FeTPPS
(Synonyms: MESO-四(4-磺酰苯基)卟吩氯化铁) 目录号 : GC43663A peroxynitrite decomposition catalyst
Cas No.:90384-82-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Peroxynitrite is a highly reactive nitrogen species formed from the reaction of nitric oxide (NO) and superoxide.[1] FeTPPS is a ferric porphyrin complex that causes the decomposition of peroxynitrite by catalytic isomerization to produce nitrate both in vitro and in vivo. The conversion of this reactive nitrogen species to nitrate results in cytoprotection (EC50 = 5 µM). [2][3] FeTPPS does not complex with NO and does not alter superoxide directly. It is commonly used to elucidate the roles of peroxynitrite in oxidative stress, cell damage, and intracellular signaling. [4][5][6]
Reference:
[1]. Chen, X., Chen, H., Deng, R., et al. Pros and cons of current approaches for detecting peroxynitrite and their applications. Biomed.J. 37(3), 120-126 (2014).
[2]. Lauzier, B., Sicard, P., Bouchot, O., et al. A peroxynitrite decomposition catalyst: FeTPPS confers cardioprotection during reperfusion after cardioplegic arrest in a working isolated rat heart model. Fundamental Clinical Pharmacology 21, 173-180 (2007).
[3]. Misko, T.P., Highkin, M.K., Veenhuizen, A.W., et al. Characterization of the cytoprotective action of peroxynitrite decomposition catalysts. The Journal of Biological Chemisty 273(25), 15646-15653 (1998).
[4]. Ishrat, T., Kozak, A., Alhusban, A., et al. Role of matrix metalloproteinase activity in the neurovascular protective effects of angiotensin antagonism. Stroke Res.Treat. 2014, 1-9 (2014).
[5]. Li, J., Loukili, N., Rosenblatt-Velin, N., et al. Peroxynitrite is a key mediator of the cardioprotection afforded by ischemic postconditioning in vivo. PLoS One 8(7), 1-8 (2013).
[6]. Kiss, A., Tratsiakovich, Y., Gonon, A.T., et al. The role of arginase and rho kinase in cardioprotection from remote ischemic perconditioning in non-diabetic and diabetic rat in vivo. PLoS One 9(8), 1-8 (2014).
| Cas No. | 90384-82-0 | SDF | |
| 别名 | MESO-四(4-磺酰苯基)卟吩氯化铁 | ||
| 化学名 | Fe(III)5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato chloride | ||
| Canonical SMILES | [Cl-][Fe+3]123[N-]4C5=CC=C4C(C6=CC=C(S([O-])(=O)=O)C=C6)=C(C=C7)[N]1=C7C(C8=CC=C(S([O-])(=O)=O)C=C8)=C(C=C9)[N-]2C9=C(C%10=CC=C(S([O-])(=O)=O)C=C%10)C%11=[N]3C(C=C%11)=C5C%12=CC=C(S([O-])(=O)=O)C=C%12.[H+].[H+].[H+].[H+] | ||
| 分子式 | C44H24ClFeN4O12S4•4H | 分子量 | 1024.3 |
| 溶解度 | 5 mg/ml in water | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.9763 mL | 4.8814 mL | 9.7628 mL |
| 5 mM | 0.1953 mL | 0.9763 mL | 1.9526 mL |
| 10 mM | 0.0976 mL | 0.4881 mL | 0.9763 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
FeTPPS Reduces Secondary Damage and Improves Neurobehavioral Functions after Traumatic Brain Injury
Front Neurosci 2017 Feb 7;11:6.PMID:28223911DOI:10.3389/fnins.2017.00006.
Traumatic brain injury (TBI) determinate a cascade of events that rapidly lead to neuron's damage and death. We already reported that administration of FeTPPS, a 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrin iron III chloride peroxynitrite decomposition catalyst, possessed evident neuroprotective effects in a experimental model of spinal cord damage. The present study evaluated the neuroprotective property of FeTPPS in TBI, using a clinically validated model of TBI, the controlled cortical impact injury (CCI). We observe that treatment with FeTPPS (30 mg/kg, i.p.) reduced: the state of brain inflammation and the tissue hurt (histological score), myeloperoxidase activity, nitric oxide production, glial fibrillary acidic protein (GFAP) and pro-inflammatory cytokines expression and apoptosis process. Moreover, treatment with FeTPPS re-established motor-cognitive function after CCI and it resulted in a reduction of lesion volumes. Our results established that FeTPPS treatment decreases the growth of inflammatory process and the tissue injury associated with TBI. Thus our study confirmed the neuroprotective role of FeTPPS treatment on TBI.
Peroxynitrite scavenger FeTPPS effectively inhibits hIAPP aggregation and protects against amyloid induced cytotoxicity
Int J Biol Macromol 2020 Oct 15;161:336-344.PMID:32522548DOI:10.1016/j.ijbiomac.2020.06.034.
Type 2 diabetes (T2D) is associated with pancreatic β-cell dysfunction, which can be induced by oxidative stress or/and the aggregation of human islet amyloid polypeptide (hIAPP). Therefore, ONOO- and hIAPP become the crucial targets of T2D treatment. Previously, we found heme could be an effective inhibitor of hIAPP aggregation. However, heme causes serious toxic effects on cells, tissues and organs through oxidative stress, which block it as a potential drug candidate for T2D treatment. 5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrinato iron(III) chloride (FeTPPS), a water-soluble derivative of heme, is recognized as a high-efficient ONOO- decomposition catalyst, which is reported to have a great therapeutic potential in ONOO- -related diseases, including T2D. Here, we explored the potentiality of FeTPPS to be an inhibitor of hIAPP aggregation and the protective effects on cytotoxicity of hIAPP aggregation. It was found that the interaction between FeTPPS and hIAPP remarkably affected hIAPP fibrillation by both stabilizing hIAPP monomers and disaggregating the long fibrils into small oligomeric species. Furthermore, unlike heme, the addition of FeTPPS completely reversed the cytotoxicity and ROS level induced by hIAPP, which was consistent with its strong inhibitory activity. These results implied that FeTPPS could be a promising agent for the treatment of T2D.
