115103-85-0

Usage

Uses

Used in Cancer Research:
MK-571 sodium is used as an efflux inhibitor for monitoring multidrug resistance protein (MRP) function and to avoid redundancy of other transporters. This application is crucial in understanding the mechanisms behind drug resistance and developing strategies to overcome it.
Used in Glioblastoma Multiforme (GBM) Research:
In the field of GBM research, MK-571 sodium is used as a tool to assess its effect on cell proliferation and 2D-migration in vitro in various cell lines. This helps researchers understand the behavior of GBM cells and develop targeted therapies.
Used in Ovarian Cancer Research:
MK-571 sodium is used as a multidrug resistance (MDR) transporter inhibitor to study its effects in ovarian cancer cells. This application aids in the development of more effective treatments for ovarian cancer by targeting the resistance mechanisms of the cancer cells.
Used in ABCC1/2 Inhibition Studies:
MK-571 sodium is used as a specific inhibitor of ABCC1/2 to investigate transport, toxicity, flow cytometry, and arsenic efflux. This application is essential in understanding the role of these transporters in various biological processes and their potential as therapeutic targets.

Biological Activity

mk571 sodium salt is a specific cyslt1 (cysteinyl-leukotriene type 1 receptor) antagonist [1].cysteinyl leukotriene receptor 1, also termed as cysltr1, is a receptor for cysteinyl leukotrienes (lt)which mediates a large variety of allergic and hypersensitivity reactions in humans [2].

Biochem/physiol Actions

MK 571 is a potent and selective leukotriene D4 (LTD4) antagonist and ABCC multidrug resistance protein 1(MRP1) inhibitor. The cysteinyl leukotrienes (CysLTs), LTC4, LTD4, and LTE4, mediate their actions through two distinct G-protein coupled receptors. LTD4 is the preferred ligand for the CysLT1 receptor, whereas LTC4 and LTD4 bind with approximately equal affinity to the CysLT2 receptor. MK 571 is a selective, orally active CysLT1 receptor antagonist. It blocks the binding of LTD4, but not LTC4, to human and guinea pig lung membranes with Ki values of 0.22 nM and 2.1 nM, respectively. MK 571 effectively blocks LTD4 activation of recombinant human and mouse CysLT1 receptors but is ineffective at blocking LTC4 or LTD4 activation of the recombinant human or murine CysLT2 receptors. It potentially inhibits MRP1 and has been shown to overcome acquired arsenic tolerance.

in vitro

mk571 is a multidrug resistance protein-2 (abcc2, mrp2) inhibitor and had been widely used to demonstrate the role of mrp2 in the cellular efflux of drugs, xenobiotics and their conjugates. apically-applied mk571 resulted in significant reductions in both the apical and basolateral efflux of flavonol conjugates from caco-2/tc7 monolayers. the estimated ki for inhibition of the synthesis of k-4′-o-glca by mk571 is 19.7 μm. mk571 inhibited the intracellular biosynthesis of all flavonol glucuronides and sulphates by caco-2 cells in a dose-dependent manner. mk571 significantly inhibited phase-2 conjugation of kaempferol by cell-free extracts of caco-2, and competitively inhibited the production of kaempferol-4′-o-glucuronide. these data indicated that mk571, in addition to inhibiting mrp2, was a potential inhibitor of enterocyte phase-2 conjugation [3].

references

[1]. thivierge m, turcotte s, rola-pleszczynski m, et al. enhanced cysteinyl-leukotriene type 1 receptor expression in t cells from house dust mite-allergic individuals following stimulation with der p[j]. journal of immunology research, 2015, 2015.[2]. singh rk, tandon r, dastidar sg, ray a (november 2013). "a review on leukotrienes and their receptors with reference to asthma". the journal of asthma. 50 (9): 922–31.[3]. barrington r d, needs p w, williamson g, et al. mk571 inhibits phase-2 conjugation of flavonols by caco-2/tc7 cells, but does not specifically inhibit their apical efflux[j]. biochemical pharmacology, 2015, 95(3): 193-200.