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Sal 003Cellular phosphatase complex inhibitor

Sal 003

Catalog No. A4541
Size Price Stock Qty
5mg $70.00 In stock
10mg $108.00 In stock
50mg $312.00 In stock

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

Sal 003

Biological Activity

Description Sal 003 is a cell-permeable inhibitor of cellular phosphatase complexes.
Targets eIF2α          
IC50            

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Chemical Properties

Cas No. 1164470-53-4 SDF Download SDF
Chemical Name (E)-3-phenyl-N-[2,2,2-trichloro-1-[(4-chlorophenyl)carbamothioylamino]ethyl]prop-2-enamide
Canonical SMILES C1=CC=C(C=C1)C=CC(=O)NC(C(Cl)(Cl)Cl)NC(=S)NC2=CC=C(C=C2)Cl
Formula C18H15Cl4N3OS M.Wt 463.21
Solubility Soluble in DMSO > 10 mM Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Background

Eukaryotic initiation factor 2 α-subunit (eIF2α) plays a critical role in the regulation of protein synthesis. Moreover, it also plays an important role in synaptic plasticity and long-term memory consolidation. Sal003 is a selective inhibitor of eIF2α dephosphorylation.

In vitro: Sal003 specifically prevents dephosphorylation of eIF2α by blocking eIF2α phosphatases. In Sal003-treated cells polysomes dissociated and consistent with this β-actin mRNA shifted to lighter fractions, reflecting the inhibition of general translation [1].

In vivo: Intra-basolateral amygdala (BLA) infusions of Sal003 immediately after memory retrieval disrupted the reconsolidation of morphine- or cocaine-induced CPP, leading to a long-lasting suppression of drug-paired stimulus-induced craving. Moreover, inhibition of eIF2α dephosphorylation in the BLA immediately after light/tone stimulus retrieval decreased subsequent cue-induced heroin-seeking behavior in the self-administration procedure. These results demonstrate that eIF2α dephosphorylation in the BLA mediates the memory reconsolidation of drug-paired stimuli [1].

Clinical trials: Currenlty no clinical data are available.

Reference:
[1] Jian M, Luo YX, Xue YX, Han Y, Shi HS, Liu JF, Yan W, Wu P, Meng SQ, Deng JH, Shen HW, Shi J, Lu L.   eIF2α dephosphorylation in basolateral amygdala mediates reconsolidation of drug memory. J Neurosci. 2014;34(30):10010-21.