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SB 706504

CAS# 911110-38-8

SB 706504

Catalog No. BCC5615----Order now to get a substantial discount!

Product Name & Size Price Stock
SB 706504:10mg $242.00 In stock
SB 706504:20mg $411.00 In stock
SB 706504:50mg $968.00 In stock
SB 706504:100mg $1694.00 In stock
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Chemical structure

SB 706504

3D structure

Chemical Properties of SB 706504

Cas No. 911110-38-8 SDF Download SDF
PubChem ID 11853799 Appearance Powder
Formula C24H19F3N8O M.Wt 492.46
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO
Chemical Name 1-cyano-2-[2-[[8-(2,6-difluorophenyl)-4-(4-fluoro-2-methylphenyl)-7-oxopyrido[2,3-d]pyrimidin-2-yl]amino]ethyl]guanidine
SMILES CC1=C(C=CC(=C1)F)C2=C3C=CC(=O)N(C3=NC(=N2)NCCN=C(N)NC#N)C4=C(C=CC=C4F)F
Standard InChIKey ZQFBVJBAWLZLOM-UHFFFAOYSA-N
Standard InChI InChI=1S/C24H19F3N8O/c1-13-11-14(25)5-6-15(13)20-16-7-8-19(36)35(21-17(26)3-2-4-18(21)27)22(16)34-24(33-20)31-10-9-30-23(29)32-12-28/h2-8,11H,9-10H2,1H3,(H3,29,30,32)(H,31,33,34)
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.
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.
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.

Biological Activity of SB 706504

Descriptionp38 MAPK inhibitor. Inhibits LPS-induced transcription of a range of chemokines and cytokines in chronic obstructive pulmonary disease (COPD) monocyte derived macrophages (MDMs). Also inhibits LPS-induced protein expression of IL-6, IL-10, TNFα and γ-inducible protein 10 in COPD MDMs. Effects on suppression of LPS-induced gene and protein expression are enhanced in combination with dexamethasone.

SB 706504 Dilution Calculator

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Preparing Stock Solutions of SB 706504

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.0306 mL 10.1531 mL 20.3062 mL 40.6124 mL 50.7655 mL
5 mM 0.4061 mL 2.0306 mL 4.0612 mL 8.1225 mL 10.1531 mL
10 mM 0.2031 mL 1.0153 mL 2.0306 mL 4.0612 mL 5.0766 mL
50 mM 0.0406 mL 0.2031 mL 0.4061 mL 0.8122 mL 1.0153 mL
100 mM 0.0203 mL 0.1015 mL 0.2031 mL 0.4061 mL 0.5077 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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References on SB 706504

The effect of Sb-surfactant on GaInP CuPtB type ordering: assessment through dark field TEM and aberration corrected HAADF imaging.[Pubmed:28367549]

Phys Chem Chem Phys. 2017 Apr 12;19(15):9806-9810.

We report on the effect of Sb on the microstructure of GaInP layers grown by metal organic vapor phase epitaxy (MOVPE). These layers exhibit a CuPtB single variant ordering due to the intentional misorientation of the substrate (Ge(001) substrates with 6 degrees misorientation towards the nearest [111] axis). The use of Sb as a surfactant during the GaInP growth does not modify the type of ordering, but it is found that the order parameter (eta) decreases with increasing Sb flux. Dark field microscopy reveals a variation of the angle of the antiphase boundaries (APBs) with Sb amount. The microstructure is assessed through high angle annular dark field (HAADF) experiments and image simulation revealing Z-contrast loss in APBs due to the superposition of ordered domains.

Direct nucleation, morphology and compositional tuning of InAs1-x Sb x nanowires on InAs (111) B substrates.[Pubmed:28346221]

Nanotechnology. 2017 Apr 21;28(16):165601.

