2-Amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiolCAS# 162359-55-9 |
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Cas No. | 162359-55-9 | SDF | Download SDF |
PubChem ID | 107970 | Appearance | Powder |
Formula | C19H33NO2 | M.Wt | 307.47 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Synonyms | FTY720 free base | ||
Solubility | DMSO : 66.67 mg/mL (216.83 mM; Need ultrasonic) Methanol : 30 mg/mL (97.57 mM; Need ultrasonic) Ethanol : 7.69 mg/mL (25.01 mM; Need ultrasonic) | ||
Chemical Name | 2-amino-2-[2-(4-octylphenyl)ethyl]propane-1,3-diol | ||
SMILES | CCCCCCCCC1=CC=C(C=C1)CCC(CO)(CO)N | ||
Standard InChIKey | KKGQTZUTZRNORY-UHFFFAOYSA-N | ||
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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | 1. 2-Amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiol analogs to significantly decrease pulmonary vascular leakage and inflammation in vitro and in vivo. 2. 2-Amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiol significantly reduces multiple indices of alveolar and vascular permeability in a lipopolysaccharide-mediated murine model of ALI. |
Targets | Immunology & Inflammation related |
2-Amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiol Dilution Calculator
2-Amino-2-[2-(4-octylphenyl)ethyl]-1,3-propandiol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.2523 mL | 16.2617 mL | 32.5235 mL | 65.047 mL | 81.3087 mL |
5 mM | 0.6505 mL | 3.2523 mL | 6.5047 mL | 13.0094 mL | 16.2617 mL |
10 mM | 0.3252 mL | 1.6262 mL | 3.2523 mL | 6.5047 mL | 8.1309 mL |
50 mM | 0.065 mL | 0.3252 mL | 0.6505 mL | 1.3009 mL | 1.6262 mL |
100 mM | 0.0325 mL | 0.1626 mL | 0.3252 mL | 0.6505 mL | 0.8131 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Fingolimod is a sphingosine 1-phosphate (S1P) antagonist with IC50 of 0.033 nM in K562 and NK cells.
In Vitro:The monocyte-derived immature dendritic cells (iDCs) are pretreated with various concentrations of S1P for various periods of time prior to their incubation with NK cells. Four hours incubation of autologous or allogeneic iDCs with 0.2-20 μM of S1P significantly protectes these cells from NK cell lysis. The IC50 values of S1P are calculated at 160 nM for autologous iDCs, and 34 nM for allogeneic iDCs. Next, the inhibitory effect of S1P is revered by various concentrations of Fingolimod or SEW2871, with an IC50 effect of 173 or 15 nM, respectively[1]. Fingolimod has been reported to reduce LPA synthesis via inhibition of the lysophospholipase autotaxin. Fingolimod treatment correlates with a significant elevation of axonal cAMP, a crucial factor for axonal outgrowth. Additionally, Fingolimod significantly reduces LPA levels in the injured nerve. PF-8380 treatment correlates with improved myelin thickness[2].
In Vivo:Fingolimod treatment results in significantly increased nerve conduction at 14 days post-crush in wildtype C57BL/6 mice. However, Foxn1-/- mice, which are devoid of T- but not B-lymphocytes, show an improvement of nerve regeneration under fingolimod treatment. Although the mean increase in nerve conduction velocity in both fingolimod-treated and controlFoxn1-/- mice implies a potentially positive role of T-lymphocyte deficiency on nerve regeneration, only fingolimod-treated Foxn1-/- mice show a significant improvement compared to C57BL/6 controls and performed better in the functional analysis[2]. Treatment of the animals with Fingolimod for 28 d results in a clear reduction in the binding of 18F-GE180 when compare with vehicle-treated animals and evaluated by ex vivo autoradiography. Quantification of the binding of the radiotracer revealed a significant reduction in the binding potential of 18F-GE180 (P<0.0001) after treatment with Fingolimod[3].
References:
[1]. Rolin J, et al. FTY720 and SEW2871 reverse the inhibitory effect of S1P on natural killer cell mediated lysis of K562 tumor cells and dendritic cells but not on cytokine release. Cancer Immunol Immunother. 2010, 59(4), 575-586.
[2]. Szepanowski F, et al. Fingolimod promotes peripheral nerve regeneration via modulation of lysophospholipid signaling. J Neuroinflammation. 2016 Jun 10;13(1):143.
[3]. Airas L, et al. In vivo PET imaging demonstrates diminished microglial activation after fingolimod treatment in an animal model of multiple sclerosis. J Nucl Med. 2015 Feb;56(2):305-10.
[4]. Shirakabe K, et al. Modification of lymphocyte migration to Peyer's patches by inhibition of sphingosine-1-phosphate lyase ameliorates murine colitis. J Gastroenterol Hepatol. 2018 Jan 15.
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Synthetic analogs of FTY720 [2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] differentially regulate pulmonary vascular permeability in vivo and in vitro.[Pubmed:19592667]
J Pharmacol Exp Ther. 2009 Oct;331(1):54-64.
Novel therapies are needed to address the vascular endothelial cell (EC) barrier disruption that occurs in inflammatory diseases such as acute lung injury (ALI). We previously demonstrated the potent barrier-enhancing effects of both sphingosine 1-phosphate (S1P) and the structurally similar compound FTY720 [2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol] in inflammatory lung injury. In this study, we examined the therapeutic potential of several novel FTY720 analogs to reduce vascular leak. Similar to S1P and FTY720, the (R)- and (S)-enantiomers of FTY720 phosphonate and enephosphonate analogs produce sustained EC barrier enhancement in vitro, as seen by increases in transendothelial electrical resistance (TER). In contrast, the (R)- and (S)-enantiomers of FTY720-regioisomeric analogs disrupt EC barrier integrity in a dose-dependent manner. Barrier-enhancing FTY720 analogs demonstrate a wider protective concentration range in vitro (1-50 microM) and greater potency than either S1P or FTY720. In contrast to FTY720-induced EC barrier enhancement, S1P and the FTY720 analogs dramatically increase TER within minutes in association with cortical actin ring formation. Unlike S1P, these FTY720 analogs exhibit differential phosphorylation effects without altering the intracellular calcium level. Inhibitor studies indicate that barrier enhancement by these analogs involves signaling via G(i)-coupled receptors, tyrosine kinases, and lipid rafts. Consistent with these in vitro responses, the (S)-phosphonate analog of FTY720 significantly reduces multiple indices of alveolar and vascular permeability in a lipopolysaccharide-mediated murine model of ALI (without significant alterations in leukocyte counts). These results demonstrate the capacity for FTY720 analogs to significantly decrease pulmonary vascular leakage and inflammation in vitro and in vivo.