BAY 60-6583

910487-58-0

379.44

DMSO : 100 mg/mL (263.55 mM; Need ultrasonic)

GPCR/G Protein

BAY 60-6583 is a potent and high-affinity agonist of adenosine A_2B receptor (EC₅₀ = 3 nM) over A1, A2A, and A3 receptors. BAY 60-6583 binds to mouse, rabbit, and dog A2BAR with K_i values of 750 nM, 340 nM and 330 nM, respectively. BAY 60-6583 has a cardioprotective effect in a myocardial ischemia model^[1][5]. In Vitro: BAY 60-6583 exhibits EC₅₀ values for receptor activation >10, 000 nM for both A1 and A2A AR and 3 nM for A2B AR subtype in CHO cells expressing recombinant human A1, A2A or A2B ARs^[1].
BAY 60-6583(0-10 uM) exhibits the maximum agonist effect of BAY in the absence of siRNA is 68 %, which is significantly different from that in the presence of 5, 50 and 500 nM siRNA (54%, 48% and 36%, respectively). It exhibits EC₅₀ values of BAY in the absence and presence siRNA with 98+/-22, 102+/-17, 127+/-31 and 93+/-19 nM, respectively, in T24 cells^[3].
BAY 60-6583 (5 uM; 24 hours) increases the accumulation of cells at the G1 phase with a decrease in G2/M phase in RAW264.7 preosteoclasts^[4].
BAY 60-6583 (5 uM; 24 hours) specifically inhibits the activation of Akt by M-CSF, whereas M-CSF-induced ERK1/2 activation is not affected by BAY 60-6583 treatment in RAW264.7 preosteoclasts^[4].
In Vivo: BAY 60-6583 (intravenous injection; 100 mcg/kg) reduces the infarction area just prior to reperfusion in ischaemic rabbit hearts^[1].
BAY 60-6583 (intraperitoneal injection; 2 mg/kg) attenuates LPS-induced lung injury, pre-treatment with this compound can significantly decrease LPS-increased IL-6 levels in WT-mice, In contrast, BAY 60-6583 treatment is ineffective in abrogating these inflammatory parameters in A2BAR^?/? mice^[2].
BAY 60-6583 (intratumoral administration) causes a significant increase in tumor-infiltrating MDSCs, it does not affect neither their ability to suppress T-cell proliferation nor their degree of maturation, it also stimulates the production of IL-10 and CCL2 in the tumor tissue^[5].