III-V ternary nanowires are interesting due to the possibility of modulating their physical and material properties by tuning their material composition. Amongst them InAs1-x Sb x nanowires are good candidates for applications such as Infrared detectors. However, this material has not been grown directly from substrates, in a large range of material compositions. Since the properties of ternaries are alterable by tuning their composition, it is beneficial to gain access to a wide range of composition tunability. Here we demonstrate direct nucleation and growth of InAs1-x Sb x nanowires from Au seed particles over a broad range of compositions (x = 0.08-0.75) for different diameters and surface densities by means of metalorganic vapor phase epitaxy. We investigate how the nucleation, morphology, solid phase Sb content, and growth rate of these nanowires depend on the particle dimensions, and on growth conditions such as the vapor phase composition, V/III ratio, and temperature. We show that the solid phase Sb content of the nanowires remains invariant towards changes of the In precursor flow. We also discuss that at relatively high In flows the growth mechanism alters from Au-seeded to what is referred to as semi In-seeded growth. This change enables growth of nanowires with a high solid phase Sb content of 0.75 that are not feasible via Au-seeded growth. Independent of the growth conditions and morphology, we report that the nanowire Sb content changes over their length, from lower Sb contents at the base, increasing to higher amounts towards the tip. We correlate the axial Sb content variations to the axial growth rate measured in situ. We also report spontaneous core-shell formation for Au-seeded nanowires, where the core is Sb-rich in comparison to the Sb-poor shell.

Differing Mechanisms of Death Induction by Fluorinated Taxane SB-T-12854 in Breast Cancer Cells.[Pubmed:28373418]

Anticancer Res. 2017 Apr;37(4):1581-1590.

BACKGROUND/AIM: Classical taxanes are routinely used in cancer therapy. In this study, mechanisms involved in death induction by the novel fluorine-containing taxane SB-T-12854 were investigated. MATERIALS AND METHODS: We employed breast cancer SK-BR-3, MCF-7 and T47D cell lines to assess activation of individual caspases, changes in the expression of proteins of the Bcl-2 family, and the release of pro-apoptotic factors from mitochondria into the cytosol after SB-T-12854 treatment. RESULTS: Caspase-2, -8, and -9 were activated in SK-BR-3 and MCF-7 cells. Only caspase-8 was activated in T47D cells. Caspase-7 and -6 were activated in all tested cells while caspase-3 was activated only in SK-BR-3 cells. Pro-apoptotic Bad protein seems to be important for cell death induction in all tested cells. Anti-apoptotic Bcl-2 and pro-apoptotic Bim, Bok, Bid and Bik seem to be also associated with cell death induction in some of the tested cells. The mitochondrial apoptotic pathway was significantly activated in association with the release of cytochrome c and Smac from mitochondria, but only in SK-BR-3 cells, not in MCF-7 and T47D cells. CONCLUSION: Cell death induced by SB-T-12854, in the tested breast cancer cells, differs regarding activation of caspases, changes in levels of pro-apoptotic and anti-apoptotic proteins of the Bcl-2 family and activation of the mitochondrial apoptotic pathway.

Critical evaluation of strategies for single and simultaneous determinations of As, Bi, Sb and Se by hydride generation inductively coupled plasma optical emission spectrometry.[Pubmed:28340714]

Talanta. 2017 May 15;167:217-226.

