TG 100572CAS# 867334-05-2 |
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Quality Control & MSDS
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| Cas No. | 867334-05-2 | SDF | Download SDF |
| PubChem ID | 11712625 | Appearance | Powder |
| Formula | C26H26ClN5O2 | M.Wt | 475.97 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 150 mg/mL (315.15 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 4-chloro-3-[5-methyl-3-[4-(2-pyrrolidin-1-ylethoxy)anilino]-1,2,4-benzotriazin-7-yl]phenol | ||
| SMILES | CC1=C2C(=CC(=C1)C3=C(C=CC(=C3)O)Cl)N=NC(=N2)NC4=CC=C(C=C4)OCCN5CCCC5 | ||
| Standard InChIKey | AQSSMEORRLJZLU-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C26H26ClN5O2/c1-17-14-18(22-16-20(33)6-9-23(22)27)15-24-25(17)29-26(31-30-24)28-19-4-7-21(8-5-19)34-13-12-32-10-2-3-11-32/h4-9,14-16,33H,2-3,10-13H2,1H3,(H,28,29,31) | ||
| 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 | TG 100572 is a multi-targeted kinase inhibitor which inhibits receptor tyrosine kinases and Src kinases; has IC50s of 2, 7, 2, 16, 13, 5, 0.5, 6, 0.1, 0.4, 1, 0.2 nM for VEGFR1, VEGFR2, FGFR1, FGFR2, PDGFRβ, Fgr, Fyn, Hck, Lck, Lyn, Src, Yes, respectively.In Vitro:TG 100572 shows sub-nanomolar activity against the Src family as well as RTK such as VEGFR1 and R2, FGFR1 and R2, and PDGFRβ. TG 100572 inhibits vascular endothelial cell proliferation (ED50=610±71 nM) and blocks VEGF-induced phosphorylation of extracellular signal-regulated kinase. TG 100572 induces apoptosis in rapidly proliferating, but not quiescent, endothelial cell cultures[1]. TG 100572 is shown to inhibit hRMVEC cell proliferation, with an IC50 of 610±72 nM. This suggests that TG 100572 has the therapeutic potential to inhibit VEGF function in ocular endothelial cells, a contributing factor to pathological angiogenesis in diseases such as AMD and PDR[2].In Vivo:Systemic delivery of TG 100572 in a murine model of laser-induced choroidal neovascularization (CNV) causes significant suppression of CNV, but with an associated weight loss suggestive of systemic toxicity[1]. A concentration of 23.4 µM (Cmax) of TG 100572 is reached in 30 min (Tmax)=0.5 h) in the choroid and the sclera. However, the levels of TG 100572 in the retina are relatively low. The half-life of TG 100572 in ocular tissues is very short; hence, the compound is administered topically minimum t.i.d. to maintain appropriate drug levels in the eye. The maximum concentration one can achieve in formulations using TG 100572 is 0.7% w/v[2]. References: | |||||
TG 100572 Dilution Calculator
TG 100572 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.101 mL | 10.5049 mL | 21.0097 mL | 42.0195 mL | 52.5243 mL |
| 5 mM | 0.4202 mL | 2.101 mL | 4.2019 mL | 8.4039 mL | 10.5049 mL |
| 10 mM | 0.2101 mL | 1.0505 mL | 2.101 mL | 4.2019 mL | 5.2524 mL |
| 50 mM | 0.042 mL | 0.2101 mL | 0.4202 mL | 0.8404 mL | 1.0505 mL |
| 100 mM | 0.021 mL | 0.105 mL | 0.2101 mL | 0.4202 mL | 0.5252 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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TG 100572 is VEGFR2/Src kinase inhibitor and anti-inflammatory agent.
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Effects of CETP inhibition with anacetrapib on metabolism of VLDL-TG and plasma apolipoproteins C-II, C-III, and E.[Pubmed:28314859]
J Lipid Res. 2017 Jun;58(6):1214-1220.
