TCEP hydrochloride
(Synonyms: 三(2-羰基乙基)磷盐酸盐,Tris(2-carboxyethyl) phosphine hydrochloride) 目录号 : GC10529
TCEP hydrochloride 是一种不结合 Hg(2+) 的非硫醇还原剂。
Cas No.:51805-45-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
HUVEC cells |
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Preparation Method |
The NO donor SNP (100 µm), the NOS inhibitor L‐NAME (500 µm), and the cysteine thiol‐reducing agent TCEP hydrochloride hydrochloride (2 mm) were used to HUVEC cells. |
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Reaction Conditions |
2 mm; 2h |
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Applications |
TCEP hydrochloride successfully abolished NO‐induced inhibition of SOD1 monomerization in HUVECs, indicating that NO inhibited monomeric SOD1 by acting on cysteine thiol |
| Animal experiment [2]: | |
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Animal models |
adult Kunming mice |
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Preparation Method |
Total 30 adult Kunming mice were randomly divided into normal control group (0 mg/kg·d), low-dose TCEP hydrochloride group (10 mg/kg·d), and high-dose TCEP hydrochloride group (100 mg/kg·d), and administered continuously by gavage for 30 days. |
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Dosage form |
0, 10, 100 mg/kg·d; p.o. |
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Applications |
Compared with the control group, the water intake of high-dose TCEP hydrochloride group was declined significantly, and the organ index of liver and spleen were increased significantly. In addition, the escape latency of TCEP hydrochloride exposed mice were longer than that in the control group in water maze test, while the total swimming course of high-dose TCEP hydrochloride group was elevated and the swimming time in target quadrant was obviously shortened compared with the control group. |
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References: [1]. Peng H, et al. Nitric oxide inhibits endothelial cell apoptosis by inhibiting cysteine-dependent SOD1 monomerization. FEBS Open Bio. 2022 Feb;12(2):538-548. [2]. Wang C, et al. Neurotoxicity and related mechanisms of flame retardant TCEP hydrochloride exposure in mice. Toxicol Mech Methods. 2020 Sep;30(7):490-496. |
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TCEP hydrochloride is a non-thiol reducing agent which does not bind Hg(2+).[1] TCEP hydrochloride increased SOD1 monomer formation, thus preventing the NO‐induced increase in dismutase activity and the decrease in ROS.[5]
In vitro efficacy test it shown that TCEP hydrochloride promoted NF-kappaB-DNA binding in a dose-related manner in concentrations from 0.25 to 6mM. with 6mM TCEP hydrochloride , Hg(2+) prevented NF-kappaB-DNA binding at concentrations as low as 20 microM in binding reactions.[1]
In vitro experiment it indicated that treatment with 100 μM TCEP hydrochloride-HCL can improve the quality and developmental capacity of in vitro-fertilized embryos by decreasing oxidative stress in porcine oocytes.[2] In human neuronal cell line, SHSY-5Y, with 1 mM TCEP hydrochloride maximally protected against BoNT/B inhibition of [(3)H]-NA release, and has no toxic.[3] TCEP hydrochloride (0.01 mM) does not scavenge Fe(3+) from Tf and is able to protect thiol groups for the coupling to maleimide. In addition, TCEP hydrochloride does not interfere with the maleimide coupling itself.[4] In vitro, human hepatocellular (HepG2) cells were treated with 100, 200, and 400 μM TCEP hydrochloride for 3 days, the level of oxidative stress, esterase, Ca2+ influx, and ΔΨm dysfunction increased. And there were 65.96% subG1 apoptotic peak in 400 μM treated cells.[6]
In vivo, treatment with 20 mg/kg and 60 mg/kg TCEP hydrochloride orally in adult ICR mice for 9 weeks, TCEP improved body weight gain, hypertriglyceridemia, and hepatic steatosis, consistent with upregulation of hepatic lipogenesis-related gene expression. TCEP also altered the levels of several hepatic metabolites.[7]
References:
[1].Dieguez-Acu?a FJ, et al. Inhibition of NF-kappaB-DNA binding by mercuric ion: utility of the non-thiol reductant, tris(2-carboxyethyl)phosphine hydrochloride (TCEP hydrochloride), on detection of impaired NF-kappaB-DNA binding by thiol-directed agents. Toxicol In Vitro. 2000 Feb;14(1):7-16.
[2]Zeng Y, et al. Effects of tris (2-carboxyethyl) phosphine hydrochloride treatment on porcine oocyte in?vitro maturation and subsequent in?vitro fertilized embryo developmental capacity. Theriogenology. 2021 Mar 1;162:32-41.
[3]Shi X, et al. TCEP hydrochloride treatment reduces proteolytic activity of BoNT/B in human neuronal SHSY-5Y cells. J Cell Biochem. 2009 Aug 1;107(5):1021-30.
