CS-994
SAR131675
CAS: 1433953-83-3
Molecular Formula: C18H22N4O4
CS-994 - Names and Identifiers
CS-994 - Physico-chemical Properties
| Molecular Formula | C18H22N4O4 |
| Molar Mass | 358.39 |
| Density | 1.33±0.1 g/cm3(Predicted) |
| Boling Point | 592.2±50.0 °C(Predicted) |
| pKa | 12.20±0.29(Predicted) |
| Storage Condition | Keep in dark place,Inert atmosphere,Store in freezer, under -20°C |
| In vitro study | SAR131675 inhibits VEGFR-3 of the ligand VEGFC and VEGFD-induced proliferation of primary human lymph node cells and has a dose-dependent profile, with an IC50 of approximately 20 nM, and also inhibits rh-VEGFR-3-TK of the activity and has a dose-dependent profile, the IC50 was 23 nM. SAR131675 inhibited VEGR-3-TK of the activity with a Ki value of approximately 12 nM. SAR131675 inhibited the activity by VEGFR-1-TK with an IC50 greater than 3 μm and inhibited the activity by VEGFR-2-TK with an IC50 of 235 nM. SAR131675 inhibited VEGFR-1 autophosphorylation with an IC50 of about 1 μm and inhibited VEGFR-2 autophosphorylation with an IC50 of about 280 nM. SAR131675 moderately inhibited VEGFR-2 but had little effect on VEGFR-1, indicating a good selectivity for VEGFR-3. SAR131675 inhibited VEGFA-induced phosphorylation by VEGFR-2 in a dose-dependent manner with an IC50 of 239 nM. SAR131675 potently inhibited VEGFC and VEGFD-induced lymphocyte survival with an IC50 of 14nM and 17 nM, respectively, and inhibited VEGFA-induced lymphocyte survival with an IC50 of 664 nM. SAR131675 significantly inhibited VEGFC-induced Erk phosphorylation in a dose-dependent manner with an IC50 of approximately 30 nM. SAR131675 inhibits VEGFR-3 of the ligand VEGFC and VEGFD-induced proliferation of primary human lymph node cells in a dose-dependent manner with an IC50 of approximately 20 nM, it also inhibited the activity by rh-VEGFR-3-TK and had a dose-dependent profile with an IC50 of 23 nM. SAR131675 inhibited VEGR-3-TK of the activity with a K I value of about 12 nM. SAR131675 inhibited the activity by VEGFR-1-TK with an IC50 greater than 3 μm and inhibited the activity by VEGFR-2-TK with an IC50 of 235 nM. SAR131675 inhibited VEGFR-1 autophosphorylation with an IC50 of about 1 μm and inhibited VEGFR-2 autophosphorylation with an IC50 of about 280 nM. SAR131675 moderately inhibited VEGFR-2 but had little effect on VEGFR-1, indicating a good selectivity for VEGFR-3. SAR131675 inhibited VEGFA-induced phosphorylation by VEGFR-2 in a dose-dependent manner with an IC50 of 239 nM. SAR131675 potently inhibited VEGFC and VEGFD-induced lymphocyte survival with an IC50 of 14nM and 17 nM, respectively, and inhibited VEGFA-induced lymphocyte survival with an IC50 of 664 nM. SAR131675 significantly inhibited VEGFC-induced Erk phosphorylation in a dose-dependent manner with an IC50 of approximately 30 nM. |
| In vivo study | SAR131675 effectively disrupted embryonic angiogenesis in experiments using zebrafish models to study embryonic angiogenesis. SAR131675 at a dose of 100 mg/kg/day resulted in a significant decrease of VEGFR-3 and hemoglobin levels of around 50%. SAR131675 effectively disrupts fgf2-induced lymphangiogenesis and angiogenesis in vivo. VEGFR-2 mg/kg of SAR131675 can inhibit the signal of VEGFR-3 and. Treatment with SAR131675 for 5 weeks in the prevention experiment showed that SAR131675 was well tolerated and that angiogenesis was reduced by 42% in the pancreas of treated mice compared to controls. Intervention studies have shown that daily oral SAR131675 use from Week 10 to Week 4 can reduce the tumor burden by 12.5. 30 mg/kg/day and 24% mg/kg/day SAR131675 treatment resulted in a 50% and reduction in tumor volume, respectively. SAR131675 effectively disrupted embryonic angiogenesis in an experiment using a zebrafish model to study embryonic angiogenesis. SAR131675 at a dose of 100 mg/kg/day resulted in a significant decrease of VEGFR-3 and hemoglobin levels of around 50%. SAR131675 effectively disrupts fgf2-induced lymphangiogenesis and angiogenesis in vivo. VEGFR-2 mg/kg of SAR131675 can inhibit the signal of VEGFR-3 and. Treatment with SAR131675 for 5 weeks in the prevention experiment showed that SAR131675 was well tolerated and that angiogenesis was reduced by 42% in the pancreas of treated mice compared to controls. Intervention studies have shown that daily oral SAR131675 use from Week 10 to Week 4 can reduce the tumor burden by 12.5. 30 mg/kg/day and 24% mg/kg/day SAR131675 treatment resulted in a 50% and reduction in tumor volume, respectively. |
CS-994 - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 2.79 ml | 13.951 ml | 27.903 ml |
| 5 mM | 0.558 ml | 2.79 ml | 5.581 ml |
| 10 mM | 0.279 ml | 1.395 ml | 2.79 ml |
| 5 mM | 0.056 ml | 0.279 ml | 0.558 ml |
Last Update：2024-01-02 23:10:35
CS-994 - Reference Information
