HS-173novel PI3K inhibitor CAS# 1276110-06-5 |
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Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 1276110-06-5 | SDF | Download SDF |
| PubChem ID | 52936849 | Appearance | Powder |
| Formula | C21H18N4O4S | M.Wt | 422.46 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 50 mg/mL (118.35 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
| Chemical Name | ethyl 6-[5-(benzenesulfonamido)pyridin-3-yl]imidazo[1,2-a]pyridine-3-carboxylate | ||
| SMILES | CCOC(=O)C1=CN=C2N1C=C(C=C2)C3=CC(=CN=C3)NS(=O)(=O)C4=CC=CC=C4 | ||
| Standard InChIKey | SEKOTFCHZNXZMM-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C21H18N4O4S/c1-2-29-21(26)19-13-23-20-9-8-15(14-25(19)20)16-10-17(12-22-11-16)24-30(27,28)18-6-4-3-5-7-18/h3-14,24H,2H2,1H3 | ||
| 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 | HS-173 is a potent inhibitor of PI3Kα with IC50 value of 0.8 nM. | |||||
| Targets | PI3Kα | |||||
| IC50 | 0.8 nM | |||||
HS-173 Dilution Calculator
HS-173 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.3671 mL | 11.8354 mL | 23.6709 mL | 47.3418 mL | 59.1772 mL |
| 5 mM | 0.4734 mL | 2.3671 mL | 4.7342 mL | 9.4684 mL | 11.8354 mL |
| 10 mM | 0.2367 mL | 1.1835 mL | 2.3671 mL | 4.7342 mL | 5.9177 mL |
| 50 mM | 0.0473 mL | 0.2367 mL | 0.4734 mL | 0.9468 mL | 1.1835 mL |
| 100 mM | 0.0237 mL | 0.1184 mL | 0.2367 mL | 0.4734 mL | 0.5918 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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Phosphatidylinositol 3-kinase (PI3K) was first identified over 20 years ago as a lipid kinase associated with viral oncoproteins. PI3K signaling pathway regulates various cellular processes such as growth, cell cycle progression, apoptosis, migration, metabolism, and cytoskeleton rearrangement. HS-173 is a novel PI3K inhibitor.
In vitro: HS-173 inhibited the PI3K signaling pathway, and showed anti-proliferative effects on cancer cells. Also, HS-173 induced cell cycle arrest at the G2/M phase and apoptosis. In addition, HS-173 decreased the expression HIF-1a and VEGF which play an important role in angiogenesis. This effect was confirmed by the suppression of tube formation and migration assay in vitro [1].
In vivo: HS-173 diminished blood vessel formation in the Matrigel plug assay in mice. These results suggest that HS-173 has potent anti-angiogenic activity in vivo [1].
Clinical trials: Currenlty no clinical data are available.
Reference:
[1] Lee H, Jung KH, Jeong Y, Hong S, Hong SS. HS-173, a novel phosphatidylinositol 3-kinase (PI3K) inhibitor, has anti-tumor activity through promoting apoptosis and inhibiting angiogenesis. Cancer Lett. 2013 Jan 1;328(1):152-9.
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HS-173, a novel PI3K inhibitor suppresses EMT and metastasis in pancreatic cancer.[Pubmed:27793006]
Oncotarget. 2016 Nov 22;7(47):78029-78047.
Pancreatic cancer is one of the most aggressive solid malignancies prone to metastasis. Epithelial-mesenchymal transition (EMT) contributes to cancer invasiveness and drug resistance. In this study, we investigated whether HS-173, a novel PI3K inhibitor blocked the process of EMT in pancreatic cancer. HS-173 inhibited the growth of pancreatic cancer cells in a dose- and time-dependent manner. Moreover, it significantly suppressed the TGF-beta-induced migration and invasion, as well as reversed TGF-beta-induced mesenchymal cell morphology. Also, HS-173 reduced EMT by increasing epithelial markers and decreasing the mesenchymal markers by blocking the PI3K/AKT/mTOR and Smad2/3 signaling pathways in pancreatic cancer cells. In addition, HS-173 clearly suppressed tumor growth without drug toxicity in both xenograft and orthotopic mouse models. Furthermore, to explore the anti-metastatic effect of HS-173, we established pancreatic cancer metastatic mouse models and found that it significantly inhibited metastatic dissemination of the primary tumor to liver and lung. Taken together, our findings demonstrate that HS-173 can efficiently suppress EMT and metastasis by inhibiting PI3K/AKT/mTOR and Smad2/3 signaling pathways, suggesting it can be a potential candidate for the treatment of advanced stage pancreatic cancer.
