| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
EIPA inhibited TRPP3-mediated Ca2+-activated currents with IC50 values of 10.5 μM.
Cell lines | MCF-7 cells |
Preparation Method | Cells were seeded in 6-well plates for 24 h prior to 48 h-treatment with EIPA (10 µM), Akti (1 µM), U0126 (10 µM) or a combination thereof. |
Reaction Conditions | 10µM for 48 hours |
Applications | MCF-7 cells were subjected to treatment with EIPA with and without ERK and Akt inhibitors. ERK, but not Akt, activity was increased upon EIPA treatment, and both kinases were effectively inhibited by their inhibitors, U0126 and Akti, respectively. Strikingly, ERK inhibition strongly potentiated EIPA-induced CHOP upregulation and PARP cleavage. |
Animal models | Female homozygous BALB/c Nu/Nu nude mice were injected subcutaneously (s.c.) in both flanks at 7 weeks of age with 106 parental and IKKαδ MIA PaCa-2 cells or 1334 and 1444 cells mixed at a 1:1 dilution with BD Matrigel (BD Biosciences) in a total volume of 100 µl. |
Preparation Method | Mice were treated with vehicle (DMSO in PBS), EIPA (7.5 mg/kg), MRT68921 (10 mg/kg) or MRT68921+EIPA for 15 days when tumors attained an average volume of 50-100 mm3. |
Dosage form | s.c., 7.5 mg/kg/d for 7 days |
Applications | One month of EIPA treatment, initiated at age 1 month, markedly reduced pancreatic weight (a tumor burden surrogate), inhibited acinar-to-ductal metaplasia (ADM) and advanced PanIN formation, and preserved the normal pancreatic parenchyma in KrasG12D;IkkαδPEC mice, while decreasing MP. |
| 文献引用 | |
| 产品描述 | EIPA inhibited TRPP3-mediated Ca2+-activated currents with IC50 values of 10.5 μM[1]. TRPP3, a member of the transient receptor potential (TRP) superfamily of cation channels, is a Ca2+-activated channel permeable to Ca2+, Na+, and K+[1].EIPA (5-(N-ethyl-N-isopropyl)-amiloride) is a commonly used amiloride derivative modified similarly to MPA, and its Ki for NHE1, NHE2, and NHE3 are 0.3, 1.8, and 67 μM, respectively[2,3] EIPA suppressed proliferation of MKN28 cells through up-regulation of p21 expression via reduction of [Cl- ] c as a result from DIDS-sensitive Cl- /HCO3- exchanger-mediated compensation for keeping pHc normal under an NHE-inhibited condition[4]. EIPA preischemic treatment overcame the I/R-induced renal dysfunction. Histologic examination of the kidney of vehicle-treated ARF mice revealed severe lesions, and these lesions were significantly suppressed by the preischemic treatment with EIPA. In addition, EIPA suppressed the increment of renal ET-1 content after reperfusion[5]. EIPA at doses of 3 and 9 mg/kg per day inhibited tumor growth of HepG2 modle mice significantly compared with the control[6]. References: |
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