Salubrinal
目录号 : GC17331
Salubrinal是有效的选择性真核翻译起始因子2α（eIF2α）去磷酸化抑制剂。
Cas No.:405060-95-9
Sample solution is provided at 25 µL, 10mM.
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Salubrinal is a potent and selective inhibitor of eukaryotic translation initiation factor 2α (eIF2α) dephosphorylation[1]. Salubrinal acts as a dual-specificity phosphatase 2 (Dusp2) inhibitor, inhibiting anti-collagen antibody-induced arthritis[2]. Salubrinal has anti-HSV-1 viral activity and inhibits the dephosphorylation of eIF2α mediated by the HSV-1 protein ICP34.5[3].
In vitro, treatment of human skin fibroblasts with Salubrinal (0-20μM) for 1h protected cells from UVB radiation-induced cell death in a dose-dependent manner and maintained intracellular Ca2+ homeostasis[4]. Treatment of bone marrow-derived cells isolated from mice with Salubrinal (1, 2, 5μM) for 6 days inhibited osteoclast differentiation and inhibited migration and adhesion of preosteoclasts in a dose- and time-dependent manner[5].
In vivo, Salubrinal (1mg/kg/day) was treated intraperitoneally in mice with traumatic brain injury (TBI) for 20 days, which effectively reduced TBI-induced plasma membrane permeability, reduced lesion volume, improved neurological deficits, and reduced ER stress-induced autophagy activation[6]. Salubrinal (1mg/kg) was treated intraperitoneally in rats with acute myocardial infarction (MI) for 30min, which increased myocardial eIF2α phosphorylation, reduced the expression of caspase-12 and C/EBP homologous protein (CHOP), and reduced myocardial cell apoptosis and infarct size[7].
References:
[1] Wang R, Sun D Z, Song C Q, et al. Eukaryotic translation initiation factor 2 subunit α (eIF2α) inhibitor salubrinal attenuates paraquat-induced human lung epithelial-like A549 cell apoptosis by regulating the PERK-eIF2α signaling pathway[J]. Toxicology In Vitro, 2018, 46: 58-65.
[2] Hamamura K, Nishimura A, Chen A, et al. Salubrinal acts as a Dusp2 inhibitor and suppresses inflammation in anti-collagen antibody-induced arthritis[J]. Cellular signalling, 2015, 27(4): 828-835.
[3] Bryant K F, Macari E R, Malik N, et al. ICP34. 5-dependent and-independent activities of salubrinal in herpes simplex virus-1 infected cells[J]. Virology, 2008, 379(2): 197-204.
[4] Ji C, Yang B, Huang S, et al. Salubrinal protects human skin fibroblasts against UVB-induced cell death by blocking endoplasmic reticulum (ER) stress and regulating calcium homeostasis[J]. Biochemical and biophysical research communications, 2017, 493(4): 1371-1376.
[5] Yokota H, Hamamura K, Chen A, et al. Effects of salubrinal on development of osteoclasts and osteoblasts from bone marrow-derived cells[J]. BMC musculoskeletal disorders, 2013, 14: 1-11.
[6] Wang Z, Gao C, Chen W, et al. Salubrinal offers neuroprotection through suppressing endoplasmic reticulum stress, autophagy and apoptosis in a mouse traumatic brain injury model[J]. Neurobiology of learning and memory, 2019, 161: 12-25.
[7] Li R J, He K L, Li X, et al. Salubrinal protects cardiomyocytes against apoptosis in a rat myocardial infarction model via suppressing the dephosphorylation of eukaryotic translation initiation factor 2α[J]. Molecular Medicine Reports, 2015, 12(1): 1043-1049.
