1022150-57-7
6-((6-(1-methyl-1h-pyrazol-4-yl)-1,2,4-triazolo(4,3-b)pyridazin-3-yl)thio)quinoline
CAS: 1022150-57-7
Molecular Formula: C18H13N7S
1022150-57-7 - Names and Identifiers
1022150-57-7 - Physico-chemical Properties
| Molecular Formula | C18H13N7S |
| Molar Mass | 359.41 |
| Density | 1.485 |
| pKa | 3.94±0.10(Predicted) |
| Storage Condition | -20℃ |
| In vitro study | SGX-523 is a c-Met/hepatocyte growth factor receptor (HGFR) tyrosine kinase inhibitor that inactivates MET to other protein kinases. SGX523 effectively inhibits the purified MET catalytic domain, rather than the closely related receptor tyrosine kinase RON. SGX523 is an ATP-competitive inhibitor with a higher affinity for low activity and non-phosphorylated MET (MET-KD (OP), Ki = 2.7 nM). SGX523 inhibits MET-regulated signaling, cell proliferation and cell migration at nanomolar concentrations, but has no inhibitory effect on other protein kinase-dependent signaling, even at micromolar concentrations, such as RON. SGX523 inhibits MET in vivo and correlates with dose-dependent inhibition of growth of human glioblastoma, lung cancer, and gastric cancer-derived xenografts, suggesting that these tumors depend on MET catalytic activity. SGX-523 is a c-Met/hepatocyte growth factor receptor (HGFR) tyrosine kinase inhibitor that inactivates MET to other protein kinases. SGX523 effectively inhibits the purified MET catalytic domain, rather than the closely related receptor tyrosine kinase RON. SGX523 is an ATP competitive inhibitor with a higher affinity (MET-KD (OP), K I = 2.7 nM) for low activity and non-phosphorylated MET. SGX523 inhibits MET-regulated signaling, cell proliferation and cell migration at nanomolar concentrations, but has no inhibitory effect on other protein kinase-dependent signaling, even at micromolar concentrations, such as RON. SGX523 inhibits MET in vivo and correlates with dose-dependent inhibition of growth of human glioblastoma, lung cancer, and gastric cancer-derived xenografts, suggesting that these tumors depend on MET catalytic activity. |
| In vivo study | Oral treatment of SGX523 at doses ≥ 10 mg/kg, twice daily, significantly delayed the prespecified GTL16 tumor growth. SGX523 at a dose of 30 mg/kg, twice daily, effectively inhibited U87MG tumor growth. Treatment of SGX523 at a dose of 30 mg/kg twice daily also delayed H441 tumor growth with a concomitant decrease in MET autophosphorylation levels. In vivo, SGX523 inhibits MET in a dose-dependent manner, and is associated with malignant glioma, lung, and gastric cancer, indicating that tumors are associated with MET catalytic activity. SGX523 treated orally at a dose of ≥ 10 mg/kg twice daily significantly delayed the growth of a prespecified GTL16 tumor. SGX523 at a dose of 30 mg/kg, twice daily, effectively inhibited U87MG tumor growth. Treatment of SGX523 at a dose of 30 mg/kg twice daily also delayed H441 tumor growth with a concomitant decrease in MET autophosphorylation levels. In vivo, SGX523 inhibits MET in a dose-dependent manner, and is associated with malignant glioma, lung, and gastric cancer, indicating that tumors are associated with MET catalytic activity. |
1022150-57-7 - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 2.782 ml | 13.911 ml | 27.823 ml |
| 5 mM | 0.556 ml | 2.782 ml | 5.565 ml |
| 10 mM | 0.278 ml | 1.391 ml | 2.782 ml |
| 5 mM | 0.056 ml | 0.278 ml | 0.556 ml |
Last Update：2024-01-02 23:10:35
1022150-57-7 - Reference Information
| c-Met kinase inhibitor | SGX523 is also a c-MET inhibitor. Animal models show that this combination therapy can control tumor growth. Major manufacturers are conducting research and development of various drugs at met targets. At that time, volitinib did not take the lead. But as the efficacy of the drug was tested, Walitinib gradually showed its met advantage. SGX-523 similar competitors were discontinued due to severe acute kidney injury in the early stage. Compared with other met small molecule inhibitors, Walitinib has better pharmacokinetics, especially in terms of solubility. To lay the foundation for the later clinical efficacy. Walitinib (AZD6094,HMPL-504) is a highly selective oral small molecule c-Met kinase inhibitor jointly developed by Hutchison Whampoa Pharmaceutical (Shanghai) Co., Ltd. and AstraZeneca. Met gene is an oncogene that can appear in a variety of cancer species. It has a certain detection rate in non-small cell lung cancer, kidney cancer, gastric cancer and colorectal cancer. The inhibitory effect of voritinib on the met gene is 10 times that of the existing drug crizotinib. Relying on such a highly effective targeted inhibition, positive results have been obtained in multiple cancer species. |
