包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
25mg | 电议 |
100mg | 电议 |
Inositol phosphate production | RH7777 cells are incubated for 1 min with or without Ki16425, and the inositol phosphates (sum of inositol bisphosphate and inositol trisphosphate) were measured. The results were normalized to 105 dpm of the total radioactivity incorporated into the cellular inositol lipids, and the radioactivity of trichloroacetic acid (5%)-insoluble fraction was considered as the total radioactivity. |
Cell lines | MDA-MB-231 and PC3 cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reaction Conditions | 10 μM; 45 mins or 24 hrs |
Applications | In human breast and prostate cancer cells, Ki16425 inhibited heparin-binding EGF-like growth factor (HB-EGF) expression. |
Animal models | PC3 cell xenograft mouse model |
Dosage form | 25 mg/kg; s.c.; for 5 days |
Applications | A five-day treatment with Ki16425 significantly decreased both HB-EGF mRNA expression at the transplanted tumor site in mice and circulating human HB-EGF concentrations in serum. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
产品描述 | Ki16425 is a subtype-selective antagonist of lysophosphatidic acid receptor (LPA) with Ki values of 0.34 μM for LPA1, 6.5μM for LPA2, and 0.93μM for LPA3 [4]. It has been reported that Ki16425 inhibited the LPA receptor-mediated actions in the order of LPA1≥LPA3≥LPA2. Ki16425 inhibited LPA-induced guanosine 5’-O-(3-thio) triphosphate binding, membrane fractions binding, and was involved in the long-term responses, including DNA synthesis and cell migration [1]. Ki16425 attenuated LPA-mediated intracellular signaling and invasion responses in vitro. Co-treatment of Ki16425 and sunitinib prolonged the sensitivity of renal tumor cell to sunitinib in xenograft mouse models [3]. In human breast cancer cells, Ki16425 can inhibit heparin-binding EGF-like growth factor (HB-EGF) expression [4]. In mouse thoracic aorta, Ki16425 significantly reduced LPA-induced vasorelaxation [2]. Ki16425 treatment also blocked renal tumorigenesis in vivo [3]. A five-day treatment with Ki16425 significantly decreased both HB-EGF mRNA expression at the transplanted tumor site in mice and circulating human HB-EGF concentrations in serum [4]. References: |