HS-173, a novel PI3K inhibitor, attenuates the activation of hepatic stellate cells in liver fibrosis.[Pubmed:24326778]
Sci Rep. 2013 Dec 11;3:3470.
Hepatic stellate cells (HSCs) are the primary source of matrix components in liver disease such as fibrosis. Phosphatidylinositol 3-kinase (PI3K) signaling in HSCs has been shown to induce fibrogenesis. In this study, we evaluated the anti-fibrotic activity of a novel imidazopyridine analogue (HS-173) in human HSCs as well as mouse liver fibrosis. HS-173 strongly suppressed the growth and proliferation of HSCs and induced the arrest at the G2/M phase and apoptosis in HSCs. Furthermore, it reduced the expression of extracellular matrix components such as collagen type I, which was confirmed by an in vivo study. We also observed that HS-173 blocked the PI3K/Akt signaling pathway in vitro and in vivo. Taken together, HS-173 suppressed fibrotic responses such as cell proliferation and collagen synthesis by blocking PI3K/Akt signaling. Therefore, we suggest that this compound may be an effective therapeutic agent for ameliorating liver fibrosis through the inhibition of PI3K signaling.
HS-173, a novel phosphatidylinositol 3-kinase (PI3K) inhibitor, has anti-tumor activity through promoting apoptosis and inhibiting angiogenesis.[Pubmed:22929971]
Cancer Lett. 2013 Jan 1;328(1):152-9.
We synthesized a novel imidazopyridine analogue, a PI3Kalpha inhibitor HS-173 and investigated anti-cancer capacity in human cancer cells. HS-173 inhibited the PI3K signaling pathway, and showed anti-proliferative effects on cancer cells. Also, HS-173 induced cell cycle arrest at the G(2)/M phase and apoptosis. In addition, HS-173 decreased the expression HIF-1alpha and VEGF which play an important role in angiogenesis. This effect was confirmed by the suppression of tube formation and migration assay in vitro. Furthermore, HS-173 diminished blood vessel formation in the Matrigel plug assay in mice. Therefore, HS-173 is considered as a novel drug candidate to treat cancer patients.
Synergistic anticancer activity of HS-173, a novel PI3K inhibitor in combination with Sorafenib against pancreatic cancer cells.[Pubmed:23340175]
Cancer Lett. 2013 May 1;331(2):250-61.
The RAF/MEK/ERK and PI3K/AKT pathways are highly implicated in the development of pancreatic cancer. The principal objective of this study was to assess the synergic effect between Sorafenib (a RAF inhibitor) and HS-173 (a novel PI3K inhibitor) to gain insight into novel therapeutic strategies for treating pancreatic cancer. We first investigated the cytotoxic effect of co-treatment with Sorafenib and HS-173 using the Calcusyn program. Combined treatment of the two drugs synergistically inhibited the viability of Panc-1 cells (combination index<1). Concomitantly, the co-treatment induced G2/M arrest and increased apoptosis with the loss of mitochondrial membrane potential. Apoptosis resulting from the co-treatment was accompanied by increased levels of cleaved caspase-3 and PARP as well as greater numbers of TUNEL-positive apoptotic cells compared to treatment with either drug alone. Furthermore, combined treatment with these drugs decreased the expression of HIF-1alpha and VEGF which play an important role in angiogenesis. This anti-angiogenic effect was confirmed by the suppressed tube formation of VEGF-induced human umbilical vein endothelial cells and inhibition of blood vessel formation in a Matrigel plug assay in mice. Taken together, our study demonstrates that combined treatment with Sorafenib and HS-173 has a synergistic anti-cancer effect on pancreatic cancer cells, indicating that simultaneously targeting the RAF/MEK and PI3K/AKT pathways can induce a synergistic inhibitory effect on pancreatic cancers in which both pathways are activated. Based on the observations from our study, we suggest that the combined administration of these two drugs may be considered to be a new therapeutic regimen for treating pancreatic cancer.