| biological activity | SGX-523 is a selective Met inhibitor with IC50 of 4 nM and no inhibitory activity against BRAFV599E, c-Raf, Abl and p38α. Phase 1. SGX-523 is a selective Met (c-Met) inhibitor with IC50 of 4 nM and no inhibitory activity on BRAFV599E, c-Raf, Abl and p38α. Phase 1. |
| In vitro studies | SGX-523 belong to c-Met/hepatocyte growth factor receptor (HGFR) tyrosine kinase inhibitors, which make MET inactivated and unable to approach other protein kinases. SGX523 effectively inhibited the purified MET catalytic region, rather than the closely related receptor tyrosine kinase RON. SGX523 is a competitive inhibitor of ATP and has higher affinity when acting on low-activity and non-phosphorylated MET (MET-KD(0P), Ki = 2.7 nM). SGX523 inhibits MET-regulated signals, cell proliferation and cell migration at nanomolar concentrations, but has no inhibitory effect on signals that depend on other protein kinases, even at micromolar concentrations, such as RON. SGX523 inhibits MET in vivo, which is related to the dose-dependent inhibition of the growth of human malignant glioma, lung cancer, and gastric cancer-derived transplanted tumors, indicating that these tumors depend on the catalytic activity of MET. SGX-523 is a tyrosine kinase inhibitor of c-Met/hepatocyte growth factor receptor (HGFR), which makes MET inactivated and unable to approach other protein kinases. SGX523 effectively inhibited the purified MET catalytic region, rather than the closely related receptor tyrosine kinase RON. SGX523 is a competitive inhibitor of ATP and has higher affinity when acting on low-activity and non-phosphorylated MET (MET-KD(0P), K I = 2.7 nM). SGX523 inhibits MET-regulated signals, cell proliferation and cell migration at nanomolar concentrations, but has no inhibitory effect on signals that depend on other protein kinases, even at micromolar concentrations, such as RON. SGX523 inhibits MET in vivo, which is related to the dose-dependent inhibition of the growth of human malignant glioma, lung cancer, and gastric cancer-derived transplanted tumors, indicating that these tumors depend on the catalytic activity of MET. |
| in vivo study | SGX523 was orally treated at a dose of ≥ 10 mg/kg twice a day, significantly delaying the pre-set GTL16 tumor growth. SGX523 was treated at a dose of 30 mg/kg twice a day, effectively inhibiting U87MG tumor growth. SGX523, treated at a dose of 30 mg/kg twice daily, also delayed H441 tumor growth, accompanied by decreased levels of MET autophosphorylation. In vivo, SGX523 inhibits MET in a dose-dependent manner, which is related to malignant glioma, lung and gastric cancer, indicating that tumor is related to MET catalytic activity. SGX523 was treated orally at a dose of ≥ 10 mg/kg twice a day, significantly delaying the pre-set GTL16 tumor growth. SGX523 was treated at a dose of 30 mg/kg twice a day, effectively inhibiting U87MG tumor growth. SGX523, treated at a dose of 30 mg/kg twice daily, also delayed H441 tumor growth, accompanied by decreased levels of MET autophosphorylation. In vivo, SGX523 inhibits MET in a dose-dependent manner, which is related to malignant glioma, lung and gastric cancer, indicating that tumor is related to MET catalytic activity. |
| target | TargetValue c-Met (Cell-free say) 4 nM |
| Target | Value |
| c-Met (Cell-free assay) | 4 nM |
Last Update：2024-04-09 21:54:55
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Product Name: SGX-523 Visit Supplier Webpage Request for quotationCAS: 1022150-57-7
Tel: 18301782025
Email: 3008007409@qq.com
Mobile: 18021002903
QQ: 3008007409
Wechat: 18301782025
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