[4]Visser CC, et al. Coupling of metal containing homing devices to liposomes via a maleimide linker: use of TCEP to stabilize thiol-groups without scavenging metals. J Drug Target. 2004;12(9-10):569-73.
[5]Peng H, et al. Nitric oxide inhibits endothelial cell apoptosis by inhibiting cysteine-dependent SOD1 monomerization. FEBS Open Bio. 2022 Feb;12(2):538-548.
[6]M Al-Salem A, et al. Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells. Toxics. 2020 Nov 20;8(4):109.
[7]Yang D, et al. Tris (2-chloroethyl) phosphate (TCEP) induces obesity and hepatic steatosis via FXR-mediated lipid accumulation in mice: Long-term exposure as a potential risk for metabolic diseases. Chem Biol Interact. 2022 Aug 25;363:110027.
TCEP hydrochloride 是一种不结合 Hg(2+) 的非硫醇还原剂。[1] TCEP hydrochloride 增加了 SOD1 单体的形成，从而阻止了 NO 诱导的歧化酶活性增加和ROS 减少。[5]
体外功效测试表明，TCEP hydrochloride 在 0.25 至 6mM 浓度范围内以剂量相关的方式促进 NF-kappaB-DNA 结合。使用 6mM TCEP 盐酸盐，Hg(2+) 在结合反应中以低至 20 microM 的浓度阻止 NF-kappaB-DNA 结合。[1]
体外实验表明，用 100 μM TCEP 盐酸盐-HCL 处理可以通过降低猪卵母细胞的氧化应激来提高体外受精胚胎的质量和发育能力。[2] 在人类中神经元细胞系 SHSY-5Y，含 1 mM TCEP 盐酸盐，最大限度地防止 BoNT/B 抑制 [(3)H]-NA 释放，并且没有毒性。[3] TCEP 盐酸盐 (0.01 mM) 不会从 Tf 中清除 Fe(3+)，并且能够保护硫醇基团以与马来酰亚胺偶联。此外，TCEP 盐酸盐不会干扰马来酰亚胺偶联本身。[4] 在体外，人肝细胞 (HepG2) 分别用 100、200 和 400 μM TCEP 盐酸盐处理 3 天，氧化应激水平、酯酶、Ca2+ 内流和 δψm 功能障碍增加。并且在400 μM处理的细胞中有65.96%的subG1凋亡峰。[6]
在体内，成年 ICR 小鼠口服 20 mg/kg 和 60 mg/kg TCEP 盐酸盐治疗 9 周后，TCEP 改善了体重增加、高甘油三酯血症和肝脂肪变性，这与肝脂肪生成相关基因表达的上调一致. TCEP 还改变了几种肝脏代谢物的水平。[7]
| Cas No. | 51805-45-9 | SDF | |
| 别名 | 三(2-羰基乙基)磷盐酸盐,Tris(2-carboxyethyl) phosphine hydrochloride | ||
| 化学名 | 3,3',3''-phosphinetriyltripropanoic acid hydrochloride | ||
| Canonical SMILES | O=C(O)CCP(CCC(O)=O)CCC(O)=O.Cl | ||
| 分子式 | C9H16ClO6P | 分子量 | 286.65 |
| 溶解度 | ≥ 28.7mg/mL in Water | 储存条件 | Store at 2-8°C , protect from light, stored under nitrogen |
| 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 | 3.4886 mL | 17.4429 mL | 34.8857 mL |
| 5 mM | 0.6977 mL | 3.4886 mL | 6.9771 mL |
| 10 mM | 0.3489 mL | 1.7443 mL | 3.4886 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。
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Amyloid-Based Albumin Hydrogels
Amyloid fibrils may serve as building blocks for the preparation of novel hydrogel materials from abundant, low-cost, and biocompatible polypeptides. This work presents the formation of physically cross-linked, self-healing hydrogels based on bovine serum albumin at room temperature through a straightforward disulfide reduction step induced by tris (2-carboxyethyl) phosphine hydrochloride. The structure and surface charge of the amyloid-like fibrils is determined by the pH of the solution during self-assembly, giving rise to hydrogels with distinct physicochemical properties. The hydrogel surface can be readily functionalized with the extracellular matrix protein fibronectin and supports cell adhesion, spreading, and long-term culture. This study offers a simple, versatile, and inexpensive method to prepare amyloid-based albumin hydrogels with potential applications in the biomedical field.
