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Salubrinal

Catalog No. T3045 CAS 405060-95-9

Salubrinal, a phosphatases (PP1) inhibitor(IC50=1.7 μM), exhibits function on the eukaryotic translation initiation factor 2 subunit (eIF2α).

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Salubrinal, CAS 405060-95-9

Pack Size	Availability	Price/USD
2 mg	In stock	$ 35.00
5 mg	In stock	$ 56.00
10 mg	In stock	$ 85.00
25 mg	In stock	$ 166.00
50 mg	In stock	$ 288.00
100 mg	In stock	$ 490.00
500 mg	In stock	$ 1,090.00
1 mL * 10 mM (in DMSO)	In stock	$ 62.00

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Purity: 100%

Purity: 99.97%

Purity: 98.25%

Purity: 98.16%

Biological Description

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Description	Salubrinal, a phosphatases (PP1) inhibitor(IC50=1.7 μM), exhibits function on the eukaryotic translation initiation factor 2 subunit (eIF2α).
Targets&IC50	PP1:1.7 μM
In vitro	In a murine model of corneal infection, Salubrinal inhibits HSV replication and lowers viral titers in eye swabs of infected animals. Intraventricular administration of Salubrinal significantly alters the homeostatic sleep response.
In vivo	Salubrinal (EC50=15 μM) inhibits tunicamycin-induced ER stress and subsequent apoptosis in a dose-dependent manner. Additionally, Salubrinal (IC50=3 μM) hampers HSV replication by inhibiting the dephosphorylation of eIF2α. In C12 cells, it downregulates cyclin D1 while upregulating GADD34 and CHOP.
Kinase Assay	Phosphatase activities are determined on immunoprecipitates of the phosphatases. Briefly, 2×106 K562 cells are treated for 18 hr with Salubrinal (20 μM), PSI (10 nM), the combination of both drugs or okadaic acid (100 nM). After washing with PBS, cells are lysed for 15 min on ice either in PP1LB (for determination of PP1γ-activity; 20 mM Tris-HCl, pH 7.5, 1% Triton X-100, 10% glycerol, 132 mM NaCl, Roche complete protease inhibitor ) or in RIPA (for PP2A), supplemented with Roche complete protease inhibitor). Cell lysates containing 500 μg (PP1γ) or 300 μg (PP2A) protein are immunoprecipitated overnight at 4°C with 2-3 μg of the appropriate antibodies and then incubated with Protein A-Sepharose. Immunoprecipitates are washed three times in lysis buffer, followed by resuspension in phosphatase assay buffer (PP2A: 20 mM Tris-HCl, pH7.5, 0.1 mM CaCl2; PP1γ: 50 mM Tris HCl pH 7.0, 0.2 mM MnCl2, 0.1 mM CaCl2, 125 μg/mL BSA, 0.05% Tween 20), supplemented with 100 μM 6,8-difluoro-4-methyl-umbelliferyl phosphate (DiFMUP). Precipitates are allowed to react with substrate for 1 hr at 37°C on an Eppendorf Thermoshaker, centrifuged and DiFMU fluorescence is measured on a BioTek Lambda Fluoro 320 microplate reader (360 nmex/460 nmem). Phosphatase activities are given as percent change relative to the control (DMSO treated cells)[1].
Cell Research	PC12 cells are plated in 384-well plates at 5000 cells per well in 40μL phenol red-freemedium containing 3μg/ml Tm to induce ER stress. 100 nL of the DiverSet E (5 mg/mlin DMSO) or National Cancer Institute's (NCI) Structural Diversity set and Open Collections (10 mM in DMSO) (NCI) are added to the wells by robotic pin transfer. After 48 hours, cell viability is assessed using a luminescence-based ATP assay. DMSO- and zVAD.fmk-treated wells on each plate served as negative and positive controls for rescue from ER stress-induced ATP loss, respectively.(Only for Reference)

Molecular Weight	479.81
Formula	C21H17Cl3N4OS
CAS No.	405060-95-9

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 48 mg/mL (100 mM)

References and Literature

1. Boyce M, et al. Science, 2005, 307(5711), 935-939. 2. Methippara MM, et al. Am J Physiol Regul Integr Comp Physiol, 2009, 296(1), 178-184. 3. Methippara M, Neuroscience, 2012, 209, 108-118. 4. Zhang J, Zhang P, Meng C, et al. The PERK Pathway Plays a Neuroprotective Role During the Early Phase of Secondary Brain Injury Induced by Experimental Intracerebral Hemorrhage[M]//. Subarachnoid Hemorrhage. Springer, Cham, 2020: 105-119. 5. Meng C, Zhang J, Dang B, et al. PERK pathway activation promotes intracerebral hemorrhage induced secondary brain injury by inducing neuronal apoptosis both in vivo and in vitro[J]. Frontiers in neuroscience. 2018 Feb 28;12:111.

Citations

1. Meng C, Zhang J, Dang B, et al. PERK pathway activation promotes intracerebral hemorrhage induced secondary brain injury by inducing neuronal apoptosis both in vivo and in vitro. Frontiers in Neuroscience. 2018 Feb 28;12:111 2. Zhao Y, Feng Y, Ye Q, et al.The oral microbiome in young women at different stages of periodontitis: Prevotella dominant in stage III periodontitis.Frontiers in Cellular and Infection Microbiology.2022 3. Berthier A, Gheeraert C, Johanns M, et al.The Molecular Circadian Clock Is a Target of Anti-cancer Translation Inhibitors.Journal of Biological Rhythms.2023: 07487304231202561.

Related compound libraries

This product is contained In the following compound libraries：

Kinase Inhibitor Library Inhibitor Library Anti-Metabolism Disease Compound Library Phosphatase Inhibitor Library Anti-Infection Compound Library Anti-Aging Compound Library HIF-1 Signaling Pathway Compound Library Metabolism Compound Library Apoptosis Compound Library Bioactive Compound Library

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Keywords

Salubrinal 405060-95-9 Apoptosis Autophagy Metabolism Microbiology/Virology HSV PERK Phosphatase Herpes simplex virus Inhibitor inhibit inhibitor

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