All AbMole products are for research use only, cannot be used for human consumption.
Bemcentinib (R428) blocks the catalytic and procancerous activities of Axl. R428 inhibits Axl with low nanomolar activity and blocked Axl-dependent events, including Akt phosphorylation, breast cancer cell invasion, and proinflammatory cytokine production. Bemcentinib (R428) inhibited angiogenesis in corneal micropocket and tumor models.
In vitro, Bemcentinib (R428) caused a concentration-dependent inhibition of preadipocyte differentiation into mature adipocytes, as evidenced by reduced lipid uptake.
In vivo, oral administration of Bemcentinib (R428) for 5 weeks to mice kept on a high-fat diet resulted in significantly reduced weight gain and subcutaneous and gonadal fat mass. Additionally, Bemcentinib (R428) synergized with cisplatin to enhance suppression of liver micrometastasis.
Cancer Biol Ther. 2015 Oct;1535-47.
The small GTPase ADP-Ribosylation Factor 1 mediates the sensitivity of triple negative breast cancer cells to EGFR tyrosine kinase inhibitors.
Bemcentinib purchased from AbMole
.jpg) |
Source | Cancer Biology& Therapy (2015) . Figure 6.R428 (Abmole Bioscience, Houston, TX) |
| Method | Western blot and MTT assay | |
| Cell Lines | MDA-MB-231 cells and MDA-MB-231 cells that were transfected with CTL or ARF1 siRNA | |
| Concentrations | 1 µ M | |
| Incubation Time | western blot (1 h) and MTT assay (24 h) | |
| Results | Interestingly, like in the EGFR inhibitor treatment, the AXL inhibitor, R428, was effective to enhance ARF1 activity. But, more importantly, this inhibitor blocked gefitinib-induced ARF1 activation. Finally, this observation was also found in MDA-MB-157 cells. However, in cells co-treated with the AXL inhibitor, R428, and gefitinib, the depletion of ARF1 was shown to have no effect further suggesting that ARF1 is signaling downstream of AXL in gefitinib treated cells (Figure 6F). |
| Cell Experiment | |
|---|---|
| Cell lines | MDA-MB-231 or 4T1 cells |
| Preparation method | Invasion Assays: MDA-MB-231 or 4T1 cells (1 × 105) were allowed to migrate through Matrigel (Millipore) toward 20% FCS in an 8-μm pore 24-well Transwell plate (BD Bio‐sciences) at 37°C for 16 to 24 h. Noninvaded cells and Matrigel were removed by swabbing. Invaded cells were fixed in 4% formaldehyde, stained with 1% crystal violet, and quantified as for Axl cellbased assay. Cells were preincubated with R428 for 3 h. R428 was added to both upper and lower Transwell chambers. |
| Concentrations | 0, 0.03, 0.3, 3 µ M |
| Incubation time | 3 h |
| Animal Experiment | |
|---|---|
| Animal models | Female BALB/c mice 4T1 Orthotopic Model |
| Formulation | R428 was formulated for in vivo studies in 0.5% hydroxypropylmethylcellulose + 0.1% Tween 80. |
| Dosages | 7–75 mg/kg twice daily |
| Administration | oral gavage |
| Molecular Weight | 506.64 |
| Formula | C30H34N8 |
| CAS Number | 1037624-75-1 |
| Solubility (25°C) | DMSO 10 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
| Related TAM Receptor Products |
|---|
| SGI-7079
SGI-7079 is a novel Axl inhibitor. |
| UNC2250
UNC2250 is a potent and selective Mer inhibitor with IC50 of 1.7 nM, about 160- and 60-fold selectivity over the closely related kinases Axl/Tyro3. |
| UNC2881
UNC2881 is a specific Mer tyrosine kinase inhibitor with IC50 of 4.3 nM, about 83- and 58-fold selectivity over Axl and Tyro3, respectively |
| Dubermatinib
Dubermatinib (TP-0903) is a potent and selective AXL inhibitor with an IC50 value of 27 nM. |
| RU-301
RU-301 is a pan-TAM receptor inhibitor that blocks Gas6-induced TAM activation and tumorigenicity, with Kd and IC50 values of 12 μM and 10 μM, respectively. |
All AbMole products are for research use only, cannot be used for human consumption or veterinary use. We do not provide products or services to individuals. Please comply with the intended use and do not use AbMole products for any other purpose.
Products are for research use only. Not for human use. We do not sell to patients.
© Copyright 2010-2026 AbMole BioScience. All Rights Reserved.
