Amiloride (MK-870) |
| Catalog No.GC31431 |
Amiloride (MK-870) es un inhibidor tanto del canal de sodio epitelial (ENaC[1]) como del receptor de activador de plasminógeno tipo uroquinasa (uTPA[2]).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 2609-46-3
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Amiloride (MK-870) is a selective T-type calcium channel blocker and an inhibitor of epithelial sodium channels (ENaC) and urokinase-type plasminogen activator receptor (uTPA), Ki=7 µM. It is also polycystin-2 (PC2;TRPP2) channel blocker[1-3].
Amiloride(50 mg/L;24h) decreased uPAR expression (due to the presence of lipopolysaccharide) in podocytes[4].
Amiloride is a relatively selective inhibitor of the epithelial sodium channel (ENaC) with an IC50 (the concentration required to reach 50% inhibition of an ion channel) in the concentration range of 0.1 to 0.5 µM. Amiloride is a relatively poor inhibitor of the the Na+/H+ exchanger (NHE) with an IC50 as low as 3 µM in the presence of a low external [Na+] but as high as 1 mM in the presence of a high [Na+][1]. Amiloride(0.1-1mM) together with Bumetanide completely blocked cell transition through G1 and entry into S-phase in BALB/c 3T3 cells [5].
Amiloride(10 mg/kg/d;3days;i.g.) might inhibit uPAR expression in podocytes of transient proteinuria induced by lipopolysaccharid in the mouse model[4]. In ApoE(-/-) mice, administration of amiloride(high-fat diets with 0.5% (w/w) amiloride;4 weeks) significantly suppressed LPS-accelerated atherosclerosis and LPS-induced increase of NHE1 activity, and reversed LPS-induced down-regulation of Bcl-2 expression[6]. Amiloride(2mg/kg/d;30days;i.p.) treatment in tumor-bearing mice(The CT26 and LLC cachexia cell models)distinctly alleviated muscle atrophy and relieved cachexia-related features without affecting tumor growth[7].
References:
[1]. Teiwes J, Toto RD. Epithelial sodium channel inhibition in cardiovascular disease. A potential role for amiloride. Am J Hypertens. 2007 Jan;20(1):109-17. doi: 10.1016/j.amjhyper.2006.05.022. PMID: 17198922.
[2]. Tang CM, Presser F, et,al. Amiloride selectively blocks the low threshold (T) calcium channel. Science. 1988 Apr 8;240(4849):213-5. doi: 10.1126/science.2451291. PMID: 2451291.
[3]. Giamarchi A, Feng S, et,al. A polycystin-2 (TRPP2) dimerization domain essential for the function of heteromeric polycystin complexes. EMBO J. 2010 Apr 7;29(7):1176-91. doi: 10.1038/emboj.2010.18. Epub 2010 Feb 18. PMID: 20168298; PMCID: PMC2857461.
[4]. Xu LB, Chi N, et,al.Amiloride, a urokinase-type plasminogen activator receptor (uTPA) inhibitor, reduces proteinurea in podocytes. Genet Mol Res. 2015 Aug 14;14(3):9518-29. doi: 10.4238/2015.August.14.15. PMID: 26345885.
[5]. Panet R, Snyder D, et,al. Amiloride added together with bumetanide completely blocks mouse 3T3-cell exit from G0/G1-phase and entry into S-phase. Biochem J. 1986 Nov 1;239(3):745-50. doi: 10.1042/bj2390745. PMID: 3548704; PMCID: PMC1147349.
[6]. Cui GM, Zhao YX, et,al.Amiloride attenuates lipopolysaccharide-accelerated atherosclerosis via inhibition of NHE1-dependent endothelial cell apoptosis. Acta Pharmacol Sin. 2013 Feb;34(2):231-8. doi: 10.1038/aps.2012.155. Epub 2012 Dec 31. PMID: 23274414; PMCID: PMC4011619.
[7]. Zhou L, Zhang T, et,al.Amiloride ameliorates muscle wasting in cancer cachexia through inhibiting tumor-derived exosome release. Skelet Muscle. 2021 Jul 6;11(1):17. doi: 10.1186/s13395-021-00274-5. PMID: 34229732; PMCID: PMC8258996.
Average Rating: 5 (Based on Reviews and 37 reference(s) in Google Scholar.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *