Molecular Formula | C21H23N7O3S |
Molar Mass | 453.52 |
Density | 1.408±0.06 g/cm3(Predicted) |
pKa | 7.17±0.70(Predicted) |
Storage Condition | -20℃ |
In vitro study | AZD2858 is a selective GSK-3 inhibitor with IC50 of 68 nM, which inhibits phosphorylation of tau 396 site and activates Wnt signaling pathway. Treatment of isolated human osteoblasts with AZD2858 (1 μm, 12 h) resulted in a 3-fold increase in β-catenin levels. In human and rat mesenchymal stem cells, AZD2858 causes β-catenin to stabilize, activating hADSC commitment to calcification of osteoblasts and osteoblasts in vitro. AZD2858 is a selective GSK-3 inhibitor with IC50 of 68 nM, which inhibits phosphorylation of tau 396 site and activates Wnt signaling pathway. Treatment of isolated human osteoblasts with AZD2858 (1 μm, 12 h) resulted in a 3-fold increase in β-catenin levels. In human and rat mesenchymal stem cells, AZD2858 causes β-catenin to stabilize, activating hADSC commitment to calcification of osteoblasts and osteoblasts in vitro. |
In vivo study | Oral AZD2858 treatment in rats resulted in a dose-dependent increase in bone density after two weeks of treatment compared to the control group, with maximal efficacy at a dose of 20 mg/kg per day (total BMC: 172% of the control group) after two weeks of treatment. A small but significant effect was also found in the cortex (total BMC: 111% of control). Three weeks after AZD2858 treatment (30 μmol/kg), the callus showed mineral density (28% at 2 weeks and 38% at 3 weeks) and mineral content (81% at 2 weeks), 93%) increased at three weeks. AZD2858 treatment resulted in faster recovery from fracture, with Bony callus but no apparent cartilage component. After 28 days of treatment with AZD2858 in rats, there was a time-dependent change in the increase of bone turnover markers and bone density in the serum. After 7 days of treatment with AZD2858 in rats, the bone formation marker P1NP increased and the erosion marker TRAcP-5b decreased, indicating an increase in bone anabolism and a decrease in erosion. compared with the control group, rats treated with oral AZD2858 caused a dose-dependent increase in bone mineral density after two weeks of treatment, at 20 mg/kg/day (total BMC: 172% of control group). Dose has the greatest effect. A small but significant effect was also found in the cortex (total BMC: 111% of control). Three weeks after AZD2858 treatment (30 μmol/kg), the callus showed mineral density (28% at 2 weeks and 38% at 3 weeks) and mineral content (81% at 2 weeks), 93%) increased at three weeks. AZD2858 treatment resulted in faster recovery from fracture, with Bony callus but no apparent cartilage component. After 28 days of treatment with AZD2858 in rats, there was a time-dependent change in the increase of bone turnover markers and bone density in the serum. After 7 days of treatment with AZD2858 in rats, the bone formation marker P1NP increased and the erosion marker TRAcP-5b decreased, indicating an increase in bone anabolism and a decrease in erosion. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.205 ml | 11.025 ml | 22.05 ml |
5 mM | 0.441 ml | 2.205 ml | 4.41 ml |
10 mM | 0.22 ml | 1.102 ml | 2.205 ml |
5 mM | 0.044 ml | 0.22 ml | 0.441 ml |
biological activity | AZD2858 a selective GSK-3 inhibitor with IC50 of 68 nM, activating Wnt signaling pathway and enhancing bone mass in rats. AZD2858 a selective GSK-3 inhibitor, IC50 is 68 nM, which activates Wnt signaling pathway and strengthens bone mass in rats. |
in vitro study | AZD2858 is a selective GSK-3 inhibitor, IC50 is 68 nM, inhibiting phosphorylation of tau 396 site and activating Wnt signaling pathway. AZD2858 treatment (1 μM, 12 h) of isolated human osteoblasts resulted in a 3-fold increase in β-catenin levels. In human and rat mesenchymal stem cells, AZD2858 caused β-catenin stabilization, activating in vitro osteoblast and osteoblast calcified hADSC stereotyping. AZD2858 is a selective GSK-3 inhibitor, IC50 is 68 nM, inhibiting phosphorylation of tau 396 site and activating Wnt signaling pathway. AZD2858 treatment (1 μM, 12 h) of isolated human osteoblasts resulted in a 3-fold increase in β-catenin levels. In human and rat mesenchymal stem cells, AZD2858 caused β-catenin stabilization, activating in vitro osteoblast and osteoblast calcified hADSC stereotyping. |
in vivo study | compared with the control group, rats treated with oral AZD2858 for two weeks caused a dose-dependent increase in bone mineral density. after two weeks of treatment, it had the greatest effect at a dose of 20 mg/kg (total BMC: 172% of the control group). Small and significant effects are also found in the cortex (total BMC: 111% of the control group). After three weeks of AZD2858 treatment, the mineral density (28% at 2 weeks, 38% at 3 weeks) and mineral content (81% at 2 weeks and 93% at 3 weeks) increased in callus. AZD2858 treatment made fracture recovery faster, with bony callus but no obvious cartilage component. After 28 days of AZD2858 treatment, rats produced time-dependent changes in the increase of bone turnover markers and bone density in serum. After 7 days of AZD2858 treatment in rats, bone formation marker P1NP increased and dissolution marker TRAcP-5b decreased, which indicated that bone anabolism increased and dissolution was weakened. compared with the control group, rats treated with oral AZD2858 for two weeks caused a dose-dependent increase in bone mineral density. after two weeks of treatment, the rats had the greatest effect at a dose of 20 mg/kg per day (total BMC: 172% of the control group). Small and significant effects are also found in the cortex (total BMC: 111% of the control group). After three weeks of AZD2858 treatment, the mineral density (28% at 2 weeks, 38% at 3 weeks) and mineral content (81% at 2 weeks and 93% at 3 weeks) increased in callus. AZD2858 treatment made fracture recovery faster, with bony callus but no obvious cartilage component. After 28 days of AZD2858 treatment, rats produced time-dependent changes in the increase of bone turnover markers and bone density in serum. After 7 days of AZD2858 treatment in rats, bone formation marker P1NP increased and dissolution marker TRAcP-5b decreased, which indicated that bone anabolism increased and dissolution was weakened. |
target | TargetValue GSK-3 68 nM |
Target | Value |
GSK-3 | 68 nM |