CGS 21680 is a selective adenosine A2A receptor agonist with an IC50 value of 22nM[1]. This product is in free form, which is unstable, we recommend the stable salt form CGS 21680 Hydrochloride (GC11978) with the same biological activity. CGS 2168 enhances the release of excitatory transmitter amino acids in the ischemic rat cerebral cortex[2]. CGS 21680 accelerates the resequestration of cytoplasmic calcium and inhibits the proinflammatory activity of human neutrophils[3].
In vitro, CGS 21680 (1µM) treatment of human urothelial cell line (UROtsa cells) and human neutrophils for 3h significantly reduced cell migration induced by uropathogenic Escherichia coli (UPEC)[4].
In vivo, CGS 21680 (0.1mg/kg) treated humanized NSG mice by intraperitoneal injection had a dual effect, increasing weight loss, reducing T cells, and increasing serum human IL-6 concentrations, but reducing hepatic leukocyte infiltration and serum human TNF-α concentrations[5]. CGS 21680 (0.1mg/kg) was intraperitoneally injected into mice with pleurisy, which significantly reduced the levels of inflammatory factors, neutrophil infiltration and the extent of lung injury[6]. CGS 21680 (0.1mg/kg) was intraperitoneally injected into mice with spinal cord injury, which reduced tissue damage, influx of myeloperoxidase-positive leukocytes, nuclear factor-κB activation and iNOS expression in spinal cord tissue, and reduced JNK MAPK activation in spinal cord oligodendrocytes[7].
References:
[1] Varani K, Gessi S, Merighi S, et al. Adenosine A2A receptors of human circulating blood elements[J]. Drug development research, 1998, 45(3‐4): 253-260.
[2] O'regan M H, Simpson R E, Perkins L M, et al. The selective A2 adenosine receptor agonist CGS 21680 enhances excitatory transmitter amino acid release from the ischemic rat cerebral cortex[J]. Neuroscience letters, 1992, 138(1): 169-172.
[3] Anderson R, Visser S S, Ramafi G, et al. Accelerated resequestration of cytosolic calcium and suppression of the pro‐inflammatory activities of human neutrophils by CGS 21680 in vitro[J]. British journal of pharmacology, 2000, 130(4): 717-724.
[4] Säve S, Mohlin C, Vumma R, et al. Activation of adenosine A2A receptors inhibits neutrophil transuroepithelial migration[J]. Infection and immunity, 2011, 79(8): 3431-3437.
[5] Geraghty N J, Adhikary S R, Watson D, et al. The A2A receptor agonist CGS 21680 has beneficial and adverse effects on disease development in a humanised mouse model of graft-versus-host disease[J]. International Immunopharmacology, 2019, 72: 479-486.
[6] Impellizzeri D, Di Paola R, Esposito E, et al. CGS 21680, an agonist of the adenosine (A2A) receptor, decreases acute lung inflammation[J]. European journal of pharmacology, 2011, 668(1-2): 305-316.
[7] Genovese T, Melani A, Esposito E, et al. The selective adenosine A2A receptor agonist CGS 21680 reduces JNK MAPK activation in oligodendrocytes in injured spinal cord[J]. Shock, 2009, 32(6): 578-585.
CGS 21680是一种选择性腺苷A2A受体激动剂，IC50值为22nM[1]。本产品是游离形式，游离形式不稳定，推荐具有相同生物学活性的稳定盐形式CGS 21680 Hydrochloride（GC11978）。CGS 2168能够增强缺血大鼠大脑皮层的兴奋性递质氨基酸释放[2]。CGS 21680能够加速胞质钙的再隔离和抑制人中性粒细胞的促炎活性[3]。
在体外，CGS 21680（1µM）处理人尿路上皮细胞系（UROtsa细胞）和人中性粒细胞3h，显著减少了尿路致病性大肠杆菌（UPEC）引起的细胞迁移[4]。
在体内，CGS 21680（0.1mg/kg）通过腹腔注射治疗人源化NSG小鼠，具有双重影响作用，增加了体重减轻，减少了T细胞，增加了血清人IL-6浓度，但减少了肝白细胞浸润和血清人TNF-α浓度[5]。CGS 21680（0.1mg/kg）通过腹腔注射治疗胸膜炎小鼠，显著降低了炎症因子水平，减少了中性粒细胞浸润和肺损伤的程度[6]。CGS 21680（0.1mg/kg）通过腹腔注射治疗脊髓损伤小鼠，减少了脊髓组织中组织损伤、髓过氧化物酶阳性白细胞的内流、核因子-κB活化和iNOS表达，降低脊髓少突胶质细胞中的JNK MAPK活化[7]。