875787-07-8
2H-Indazole, 2-[(2-chloro-4-fluorophenyl)Methyl]-3-(4-fluorophenyl)-7-(trifluoroMethyl)-
CAS: 875787-07-8
Molecular Formula: C21H12ClF5N2
875787-07-8 - Names and Identifiers
875787-07-8 - Physico-chemical Properties
| Molecular Formula | C21H12ClF5N2 |
| Molar Mass | 422.78 |
| Density | 1.40 |
| Melting Point | 93℃ |
| Boling Point | 528.4±50.0 °C(Predicted) |
| Appearance | powder |
| Color | white to beige |
| pKa | -1.87±0.30(Predicted) |
| Storage Condition | room temp |
| In vitro study | LXR-623 inhibits LDLR expression, increases expression of ABCA1 efflux transporters and induces substantial cell death in GBM cells. Brain Metastatic breast cancer cells MDA-MB-361 are highly sensitive to LXR-623-dependent cell death. In GBM cells, LXR-623 inhibited LDL uptake and induced cholesterol efflux, resulting in a significant decrease in intracellular cholesterol content. Normal brain cells are insensitive to LXR-623, probably due to the negative feedback effect that normal cells rely on endogenous cholesterol synthesis to maintain integrity through the synthesis of hydroxysterols. |
| In vivo study | LXR-623 is rapidly absorbed in vivo, with peak concentrations (Cmax) occurring approximately 2 hours after administration. The Cmax and the area under the concentration-time curve are proportional to the dose. The average half-life was 41-43 hours. In a LDLr knockout mouse model of atherosclerosis, oral administration of LXR-623 upregulates its intestinal ABCG2 and ABCG2 expression, reducing the burden of atherogenesis, without affecting serum or liver cholesterol and triglycerides. In mice with glioblastoma, LXR-623 had brain permeability and resulted in tumor regression, reduced cholesterol levels and induced cell death. |
875787-07-8 - Risk and Safety
| UN IDs | UN 2811 6.1 / PGIII |
875787-07-8 - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 2.365 ml | 11.827 ml | 23.653 ml |
| 5 mM | 0.473 ml | 2.365 ml | 4.731 ml |
| 10 mM | 0.237 ml | 1.183 ml | 2.365 ml |
| 5 mM | 0.047 ml | 0.237 ml | 0.473 ml |
Last Update：2024-01-02 23:10:35
875787-07-8 - Reference Information
| biological activity | LXR-623 (WAY-252623) is a new type of liver X-receptor(LXR) agonist with IC50 values of 179 nM and 24 nM for LXR-α and LXR-β respectively. It has biological oral activity and can pass through the blood-brain barrier. |
| target | TargetValue LXR-β 24 nM LXR-α 179 nM |
| Target | Value |
| LXR-β | 24 nM |
| LXR-α | 179 nM |
| in vitro study | LXR-623 inhibit LDLR expression, increase ABCA1 efflux transporter expression and induce large-scale cell death of GBM cells. Brain metastatic breast cancer cell MDA-MB-361 is highly sensitive to LXR-623-dependent cell death. In GBM cells, LXR-623 inhibits LDL absorption and induces cholesterol outflow, resulting in a significant decrease in intracellular cholesterol content. Normal brain cells are not sensitive to LXR-623, which may be due to the negative feedback effect that normal cells rely on endogenous cholesterol synthesis and maintain complete through the synthesis of hydroxysterol. |
| in vivo studies | LXR-623 can be quickly absorbed in the body, and the peak concentration (Cmax) appears about 2 hours after administration. Cmax and concentration time curve below the product into a dose proportional relationship. The average half-life is 41-43 hours. In a mouse model of LDLr knockout atherosclerosis, oral administration of LXR-623 can up-regulate the expression of ABCG5 and ABCG8 in intestinal tract and reduce the burden of atherosclerosis without affecting serum or liver cholesterol and triglyceride. In mice with malignant gliomas, LXR-623 have brain permeability and cause tumor regression, reduce cholesterol levels and induce cell death. |
Last Update：2024-04-09 20:49:11
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