FeTPPS protects against global cerebral ischemic-reperfusion injury in gerbils
Pharmacol Res 2007 Apr;55(4):335-42.PMID:17292620DOI:10.1016/j.phrs.2007.01.002.
Neuronal damage following cerebral ischemia is mediated by various mechanisms, among which nitrosative stress plays an important role. Peroxynitrite, a powerful oxidant, contributes heavily to the neuronal damage in cerebral ischemic-reperfusion (IR) injury. In the present study, we have investigated the neuroprotective effects of a peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrinato iron(III) [FeTPPS] in global cerebral IR injury in gerbils. Neurological damage was significantly attenuated by FeTPPS treatment (1 and 3mgkg(-1), i.p.) as evident from reduction in neurological symptoms, hyperlocomotion, memory impairment and CA1 hippocampal neuronal damage in IR challenged gerbils. FeTPPS treatment also attenuated the increased malondialdehyde (MDA) levels and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cells after cerebral IR injury. Results of this study demonstrates the neuroprotective activity of FeTPPS in global cerebral IR injury and its neuroprotective effects may be attributed to reduction in oxidative stress and DNA fragmentation.
The metalloporphyrin FeTPPS but not by cyclosporin A antagonizes the interaction of peroxynitrate and hydrogen peroxide on cardiomyocyte cell death
Naunyn Schmiedebergs Arch Pharmacol 2009 Feb;379(2):149-61.PMID:18773197DOI:10.1007/s00210-008-0342-3.
The objective of this study was to determine whether the metalloporphyrin, 5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrinato iron (III) chloride (FeTPPS), antagonized the effect of peroxynitrite, oxygen-free radicals, and the combination of the two, on cardiomyocyte cell viability. We further sought to compare the effects of FeTPPS to an inhibitor of the mitochondrial transmembrane permeability transition pores (PTP)-cyclosporin A. Cardiomyocytes from embryonic chick heart were treated with 3-morpholinosydnonimine (SIN-1), which decomposes to liberate NO and superoxide anion (O(2) (-)) which in turn generates peroxynitrite. FeTPPS antagonized cell death induced by either SIN-1 or H(2)O(2). The combination of H(2)O(2) plus SIN-1 further enhanced the amount of cell death over SIN-1 alone. FeTPPS rescued cells from almost complete cell death with the combination of SIN-1 plus H(2)O(2). SIN-1 induced cardiac protein nitration, including mitochondrial proteins as demonstrated by Western blotting with nitrotyrosine-specific antibodies. FeTPPS reduced cellular protein nitration. SIN-1-induced loss of mitochondrial transmembrane permeability transition pores potential was visualized with fluorescent dye staining and was reversed by FeTPPS. In contrast, the mitochondrial PTP blocker cyclosporin A did not alter SIN-1-induced cell death. In summary, these data demonstrate the enhanced cellular lethality of the combination of peroxynitrite and reactive oxygen species from hydrogen peroxide. A mitochondrial death pathway was implicated as nitration of mitochondrial proteins was induced by peroxynitrite that also induced a loss of DeltaPsim that was prevented by FeTPPS. In contrast, cyclosporin did not antagonize the effects of SIN-1. The ability of FeTPPS to reduce reactive nitrogen-induced cell death, and protein nitration suggests that FeTPPS is a useful agent to maintain cell viability and is better than cyclosporin in this situation.
Study on the detoxification mechanisms to 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrinato iron(III) chloride (FeTPPS), an efficient pro-oxidant of heme water-soluble analogue
J Inorg Biochem 2018 Dec;189:40-52.PMID:30218889DOI:10.1016/j.jinorgbio.2018.08.016.
5,10,15,20-Tetrakis (4-sulfonatophenyl) porphyrinato iron(III) chloride (FeTPPS) is a water-soluble analog of heme and widely employed as peroxynitrite scavenger in vivo. However, previous studies have showed that like heme, FeTPPS could also act as an effective pro-oxidant towards appreciable substrates in vitro in the presence of oxidant. The reason that FeTPPS did not show any pro-oxidative damage in previous studies when it was used as peroxynitrite decomposition catalyst in vivo, has not been studied. Herein, the effects of two main detoxification mechanisms of heme, i.e., serum albumin (SA) binding and heme oxygenase-1 (HO-1) induction, were examined on FeTPPS in vitro. Fluorescence quenching studies showed bovine serum albumin (BSA) could bind to FeTPPS with high affinity (Kb ~ 109 M-1). Molecular docking studies presented us the details of the binding site that is not a heme pocket. Furthermore, the intrinsic pro-oxidative activity of FeTPPS was found effectively inhibited by forming BSA-FeTPPS complex of low reactivity, which could be thought to protect against the potentially toxic effects of FeTPPS on blood components. In addition, this binding could protect FeTPPS against oxidative degradation. In albumin-free cell system, cell viability results indicated FeTPPS was innoxious to living cells and could protect cells against the oxidative impairment of H2O2 effectively rather than promoting damage. Using western blot, we illustrated that HO-1 expression could not be induced by FeTPPS, which suggested that HO-1 was not related to the protective capacity of FeTPPS. Our results provide a better understanding of FeTPPS and lead to a new guidance to its application.