WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 530967
CAS#: 1164470-53-4
Description: SAL-003 is a cell-permeable inhibitor of eIF2α dephosphorylation. SAL003 is an Analog of salubrinal (Cat. No. 2347) with improved aqueous solubility. Sal003‑mediated upregulation of eIF2α phosphorylation suppressed cisplatin‑induced p53 activation. Furthermore, reduction of eIF2α phosphorylation by PERK knockdown enhanced cisplatin-induced p53 activation and apoptosis.
MedKoo Cat#: 530967
Name: SAL003
CAS#: 1164470-53-4
Chemical Formula: C18H15Cl4N3OS
Exact Mass: 460.969
Molecular Weight: 463.198
Elemental Analysis: C, 46.68; H, 3.26; Cl, 30.61; N, 9.07; O, 3.45; S, 6.92
Synonym: SAL-003; SAL 003; SAL003.
IUPAC/Chemical Name: 3--Phenyl-N-(2,2,2-trichloro-1-((((4-chlorophenyl)amino)carbonothioyl)amino)ethyl)acrylamide
InChi Key: TVNBASWNLOIQML-IZZDOVSWSA-N
InChi Code: InChI=1S/C18H15Cl4N3OS/c19-13-7-9-14(10-8-13)23-17(27)25-16(18(20,21)22)24-15(26)11-6-12-4-2-1-3-5-12/h1-11,16H,(H,24,26)(H2,23,25,27)/b11-6+
SMILES Code: O=C(NC(NC(NC1=CC=C(Cl)C=C1)=S)C(Cl)(Cl)Cl)/C=C/C2=CC=CC=C2
Appearance: Solid powder
Purity: >98% (or refer to the Certificate of Analysis)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility: Soluble in DMSO
Shelf Life: >2 years if stored properly
Drug Formulation: This drug may be formulated in DMSO
Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code: 2934.99.9001
The following data is based on the product molecular weight 463.198 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
| Concentration / Solvent Volume / Mass | 1 mg | 5 mg | 10 mg |
|---|---|---|---|
| 1 mM | 1.15 mL | 5.76 mL | 11.51 mL |
| 5 mM | 0.23 mL | 1.15 mL | 2.3 mL |
| 10 mM | 0.12 mL | 0.58 mL | 1.15 mL |
| 50 mM | 0.02 mL | 0.12 mL | 0.23 mL |
1: Ju SM, Jo YS, Jeon YM, Pae HO, Kang DG, Lee HS, Bae JS, Jeon BH.
Phosphorylation of eIF2α suppresses cisplatin-induced p53 activation and
apoptosis by attenuating oxidative stress via ATF4-mediated HO-1 expression in
human renal proximal tubular cells. Int J Mol Med. 2017 Oct 10. doi:
10.3892/ijmm.2017.3181. [Epub ahead of print] PubMed PMID: 29039478.
2: 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 Jul 23;34(30):10010-21. doi:
10.1523/JNEUROSCI.0934-14.2014. PubMed PMID: 25057203.
3: Costa-Mattioli M, Gobert D, Stern E, Gamache K, Colina R, Cuello C, Sossin W,
Kaufman R, Pelletier J, Rosenblum K, Krnjević K, Lacaille JC, Nader K, Sonenberg
N. eIF2alpha phosphorylation bidirectionally regulates the switch from short- to
long-term synaptic plasticity and memory. Cell. 2007 Apr 6;129(1):195-206. PubMed
PMID: 17418795; PubMed Central PMCID: PMC4149214.
4: Yahiro K, Tsutsuki H, Ogura K, Nagasawa S, Moss J, Noda M. Regulation of
subtilase cytotoxin-induced cell death by an RNA-dependent protein kinase-like
endoplasmic reticulum kinase-dependent proteasome pathway in HeLa cells. Infect
Immun. 2012 May;80(5):1803-14. doi: 10.1128/IAI.06164-11. Epub 2012 Feb 21.
PubMed PMID: 22354021; PubMed Central PMCID: PMC3347452.
Cisplatin is one of the most widely used chemotherapeutic agents for the treatment of human cancers. However, the nephrotoxicity of cisplatin limits its use as a therapeutic agent. It has been suggested that oxidative stress and p53 activation play important roles in cisplatin-induced nephrotoxicity. It has been demonstrated that the eukaryotic translation initiation factor 2α (eIF2α) may protect HK-2 human renal proximal tubular cells against cisplatin-induced apoptosis through inhibition of reactive oxygen species (ROS)‑mediated p53 activation.