A systematic study of hydride generation (HG) of As, Bi, Sb and Se from solutions containing As(III), As(V), Bi(III), Sb(III), Sb(V), Se(IV) and Se(VI) was presented. Hydrides were generated in a gas-liquid phase separation system using a continuous flow vapor generation accessory (VGA) by mixing acidified aqueous sample, HCl and sodium borohydride reductant (NaBH4) solutions on-line. For detection, a simultaneous axially viewed inductively coupled plasma optical emission spectrometer (ICP-OES) was applied. Effects of the HCl concentration (related to sample and additional acid solutions) and type of the pre-reducing agents used for reduction of As(V), Sb(V) and Se(VI) into As(III), Sb(III) and Se(IV) on the analytical responses of As, Bi, Sb and Se were studied and discussed. Two compromised HG reaction conditions for simultaneous measurements of As+Bi+Sb (CC1) or As+Sb+Se (CC2) were established. It was found that choice of the pre-reductant prior to formation of the hydrides is critical in obtaining the dependable results of the analysis. Accordingly, for a As(III)+As(V)+Bi(III)+Sb(III)+Sb(V) mixture and using CC1, thiourea/thiourea-ascorbic acid interfered in Bi determination and hence, total As+Sb could be measured. If L-cysteine/L-cysteine-ascorbic acid were used, measurements of total Bi+Sb was possible in these HG reaction conditions. For a As(III)+As(V)+Sb(III)+Sb(V)+Se(IV)+Se(VI) mixture and using CC2, thiourea/thiourea-ascorbic acid and L-cysteine/L-cysteine-ascorbic acid influenced HG of Se but ensured total As+Sb determination. In contrast, heating a sample solution with HCl, although did not pre-reduce As(V) and Sb(V), assured quantitative reduction of Se(VI) to Se(IV). Finally, considering all favorable pre-reducing and HG conditions, methodologies for reliable determination of total As, Bi, Sb and Se by HG-ICP-OES were proposed. Strategies for single-, two- and three-element measurements were evaluated and validated, obtaining the detection limits (DLs) below 0.1ngg(-1) and precision typically in the range of 1.4-3.9% RSD.

Inhibition of lipopolysaccharide-stimulated chronic obstructive pulmonary disease macrophage inflammatory gene expression by dexamethasone and the p38 mitogen-activated protein kinase inhibitor N-cyano-N'-(2-{[8-(2,6-difluorophenyl)-4-(4-fluoro-2-methylphenyl)-7-oxo-7,8-dihy dropyrido[2,3-d] pyrimidin-2-yl]amino}ethyl)guanidine (SB706504).[Pubmed:19004925]

J Pharmacol Exp Ther. 2009 Feb;328(2):458-68.

p38 mitogen-activated protein kinase (MAPK) signaling is known to be increased in chronic obstructive pulmonary disease (COPD) macrophages. We have studied the effects of the p38 MAPK inhibitor N-cyano-N'-(2-{[8-(2,6-difluorophenyl)-4-(4-fluoro-2-methylphenyl)-7-oxo-7,8-dihy dropyrido[2,3-d]-pyrimidin-2-yl]amino}ethyl)guanidine (SB706504) and dexamethasone on COPD macrophage inflammatory gene expression and protein secretion. We also studied the effects of combined SB706504 and dexamethasone treatment. Lipopolysaccharide (LPS)-stimulated monocyte derived macrophages (MDMs) and alveolar macrophages (AMs) were cultured with dexamethasone and/or SB706504. MDMs were used for gene array and protein studies, whereas tumor necrosis factor (TNF) alpha protein production was measured from AMs. SB706504 caused transcriptional inhibition of a range of cytokines and chemokines in COPD MDMs. The use of SB706504 combined with dexamethasone caused greater suppression of gene expression (-8.90) compared with SB706504 alone (-2.04) or dexamethasone (-3.39). Twenty-three genes were insensitive to the effects of both drugs, including interleukin (IL)-1beta, IL-18, and chemokine (CC motif) ligand (CCL) 5. In addition, the chromosome 4 chemokine cluster members, CXCL1, CXCL2, CXCL3, and CXCL8, were all glucocorticoid-resistant. SB706504 significantly inhibited LPS-stimulated TNFalpha production from COPD and smoker AMs, with near-maximal suppression caused by combination treatment with dexamethasone. We conclude that SB706504 targets a subset of inflammatory macrophage genes and when used with dexamethasone causes effective suppression of these genes. SB706504 and dexamethasone had no effect on the transcription of a subset of LPS-regulated genes, including IL-1beta, IL-18, and CCL5, which are all known to be involved in the pathogenesis of COPD.

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