TCEP treatment reduces proteolytic activity of BoNT/B in human neuronal SHSY-5Y cells
The light chain (LC) of botulinum neurotoxin B (BoNT/B) is unable to enter target neuronal cells by itself. It is brought into the cell in association with the BoNT/B heavy chain (HC) through endocytosis. The BoNT HC-LC subunits are held together by a single disulfide bond. Intracellular reduction of this bond and separation of the two subunits activates the endopeptidase activity of the LC. This requirement suggests a strategy to prevent uptake by prophylactic reduction to disrupt the disulfide bond prior to endocytosis of the complex. We examined the utility of tris-(2-carboxyethyl)-phosphine hydrochloride (TCEP), a relatively non-toxic, non-sulfur containing disulfide bond reducing agent that lacks the undesirable properties of mercapto-containing reducing agents. We found that TCEP was as effective as DTT with maximal LC endopeptidase activation occurring at 1 mM, a concentration not toxic to the human neuronal cell line, SHSY-5Y. In these cells, 1 mM TCEP maximally protected against BoNT/B inhibition of [(3)H]-NA release, achieving 72% of the release from un-intoxicated controls. This effect appears to be due to the sparing of SNARE proteins as the levels of VAMP-2, the specific target of BoNT/B, were protected. These results show that TCEP disrupts the structure of BoNT/B by reduction of the LC and HC bridging disulfide bond and prevents neuronal intoxication. Since disulfide bond coupling between toxin subunits is a general motif for many toxins, e.g., ricin, snake venom, and all BoNT serotypes, this suggests that TCEP is a promising means to protect against these toxins by preventing cell penetration.
Amyloid-Like Protein Aggregation Toward Pesticide Reduction
Pesticide overuse is a major global problem and the cause of this problem is noticeable pesticide loss from undesired bouncing of sprayed pesticide droplets and rain erosion. This further becomes a primary source of soil and groundwater pollution. Herein, the authors report a method that can enhance pesticide droplet deposition and adhesion on superhydrophobic plant leave surfaces by amyloid-like aggregation of bovine serum albumin (BSA). Through the reduction of the disulfide bond of BSA by tris(2-carboxyethyl) phosphine hydrochloride (TCEP), the amyloid-like phase transition of BSA is triggered that rapidly affords abundant phase-transitioned BSA (PTB) oligomers to facilitate the invasion of the PTB droplet into the nanostructures on a leaf surface. Such easy penetration is further followed by a robust amyloid-mediated interfacial adhesion of PTB on leaf surface. As a result, after mixing with pesticides, the PTB system exhibits a remarkable pesticide adhesion capacity that is more than 10 times higher than conventional fixation of commercial pesticides. The practical farmland experiments show that the use of PTB aggregation could reduce the use of pesticides by 70-90% while ensuring yield. This work demonstrates that current pesticide dosage in actual agriculture production may be largely reduced by utilizing eco-friendly amyloid-like protein aggregation.
Effects of tris (2-carboxyethyl) phosphine hydrochloride treatment on porcine oocyte in vitro maturation and subsequent in vitro fertilized embryo developmental capacity
Oocyte in vitro maturation (IVM) is a crucial process that determines subsequent in vitro embryo production. The present study investigated the effects of the antioxidant tris (2-carboxyethyl) phosphine hydrochloride (TCEP-HCL) on the in vitro maturation of porcine oocytes and in vitro developmental competence of fertilized embryos. Oocytes were matured in IVM medium based on four concentration groups of TCEP-HCL (0, 50, 100, and 200 μM) treatment. 100 μM TCEP-HCL treatment significantly increased the oocyte first polar body extrusion rate, monospermy rate and subsequent in vitro fertilized embryo developmental capacity (cleavage rate, blastocyst formation rate, and blastocyst total cell number) compared to those in the control group. Furthermore, 100 μM TCEP-HCL treatment significantly reduced the levels of reactive oxygen species, significantly increased glutathione levels and mitochondrial content compared to those in the control group. Moreover, 100 μM TCEP-HCL treatment significantly decreased the oocyte apoptosis, blastocyst apoptosis compared to that in the controls. In summary, these results indicate that 100 μM TCEP-HCL treatment improves the quality and developmental capacity of in vitro-fertilized embryos by decreasing oxidative stress in porcine oocytes.
Thiol Catalysis of Selenosulfide Bond Cleavage by a Triarylphosphine
The arylthiol 4-mercaptophenylacetic acid (MPAA) is a powerful catalyst of selenosulfide bond reduction by the triarylphosphine 3,3',3″-phosphanetriyltris(benzenesulfonic acid) trisodium salt (TPPTS). Both reagents are water-soluble at neutral pH and are particularly adapted for working with unprotected peptidic substrates. Contrary to trialkylphosphines such as tris(2-carboxyethyl)phosphine hydrochloride (TCEP), TPPTS has the advantage of not inducing deselenization reactions. We believe that the work reported here will be of value for those manipulating selenosulfide bonds in peptidic or protein molecules.