[CAS NO. 345630-40-2] SF1670
PRODUCTS SPECIFICATIONS [345630-40-2]
DESCRIPTION [345630-40-2]
Overview
| MDL | MFCD06411448 |
|---|---|
| Molecular Weight | 307.34 |
| Molecular Formula | C19H17NO3 |
| SMILES | CC(C)(C)C(NC(C=C1C2=O)=CC=C1C3=C(C2=O)C=CC=C3)=O |
13 Publications Citing Use of MCE
- [1]Autophagy. 2021 Mar 22.
- [2]Oncogene. 2020 Feb;39(8):1739-1755.
- [3]Cell Death Dis. 2020 Aug 3;11(8):646.
- [4]Cell Death Dis. 2019 Mar 13;10(3):248.
- [5]Biochem Pharmacol. 2020 Jan;171:113674.
- [6]Front Pharmacol. 2022 May 16;13:848957.
- [7]Exp Cell Res. 2021 Oct 6;112864.
- [8]Eur Rev Med Pharmacol Sci. 2019 Apr;23(7):3080-3087.
- [9]Mol Med Rep. 2021 Nov;24(5):766.
- [10]Mol Med Rep. 2018 Jul;18(1):349-357.
- [11]Int J Clin Exp Med. 2019;12(7):8992-8998.
- [12]Int J Clin Exp Med. 2019;12(7):8739-8745.
- [13]Materials Express. 1045-1050, 2021.
Summary
SF1670 is a potent and specific phosphatase and tensin homolog deleted on chromosome 10 ( PTEN ) inhibitor [1] .
IC50 & Target
PTEN [1]
In Vitro
SF1670 is a specific PTEN inhibitor with prolonged intracellular retention in neutrophils. SF1670 enhances PtdIns(3,4,5)P3 signaling in transplanted neutrophils. SF1670 also elevates Akt phosphorylation in murine cells. Consistent with the enhanced Akt phosphorylation, pretreatment with SF1670 also significantly augments PtdIns(3,4,5)P3 level in mouse neutrophils. SF1670-induced Akt hyperactivation is abolished in PTEN-null neutrophils, further demonstrating that this effect is mediated by specific inhibition of PTEN activity. At 500 nM fMLP stimulation, SF1670 (500 nM)–pretreated neutrophils show nearly 70% higher (maximal) superoxide production than untreated neutrophils [1] . HCT116 cells are pre-treated with the PTEN inhibitor SF1670 (2 μM) for 24 h (untreated HCT116 cells served as control); treated cells are subsequently plated under non-adherent conditions with added MET (60 μM), Lun (2 μM), or Gen (2 μM). SF1670 binds to the PTEN active site, resulting in elevated phosphatidylinositol (3,4,5) triphosphate signaling [2] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
SF1670 (3 mg/kg; i.p.) triggers postconditioning after inducing cerebral global ischaemia (17 min) and reperfusion (24 h)‐induced injury via occlusion of both carotid arteries in mice [1] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: | Swiss albino male mice (bodyweight 25-30 g) [1] |
| Dosage: | 3 mg/kg |
| Administration: | Treatment with i.p. |
| Result: | Lead to attenuation of cerebral I/R-induced increase in thiobarbituric acid reactive substances (TBARS). |
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : ≥ 50 mg/mL ( 162.69 mM )
* "≥" means soluble, but saturation unknown.
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 3.2537 mL | 16.2686 mL | 32.5373 mL |
| 5 mM | 0.6507 mL | 3.2537 mL | 6.5075 mL |
| 10 mM | 0.3254 mL | 1.6269 mL | 3.2537 mL |
-
1.
Add each solvent one by one: 10% DMSO >> 90% corn oil
Solubility: ≥ 2.5 mg/mL (8.13 mM); Clear solution
References
- [1] Li Y, et al. Pretreatment with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor SF1670augments the efficacy of granulocyte transfusion in a clinically relevant mouse model. Blood. 2011 Jun 16;117(24):6702-13.
- [2] Montales MT, et al. Metformin and soybean-derived bioactive molecules attenuate the expansion of stem cell-like epithelial subpopulation and confer apoptotic sensitivity in human colon cancer cells. Genes Nutr. 2015 Nov;10(6):49.
- [3] Amarjot Kaur Grewal, et al. Neuroprotective effect of pharmacological postconditioning on cerebral ischaemia-reperfusion-induced injury in mice. J Pharm Pharmacol. 2019 Jun;71(6):956-970.