Cholesteryl ester transfer protein (CETP) mediates the transfer of HDL cholesteryl esters for triglyceride (TG) in VLDL/LDL. CETP inhibition, with anacetrapib, increases HDL-cholesterol, reduces LDL-cholesterol, and lowers TG levels. This study describes the mechanisms responsible for TG lowering by examining the kinetics of VLDL-TG, apoC-II, apoC-III, and apoE. Mildly hypercholesterolemic subjects were randomized to either placebo (N = 10) or atorvastatin 20 mg/qd (N = 29) for 4 weeks (period 1) followed by 8 weeks of anacetrapib, 100 mg/qd (period 2). Following each period, subjects underwent stable isotope metabolic studies to determine the fractional catabolic rates (FCRs) and production rates (PRs) of VLDL-TG and plasma apoC-II, apoC-III, and apoE. Anacetrapib reduced the VLDL-TG pool on a statin background due to an increased VLDL-TG FCR (29%; P = 0.002). Despite an increased VLDL-TG FCR following anacetrapib monotherapy (41%; P = 0.11), the VLDL-TG pool was unchanged due to an increase in the VLDL-TG PR (39%; P = 0.014). apoC-II, apoC-III, and apoE pool sizes increased following anacetrapib; however, the mechanisms responsible for these changes differed by treatment group. Anacetrapib increased the VLDL-TG FCR by enhancing the lipolytic potential of VLDL, which lowered the VLDL-TG pool on atorvastatin background. There was no change in the VLDL-TG pool in subjects treated with anacetrapib monotherapy due to an accompanying increase in the VLDL-TG PR.
Does fragility of glass formation determine the strength of Tg-nanoconfinement effects?[Pubmed:28298103]
J Chem Phys. 2017 Mar 14;146(10):104902.
Nanoscale confinement has been shown to alter the glass transition and associated mechanical and transport properties of glass-forming materials. Inspired by expected interrelations between nanoconfinement effects, cooperative dynamics in supercooled liquids, and the "fragility" (or temperature-abruptness) of the glass transition, it is commonly expected that nanoconfinement effects on Tg should be more pronounced for more fragile glass formers. Here we employ molecular dynamics simulations of glass formation in the bulk and under nanoconfinement of model polymers in which we systematically tune fragility by several routes. Results indicate that a correlation between fragility and the strength of nanoconfinement effects is weak to modest at best when considering all systems but can appear to be stronger when considering a subset of systems. This outcome is consistent with a reanalysis of the Adam-Gibbs theory of glass formation indicating that fragility does not necessarily track in a universal way with the scale of cooperative motion in glass-forming liquids. Finally, we find that factors such as composition gradients or variability in measurement sensitivity to different parts of the dynamic gradient have the potential to significantly confound efforts to identify trends in Tg-nanoconfinement effects with variables such as fragility, emphasizing the importance of employing diverse data sets and multiple metrologies in the study of this problem.
The predictive value of baseline LDL-TG level on major adverse cardiovascular events in a followed up cohort population.[Pubmed:28338187]
Eur Rev Med Pharmacol Sci. 2017 Mar;21(5):1060-1064.
OBJECTIVE: We aimed at identifying the predictive roles of Low-Density Lipoprotein Triglycerides (LDL-TG) for major adverse cardiovascular events (MACEs). PATIENTS AND METHODS: A longitudinal study in a routine health check-up population was performed with an average follow-up of 4.8 years. The participants involved in this study were 1680, from 2007 to 2009, and all had followed-up for all-cause mortality, cardiovascular disease mortality, and the development of MACEs. The demographic information and anthropometric parameters at baseline were recorded. The baseline and follow-up conventional lipid parameters were measured. We also examined the level LDL-TG, as well as the relationship between its level and MACEs. RESULTS: MACEs individuals were characterized by statistically higher baseline LDL-TG (17.22 +/- 8.05 vs. 16.39 +/-7.35 nmol/l, p = 0.017). The univariate regression for MACEs group indicated that the LDL-TG (b = 0.813, HR = 2.254, 95% CI: 1.454-3.494, p < 0.001), older age, sex and other factors were a significant risk for MACEs. Furthermore, in the adjusted Cox model showed that only higher baseline LDL-TG (b =0.512, HR = 1.669, 95% CI: 1.013-2.748, p = 0.044) and older age (b = 0.062, HR = 1.064, 95% CI: 1.034-1.094, p < 0.001, Table IV) were still predictors for MACEs. CONCLUSIONS: Higher baseline LDL-TG closely associated with MACEs and it is a moderate and independent predictive factor for MACEs.
Iodinated TG in Thyroid Follicular Lumen Regulates TTF-1 and PAX8 Expression via TSH/TSHR Signaling Pathway.[Pubmed:28322461]
J Cell Biochem. 2017 Oct;118(10):3444-3451.
Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the follicular lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid follicular lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. (c) 2017 Wiley Periodicals, Inc.