| biological activity | SAR131675 is a VEGFR3 inhibitor with an IC50/Ki of 23 nM/12 nM, acting on VEGFR3 is 50 and 10 times more selective than acting on VEGFR1/2, and has little activity on Akt1, CDKs, PLK1, EGFR, IGF-1R, c-Met, Flt2, etc. SAR131675 is a VEGFR3 inhibitor with an IC50/Ki of 23 nM/12 nM in a cell-free assay, which is 50-and 10-fold more selective for VEGFR3 than for VEGFR1/2, there was almost no activity against Akt1, CDKs, PLK1, EGFR, IGF-1R, c-Met, Flt2, etc. |
| in vitro study | SAR131675 inhibits VEGFR-3 ligand VEGFC and VEGFD-induced proliferation of primary human lymph node cells in a dose-dependent manner, the IC50 is approximately 20 nM and also inhibits rh-VEGFR-3-TK of the activity in a dose-dependent manner with an IC50 of 23 nM. SAR131675 inhibited VEGR-3-TK of the activity with a Ki value of approximately 12 nM. SAR131675 inhibited the activity by VEGFR-1-TK with an IC50 greater than 3 μm and inhibited the activity by VEGFR-2-TK with an IC50 of 235 nM. SAR131675 inhibited VEGFR-1 autophosphorylation with an IC50 of about 1 μm and inhibited VEGFR-2 autophosphorylation with an IC50 of about 280 nM. SAR131675 moderately inhibited VEGFR-2 but had little effect on VEGFR-1, indicating a good selectivity for VEGFR-3. SAR131675 inhibited VEGFA-induced phosphorylation by VEGFR-2 in a dose-dependent manner with an IC50 of 239 nM. SAR131675 potently inhibited VEGFC and VEGFD-induced lymphocyte survival with an IC50 of 14nM and 17 nM, respectively, and inhibited VEGFA-induced lymphocyte survival with an IC50 of 664 nM. SAR131675 significantly inhibited VEGFC-induced Erk phosphorylation in a dose-dependent manner with an IC50 of approximately 30 nM. SAR131675 inhibits VEGFR-3 of the ligand VEGFC and VEGFD-induced proliferation of primary human lymph node cells in a dose-dependent manner with an IC50 of approximately 20 nM, it also inhibited the activity by rh-VEGFR-3-TK and had a dose-dependent profile with an IC50 of 23 nM. SAR131675 inhibited VEGR-3-TK of the activity with a K I value of about 12 nM. SAR131675 inhibited the activity by VEGFR-1-TK with an IC50 greater than 3 μm and inhibited the activity by VEGFR-2-TK with an IC50 of 235 nM. SAR131675 inhibited VEGFR-1 autophosphorylation with an IC50 of about 1 μm and inhibited VEGFR-2 autophosphorylation with an IC50 of about 280 nM. SAR131675 moderately inhibited VEGFR-2 but had little effect on VEGFR-1, indicating a good selectivity for VEGFR-3. SAR131675 inhibited VEGFA-induced phosphorylation by VEGFR-2 in a dose-dependent manner with an IC50 of 239 nM. SAR131675 potently inhibited VEGFC and VEGFD-induced lymphocyte survival with an IC50 of 14nM and 17 nM, respectively, and inhibited VEGFA-induced lymphocyte survival with an IC50 of 664 nM. SAR131675 significantly inhibited VEGFC-induced Erk phosphorylation in a dose-dependent manner with an IC50 of approximately 30 nM. |
| in vivo study | in the study of embryonic angiogenesis using zebrafish model, SAR131675 effectively disrupts embryonic angiogenesis. SAR131675 at a dose of 100 mg/kg/day resulted in a significant decrease of VEGFR-3 and hemoglobin levels of around 50%. SAR131675 effectively disrupts fgf2-induced lymphangiogenesis and angiogenesis in vivo. VEGFR-2 mg/kg of SAR131675 can inhibit the signal of VEGFR-3 and. Treatment with SAR131675 for 5 weeks in the prevention experiment showed that SAR131675 was well tolerated and that angiogenesis was reduced by 42% in the pancreas of treated mice compared to controls. Intervention studies have shown that daily oral SAR131675 use from Week 10 to Week 4 can reduce the tumor burden by 12.5. 30 mg/kg/day and 24% mg/kg/day SAR131675 treatment resulted in a 50% and reduction in tumor volume, respectively. SAR131675 effectively disrupted embryonic angiogenesis in an experiment using a zebrafish model to study embryonic angiogenesis. SAR131675 at a dose of 100 mg/kg/day resulted in a significant decrease of VEGFR-3 and hemoglobin levels of around 50%. SAR131675 effectively disrupts fgf2-induced lymphangiogenesis and angiogenesis in vivo. VEGFR-2 mg/kg of SAR131675 can inhibit the signal of VEGFR-3 and. Treatment with SAR131675 for 5 weeks in the prevention experiment showed that SAR131675 was well tolerated and that angiogenesis was reduced by 42% in the pancreas of treated mice compared to controls. Intervention studies have shown that daily oral SAR131675 use from Week 10 to Week 4 can reduce the tumor burden by 12.5. 30 mg/kg/day and 24% mg/kg/day SAR131675 treatment resulted in a 50% and reduction in tumor volume, respectively. |
| characteristic | SAR131675 is a potent and selective VEGFR-3 tyrosine kinase inhibitor |
| Target | TargetValue VEGFR3 (Cell-free assay) 23 nM |
| Target | Value |
| VEGFR3 (Cell-free assay) | 23 nM |
Last Update：2024-04-09 21:54:55
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