BAY 60-6583 is a high-affinity, highly selective adenosine A2B receptor agonist (EC50 = 2.8nM) [1]. BAY 60-6583 activates the A2B receptor, triggering cAMP signaling and preferential activation of ERK1/2 kinases, thereby exerting anti-inflammatory, antioxidant, and protective effects against cardiac, renal, and cerebral ischemia [2-3]. BAY 60-6583 is primarily used to study ischemia-related injury [4].
In RAW264.7 cells, BAY 60-6583 (0-5μM; 48h) significantly reduced proliferation of cell in a dose-dependent manner [5]. In bone marrow osteoclast, BAY 60-6583 (5μM; 48h) stimulation significantly reduces macrophage colony-stimulating factor-induced osteoclast proliferation [6]. In A549 cells, BAY 60-6583 (1μM; 96h) enhances cell migration and actin remodeling [7].
In MDA-MB-453-luc cells xenograft tumor mouse model, BAY 60-6583 (20μg; iv; 25d) enhances the anti-tumor activity of CAR-T cells [8]. In C57BL6 mice, BAY 60-6583 (100μg/kg; iv; 15min) increases p-Akt and IL-10 levels [9].
References:
[1]. Aherne C M, Saeedi B, Collins C B, et al. Epithelial-specific A2B adenosine receptor signaling protects the colonic epithelial barrier during acute colitis[J]. Mucosal immunology, 2015, 8(6): 1324-1338.
[2]. Bulli I. Adenosine A2B receptors and carbonic anhydrase: new therapeutic targets for cerebral ischemia[J]. 2022.
[3]. Khayat M T, Hanif A, Geldenhuys W J, et al. Adenosine receptors and drug discovery in the cardiovascular system[M]//Frontiers in Cardiovascular Drug Discovery: Volume 4. Bentham Science Publishers, 2019: 16-64.
[4]. Tian Y, Piras B A, Kron I L, et al. Adenosine 2B receptor activation reduces myocardial reperfusion injury by promoting anti‐inflammatory macrophages differentiation via PI3K/Akt pathway[J]. Oxidative medicine and cellular longevity, 2015, 2015(1): 585297.
[5]. Oh Y T, Lee N K. A2b adenosine receptor stimulation down-regulates M-CSF-mediated osteoclast proliferation[J]. Biomedical Science Letters, 2017, 23(3): 194-200.
[6]. Kim H S, Lee N K. The Regulation of p27Kip-1 and Bcl2 Expression Is Involved in the Decrease of Osteoclast Proliferation by A2B Adenosine Receptor Stimulation[J]. Biomedical Science Letters, 2017, 23(4): 327-332.
[7]. Oyama M, Sakamoto M, Kitabatake K, et al. Involvement of cannabinoid receptors and adenosine A2B receptor in enhanced migration of lung cancer A549 cells induced by γ-Ray irradiation[J]. Biological and Pharmaceutical Bulletin, 2024, 47(1): 60-71.
[8]. Tang J, Zou Y, Li L, et al. BAY 60-6583 enhances the antitumor function of chimeric antigen receptor-modified T cells independent of the adenosine A2b receptor[J]. Frontiers in pharmacology, 2021, 12: 619800.
[9]. Ni Y, Liang D, Tian Y, et al. Infarct-sparing effect of adenosine A2B receptor agonist is primarily due to its action on splenic leukocytes via a PI3K/Akt/IL-10 pathway[J]. Journal of Surgical Research, 2018, 232: 442-449.
BAY 60-6583是一种高亲和力、高选择性腺苷A2B受体激动剂（EC50 = 2.8nM） [1]。BAY 60-6583可激活A2B受体，触发cAMP信号传导并优先激活ERK1/2激酶，从而发挥抗炎、抗氧化和保护心脏、肾脏和脑缺血的作用 [2-3]。BAY 60-6583主要用于研究缺血相关损伤 [4]。
在RAW264.7细胞中，BAY 60-6583（0-5μM；48h）以剂量依赖性方式显著降低细胞的增殖 [5]。在骨髓破骨细胞中，BAY 60-6583（5μM；48h）刺激可显著降低巨噬细胞集落刺激因子诱导的破骨细胞增殖 [6]。在A549细胞中，BAY 60-6583（1μM；96h）可增强细胞迁移和肌动蛋白重塑 [7]。
在MDA-MB-453-luc细胞异种移植肿瘤小鼠模型中，BAY 60-6583（20μg/kg；iv；25d）可增强CAR-T细胞的抗肿瘤活性 [8]。在C57BL6小鼠中，BAY 60-6583（100μg/kg；iv；15min）可提高p-Akt和IL-10水平 [9]。