Salubrinal是有效的选择性真核翻译起始因子2α（eIF2α）去磷酸化抑制剂[1]。Salubrinal可作为双特异性磷酸酶2（Dusp2）抑制剂，抑制抗胶原蛋白抗体诱导的关节炎[2]。Salubrinal具有抗HSV-1病毒的活性，并抑制由HSV-1蛋白 ICP34.5介导的eIF2α的去磷酸化[3]。
在体外，Salubrinal（0-20μM）处理人类皮肤成纤维细胞1h，以剂量依赖性方式保护了细胞免受UVB辐射引起的细胞死亡，维持细胞内Ca2+稳态[4]。Salubrinal（1、2、5μM）处理小鼠中分离的骨髓源性细胞6天，以剂量和时间依赖性方式抑制了破骨细胞分化，抑制了前破骨细胞的迁移和粘附[5]。
在体内，Salubrinal（1mg/kg/day）通过腹腔注射治疗创伤性脑损伤（TBI）小鼠20天，有效降低了TBI诱导的质膜通透性，减少了病变体积并改善神经功能缺损，降低了ER应激自噬激活[6]。Salubrinal（1mg/kg）通过腹膜内注射治疗急性心肌梗死（MI）大鼠30min，增加了心肌细胞eIF2α磷酸化，减少了caspase-12和C/EBP同源蛋白（CHOP）的表达，减少了心肌细胞凋亡和梗死面积[7]。
| Cell experiment [1]: | |
Cell lines | Human skin fibroblasts |
Preparation Method | Human skin fibroblasts were pretreated with 0-20μM Salubrinal for 1h and then irradiated with UVB (15mJ/cm2). Cell viability was determined by MTT. |
Reaction Conditions | 0-20μM; 1h |
Applications | Salubrinal protects human skin fibroblasts against UVB radiation-induced cell death in a dose dependent manner. |
| Animal experiment [2]: | |
Animal models | Adult male ICR mice |
Preparation Method | Mice were subjected to Traumatic brain injury (TBI) in the left part of the brain using a weightdrop controlled cortical impact device. After injury, the scalp was sutured and mice returned to their cages to recover from anesthesia. After TBI, mice were sacrificed 6 h, 1 d, 2 d, 3 d, 7 d, 10 d and 14 d after surgery, and control mice were sacrificed on day 2. The groups of this experiment were as follows: vehicle-treated sham group (Sha+Veh), Salubrinal-treated sham group (Sha+Sal), vehicletreated TBI group (TBI+Veh) and Salubrinal-treated TBI group (TBI+Sal). Salubrinal (1mg/kg, first solubilized in DMSO to 100mg/kg and then in saline to the final concentration) was administered by intraperitoneal injection 2h after the onset of TBI and subsequent daily dose for 2 or 21d after TBI. Solvent control mice received a vehicle injection (1% DMSO in saline) at the same time points after TBI. Sham animals also received vehicle or Salubirnal. |
Dosage form | 1mg/kg/day for 20 days; i.p. |
Applications | Salubrinal ameliorated neurological deficits after TBI. Salubrinal reduced lesion volume after TBI. Salubrinal decreased TBI-induced ER stress-autophagic activation. |
References: [1]Ji C, Yang B, Huang S, et al. Salubrinal protects human skin fibroblasts against UVB-induced cell death by blocking endoplasmic reticulum (ER) stress and regulating calcium homeostasis[J]. Biochemical and biophysical research communications, 2017, 493(4): 1371-1376. [2]Wang Z, Gao C, Chen W, et al. Salubrinal offers neuroprotection through suppressing endoplasmic reticulum stress, autophagy and apoptosis in a mouse traumatic brain injury model[J]. Neurobiology of learning and memory, 2019, 161: 12-25. | |
| Cas No. | 405060-95-9 | SDF | |
| 化学名 | (E)-3-phenyl-N-[2,2,2-trichloro-1-(quinolin-8-ylcarbamothioylamino)ethyl]prop-2-enamide | ||
| Canonical SMILES | C1=CC=C(C=C1)C=CC(=O)NC(C(Cl)(Cl)Cl)NC(=S)NC2=CC=CC3=C2N=CC=C3 | ||
| 分子式 | C21H17Cl3N4OS | 分子量 | 479.81 |
| 溶解度 | ≥ 48mg/mL in DMSO | 储存条件 | 4°C, protect from light |
| 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 | 2.0842 mL | 10.4208 mL | 20.8416 mL |
| 5 mM | 0.4168 mL | 2.0842 mL | 4.1683 mL |
| 10 mM | 0.2084 mL | 1.0421 mL | 2.0842 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。
Quality Control & SDS
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- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet