsopanoglou NE, et al. On the mode of action of thrombin-induced angiogenesis: thrombin peptide, TP508, mediates effects in endothelial cells via alphavbeta3 integrin. Thromb Haemost. 2004 Oct;92(4):846-57.

Chemical Properties

Cas No. 121341-81-9 SDF
Canonical SMILES Ala-Gly-Tyr-Lys-Pro-Asp-Glu-Gly-Lys-Arg-Gly-Asp-Ala-Cys-Glu-Gly-Asp-Ser-Gly-Gly-Pro-Phe-Val
分子式 C97H146N28O36S 分子量 2312.44
溶解度 Soluble in Water 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 0.4324 mL 2.1622 mL 4.3244 mL
5 mM 0.0865 mL 0.4324 mL 0.8649 mL
10 mM 0.0432 mL 0.2162 mL 0.4324 mL
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Research Update

Thrombin peptide TP508 stimulates cellular events leading to angiogenesis, revascularization, and repair of dermal and musculoskeletal tissues

J Bone Joint Surg Am 2006 Nov;88 Suppl 3:132-9.PMID:17079379DOI:10.2106/JBJS.F.00892.

The thrombin peptide, TP508, also known as Chrysalin (OrthoLogic, Tempe, Arizona), is a twenty-three-amino-acid peptide that represents a portion of the receptor-binding domain of the native human thrombin molecule that has been identified as the binding site for a specific class of receptors on fibroblasts and other cells. Preclinical studies with this peptide have shown that it can accelerate tissue repair in both soft and hard tissues by mechanisms that appear to involve up-regulation of genes that initiate a cascade of healing events. These events include recruitment and activation of inflammatory cells, directed migration of cells (chemotaxis), cell proliferation, elaboration of extra-cellular matrix, and accelerated revascularization of the healing tissues. Early preclinical dermal wound-healing studies showed that TP508 accelerated healing of both incisional wounds and full-thickness excisional wounds in normal and ischemic skin. In all of these studies, the accelerated healing was associated with increased neovascularization across the incision or in the granulating wound bed. Studies in a rat fracture model have also shown that TP508 accelerates the rate of fracture repair. Gene array analysis of fracture callus from control and TP508-treated fractures indicated that TP508 treatment was associated with an up-regulation of early response elements, inflammatory mediators, and genes related to angiogenesis. Similar to what had been seen in dermal wounds, histology from rat fracture callus twenty-one days after treatment indicated that fractures treated with TP508 had significantly more large functional blood vessels than did fractures in the control animals. In vitro studies support these in vivo data and indicate that TP508 may have a direct angiogenic effect by promoting the rate of new vessel growth. The results from phase-1 and phase-2 human clinical studies have shown a positive stimulatory effect of TP508 in the healing of diabetic ulcers and in the repair of fractures to the distal aspect of the radius. Collectively, these studies suggest that TP508 accelerates tissue repair by initiating a cascade of events that lead to an increased rate of tissue revascularization and regeneration.

Thrombin peptide, TP508, stimulates angiogenic responses in animal models of dermal wound healing, in chick chorioallantoic membranes, and in cultured human aortic and microvascular endothelial cells

Gen Pharmacol 2000 Nov;35(5):249-54.PMID:11888680DOI:10.1016/s0306-3623(01)00118-5.

The alpha-thrombin peptide, TP508, accelerates the healing of full-thickness wounds in both normal and ischemic skin. In wounds treated with TP508, a pattern of increased vascularization is consistently observed both grossly and microscopically when compared to wounds treated with saline. One possible mechanism by which the peptide accelerates wound healing is by promoting revascularization of granulation tissue at the injured site. To evaluate the angiogenic potential of TP508, the peptide was tested in the chick embryo chorioallantoic membrane (CAM), where it increased the density and size of CAM blood vessels relative to controls. Additionally, TP508 stimulated chemokinesis and chemotaxis in a dose-dependent fashion in cultured human aortic and human microvascular endothelial cells. Taken together, these in vivo and in vitro data support an angiogenic role for TP508 in wound healing. A working model is presented to explain how this 23-amino-acid peptide, which lacks proteolytic activity, is generated during wound healing and contributes to the nonproteolytic functions associated with alpha-thrombin during tissue repair.

TP508 (Chrysalin) reverses endothelial dysfunction and increases perfusion and myocardial function in hearts with chronic ischemia

J Cardiovasc Pharmacol Ther 2008 Sep;13(3):214-25.PMID:18757834DOI:10.1177/1074248408321468.

Endothelial dysfunction (ED) is characterized by impaired nitric oxide (NO) signaling, decreased NO-dependent vasodilatation, increased vascular inflammation, and diminished response to angiogenic factors. TP508 (Chrysalin), an angiogenic tissue repair peptide, was tested for potential effects on myocardial revascularization and ED using a porcine model of chronic myocardial ischemia. TP508 increased perfusion in ischemic regions up to16-fold (P < .02) and doubled myocardial wall thickening (P < .02) relative to placebo controls. Ischemic arterioles exhibited impaired NO-mediated vasodilation and diminished NO production. TP508 reversed ischemic effects, increasing NO-mediated vasodilation (P < .05), endothelial nitric oxide synthase (eNOS) expression, and NO production. In human endothelial cells, TP508 stimulated eNOS activation (1.84 +/- 0.2-fold; P < .02), increased NO production (85 +/- 18%; P < .02), and prevented hypoxia-induced eNOS downregulation (P < .01). Thus, TP508 reverses ED both in porcine ischemic hearts and cultured human endothelial cells. These results suggest potential therapeutic benefit of TP508 in myocardial revascularization and treatment of ED-related diseases.

TP508 accelerates fracture repair by promoting cell growth over cell death

Biochem Biophys Res Commun 2007 Dec 7;364(1):187-93.PMID:17942078DOI:10.1016/j.bbrc.2007.07.202.

TP508 is a synthetic 23-amino acid peptide representing a receptor-binding domain of human thrombin. We have previously shown that a single injection of TP508 accelerates fracture healing in a rat femoral fracture model. To understand how TP508 acts at the protein level during fracture healing, we compared the translational profiles between saline-control and fractured femur at six time points after TP508 treatment using the second generation of BD Clontechtrade mark Antibody Microarray. Here, we demonstrate that TP508 accelerates fracture healing by modulating expression levels of proteins primarily involved in the functional categories of cell cycle, cellular growth and proliferation, and cell death. The majority of those proteins are physically interrelated and functionally overlapped. The action of those proteins is highlighted by a central theme of promoting cell growth via balance of cell survival over cell death signals. This appears to occur through the stimulation of several bone healing pathways including cell cycle-G1/S checkpoint regulation, apoptosis, JAK/STAT, NF-kappaB, PDGF, PI3K/AKT, PTEN, and ERK/MAPK.

Effect of thrombin fragment (TP508) on myocardial ischemia-reperfusion injury in hypercholesterolemic pigs

J Appl Physiol (1985) 2009 Jun;106(6):1993-2001.PMID:19372304DOI:10.1152/japplphysiol.00071.2009.

Myocardial ischemia-reperfusion (IR) injury occurs frequently in the setting of hypercholesterolemia. We investigated the potential efficacy of a novel thrombin fragment (TP508) on IR injury in a hypercholesterolemic porcine model. Twenty-one hypercholesterolemic male Yucatan pigs underwent 60 min of mid-left anterior descending coronary artery occlusion followed by 120 min of reperfusion. Pigs received either placebo (control, n = 7) or TP508 in two doses (TP508 low dose, n = 7, as bolus of 0.5 mg/kg 50 min into ischemia and an infusion of 1.25 mg.kg(-1).h(-1) during reperfusion period or TP508 high dose, n = 7, a double dose of TP508 low-dose group). Myocardial function was monitored throughout the experiment. The area at risk and myocardial necrosis were determined by Monastryl blue/triphenyl tetrazolium chloride staining. Apoptosis in the ischemic territory was assessed. Coronary microvascular reactivity to endothelium-dependent and -independent factors was measured. Myocardial necrosis was lower in both TP508-treated groups vs. control (P < 0.05). Regional left ventricular function was improved only in the TP508 high-dose group (P < 0.05). Endothelium-dependent coronary microvascular reactivity was greater in both TP508-treated groups (P < 0.05) vs. control. The expression of proteins favoring cell survival, 90-kDa heat shock protein and phospho-Bad (Ser112) was higher in the TP508 high-dose group (P < 0.05). The expression of the cell death signaling proteins, cleaved caspase-3 (P < 0.05), apoptosis-inducing factor (P < 0.05), and poly-ADP ribose polymerase (P = 0.07) was lower in the TP508 low-dose group vs. TP508 high-dose and control. The terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling positive cell count was lower in both TP508 groups compared with the control (P < 0.05). This study demonstrates that, in hypercholesterolemic pigs, TP508 decreases myocardial necrosis and apoptosis after IR. Thus TP508 may offer a novel approach in protecting the myocardium from IR injury.