PSB-1115 (potassium salt) is a selective A2B Adenosine Receptor antagonist [1]. PSB-1115 (potassium salt) can inhibit the expression of the TRPV1 gene, reduce calcium ion influx, and thereby regulate the sensory hypersensitivity and pain-related behaviors in animals[2]. PSB-1115 (potassium salt) has been widely used in mouse models of middle cerebral artery occlusion to reduce the infarct area[3].
In vitro, PSB-1115 (potassium salt) treatment for 15 minutes significantly inhibited the increase in cAMP induced by adenosine (100μM) in T84 cells, with an IC50 value of 84nM[4]. Treatment with 1µM PSB-1115 (potassium salt) for 24 hours resulted in a significant increase in the expression levels of p-JNK1/2 and JNK1/2 in MDA-MB-231 cells[5].
In vivo, PSB-1115 (potassium salt) treatment at a dose of 1mg/kg/day via peritumoral injection for 4 consecutive days significantly inhibited tumor growth in the melanoma mouse model and led to a significant reduction in the number of tumor-infiltrating CD11b+ Gr1+ cells in the in the tumors of mice[6]. A single intravenous injection of 10mg/kg dose of PSB-1115 (potassium salt) for 10min significantly inhibited the tachycardia and the dilation of the kidneys and mesenteric blood vessels caused by A1-receptor bitopic ligand VCP746 in rats[7]. For a consecutive week, 1mg/kg dose of PSB-1115 (potassium salt) was intraperitoneally injected into mice carrying B16.F10 tumors every day, resulting in a significant decrease in VEGF expression and microvessel density in the tumor tissues[8].
References:
[1] Rüsing D, Müller C E, Verspohl E J. The impact of adenosine and A2B receptors on glucose homoeostasis[J]. Journal of Pharmacy and Pharmacology, 2006, 58(12): 1639-1645.
[2] Hu X, Adebiyi M G, Luo J, et al. Sustained elevated adenosine via ADORA2B promotes chronic pain through neuro-immune interaction[J]. Cell Reports, 2016, 16(1): 106-119.
[3] Weitzel L B, Grewal H, Herson P S, et al. Abstract T P82: The Role of the A2B Receptor in a Mouse Model Of Stroke[J]. Stroke, 2015, 46(suppl_1): ATP82-ATP82.
[4] Asano T, Noda Y, Tanaka K I, et al. A2B adenosine receptor inhibition by the dihydropyridine calcium channel blocker nifedipine involves colonic fluid secretion[J]. Scientific Reports, 2020, 10(1): 3555.
[5] Zelepuga E A, Chingizova E A, Menchinskaya E S, et al. Anticancer Activity of Triterpene Glycosides Cucumarioside A0-1 and Djakonovioside A Against MDA-MB-231 as A2B Adenosine Receptor Antagonists[J]. International Journal of Molecular Sciences, 2025, 26(21): 10327.
[6] Iannone R, Miele L, Maiolino P, et al. Blockade of A2b adenosine receptor reduces tumor growth and immune suppression mediated by myeloid-derived suppressor cells in a mouse model of melanoma[J]. Neoplasia, 2013, 15(12): 1400-IN10.
[7] Cooper S L, Wragg E, March J, et al. Effects of an Adenosine Receptor Bitopic Ligand on The Cardiovascular System[J]. The FASEB Journal, 2020, 34(S1): 1-1.
[8] Sorrentino C, Miele L, Porta A, et al. Myeloid-derived suppressor cells contribute to A2B adenosine receptor-induced VEGF production and angiogenesis in a mouse melanoma model[J]. Oncotarget, 2015, 6(29): 27478.
PSB-1115 (potassium salt)是一种选择性A2B腺苷受体拮抗剂[1]。PSB-1115 (potassium salt)通过抑制TRPV1基因表达，减少钙离子内流，从而调节动物的感觉过敏和疼痛相关行为[2]。PSB-1115 (potassium salt)已广泛应用于大脑中动脉闭塞小鼠模型中以减少梗死面积[3]。
在体外，PSB-1115 (potassium salt)处理15分钟可显著抑制腺苷（100μM）诱导的T84细胞内cAMP升高，IC50值为84nM[4]。使用1µM的PSB-1115 (potassium salt)处理MDA-MB-231细胞24小时，能显著提高p-JNK1/2和JNK1/2的表达水平[5]。
在体内，连续4天每日瘤周注射1mg/kg剂量的PSB-1115 (potassium salt)，可显著抑制黑色素瘤小鼠模型的肿瘤生长，并显著减少肿瘤组织中CD11b+ Gr1+肿瘤浸润细胞的数量[6]。单次静脉注射10mg/kg剂量的PSB-1115 (potassium salt) 10分钟，能显著抑制由A1受体双位点配体VCP746引起的大鼠心动过速及肾脏和肠系膜血管扩张[7]。在携带B16.F10肿瘤的小鼠中连续一周每日腹腔注射1mg/kg剂量的PSB-1115 (potassium salt)，可显著降低肿瘤组织中VEGF表达水平和微血管密度[8]。