Amg487

Manufactured by Merck Group

Sourced in United Kingdom, United States

AMG487 is a laboratory equipment product offered by the Merck Group. It is designed for use in various scientific research and testing applications. The core function of AMG487 is to provide a reliable and versatile platform for performing targeted analyses and experiments. No further details about the intended use or capabilities of this product can be provided in an unbiased and factual manner.

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Lab products found in correlation

5 protocols using amg487

Chemokine Receptor Antagonist Effects on RA-FLS Viability

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RA-FLS were seeded into 96-well plates at a density of 5x10³ cells/well for 24 h and subsequently treated with different concentrations of several chemokine receptor antagonists: BX471 (50, 100 and 150 nM; CCR1 antagonist, Sigma-Aldrich; Merck KGaA), AMG487 (0.5, 1 and 2 µM; CXCR3 antagonist, Sigma-Aldrich; Merck KGaA) and SB225002 (0.1, 0.2 and 0.4 µM; CXCR2 antagonist, Sigma-Aldrich; Merck KGaA). Following incubation for 24 h at 37˚C, 10 µl Cell Counting Kit-8 (CCK-8; Absin Bioscience, Inc.) reagent was added to each well and the optical density was measured at a wavelength of 450 nm.

Wang W., Deng Z., Liu G., Yang J., Zhou W., Zhang C., Shen W, & Zhang Y. (2021). Platelet-derived extracellular vesicles promote the migration and invasion of rheumatoid arthritis fibroblast-like synoviocytes via CXCR2 signaling. Experimental and Therapeutic Medicine, 22(4), 1120.

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Pharmacologic Inhibition of CXCR3 Signaling

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AMG487, a pharmacologic inhibitor of CXCR3 signaling, was purchased from Tocris Bioscience (Bristol, United Kingdom). For in vitro treatment, AMG487 was prepared as a 10 mmol/L stock solution with DMSO; tumor cells or monocytes were cultured in fresh medium containing 1μmol/L AMG487 for 18 h at 37 °C, then washed and injected. For in vivo administration, AMG487 was prepared in a vehicle (hydroxypropyl-β-cyclodextrain [Sigma, St. Louis, MO]) by incubation in a sonicating water bath for 2 h with intermittent vortexing. Distilled water was used to bring the final concentration of AMG487 to 20% of hydroxypropyl-β-cyclodextrain. Mice received 5 mg/kg of AMG487 or vehicle control by subcutaneous injection.

Butler K.L., Clancy-Thompson E, & Mullins D.W. (2017). CXCR3+ monocytes/macrophages are required for establishment of pulmonary metastases. Scientific Reports, 7, 45593.

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Blocking CXCR3 Attenuates LPS-Induced Bone Loss

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Seven-week-old male C57BL/6J mice purchased from the Jackson Laboratory were utilized. (±)-AMG-487 (Tocris, R&D Systems), a Cxcr3 antagonist (a small molecular-weight peptide), was utilized to block Cxcr3 in vivo. Mice were divided into three groups: Control (local vehicle injection) + i.p. vehicle injection), LPS + vehicle injection, and LPS + AMG-487. AMG-487 was initially dissolved in a 50% hydroxypropyl-β-cyclodextrin (Sigma-Aldrich) in a sonicating water bath for 2 hours with occasional vortexing. After the AMG-487 powder had completely dissolved, distilled water was added to make a final concentration of 20% hyroxypropyl-β-cyclodextrin solution. Vehicle injections consisted of a 20% hyroxypropyl-β-cyclodextrin solution without AMG-487. At the start of LPS injections, mice received the first injection of AMG-487 at a concentration of 5 mg/g twice a day for the whole duration of the experiment.^{(37 (link))}P.g.-LPS injections were performed as described above. Mice were euthanized after a total of 12 LPS injections (6 weeks). Bone loss measurements, histology, and osteoclast counts (n = 5 slides per mouse, n ≥ 5 mice/group) were performed as described above.

Hiyari S., Green E., Pan C., Lari S., Davar M., Davis R., Camargo P.M., Tetradis S., Lusis A.J, & Pirih F.Q. (2018). Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 33(8), 1450-1463.

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Quantifying Platelet Mitochondrial Activity

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Anti-human CD3 (clone UCHT1) and CD28 (clone 37407) monoclonal antibodies (MAbs), rabbit anti-human TGFβ neutralizing antibody (cat# AB-100-NA), goat anti-human RANTES neutralizing antibody (cat# AF-278-NA), and recombinant human (rh) CXCL4/PF4 protein (795-P4-025, with an endotoxin test<0.01 EU/µg recombinant protein) were purchased from R&D Systems (Minneapolis, MN, USA). Prostaglandin E 1 (PGE 1 ), aspirin, apyrase, nonspecific rabbit and goat IgG antibodies, and bovine serum albumin (BSA) were from Sigma (St Louis, MO, USA). Rabbit anti-human PF4 polyclonal antibodies (500-p05) were from PeproTech (London, UK). MitoTracker Green FM and MitoTracker Deep Red FM were purchased from ThermoFisher (Waltham, MA, USA). Anti-actin antibody (cat nr: A5441) was from Sigma, and the antibodies for the total Akt (cat #: 9272) and p-Akt (cat #: 9271) were from Cell Signaling Technology (Danvers, MA, USA). The mitochondrial complex I inhibitor rotenone (cat# R8875) and the CXCR3 antagonist (±)-AMG487 were from was from Sigma and Tocris Bioscience (Bristol, UK), respectively.

Tan S., Zhang J., Sun Y., Gisterå A., Sheng Z., Malmström R.E., Hou M., Peng J., Ma C., Liao W, & Li N. (2022). Platelets enhance CD4+ central memory T cell responses via platelet factor 4-dependent mitochondrial biogenesis and cell proliferation. Platelets, 33(3).

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Modulating PAG to Investigate Morphine Analgesia

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Animals were anesthetized with pentobarbital sodium (60 mg/kg, intraperitoneally). In order to facilitate injection, stainless cannula guides (0.60 mm external and 0.35 mm internal diameters) was implanted unilaterally into dorsal part of PAG (-4.6 mm posterior to bregma, +/-0 mm lateral to the midline and -2 mm ventral to the dorsal surface of the skull) according to the previous study (Masse et al., 2008) . A metallic cannula dummy was placed in the cannula guides after surgery to avoid blood clots.
Animals were allowed a 7-day recovery period before the following experiments.
The following drugs were micro-injected into PAG 30 min before morphine administration, respectively: CXCR3 inhibitor AMG487 (10 or 20 μg, 0.25 μL, diluted in 20 % 2-hydroxypropyl-β-cyclodextrin, once daily; Sigma, St. Louis, MO, USA), microglia inhibitor minocycline (10 pmol, 0.25 μL, diluted in saline, once daily; Sigma, St. Louis, MO, USA) (Wei et al., 2008; Eidson and Murphy, 2013a) , recombinant mouse CXCL10 protein (rmCXCL10; 20 μg, 0.25 μL, diluted in saline, once daily; ProSpec-Tany TechnoGene, Rehovot, Israel).

Wang W., Peng Y., Yang H., Bu H., Guo G., Liu D., Shu B., Tian X., Luo A., Zhang X, & Gao F. (2017). Potential role of CXCL10/CXCR3 signaling in the development of morphine tolerance in periaqueductal gray. Neuropeptides, 65.

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