2-BFI hydrochloride is a high-affinity, selective agonist of the imidazoline I2 receptor (I2R) with a Ki of 70.1nM[1]. I2R is an allosteric binding site on monoamine oxidase-B that modulates neurotransmitter metabolism and neuroprotection[2]. 2-BFI hydrochloride is commonly used in studies of neuroprotection, anti-inflammation, and traumatic brain injury (TBI)[3].
In vitro, treatment of cultured rat cortical neurons with 2-BFI hydrochloride (30-1000µM; 2-3min) selectively inhibits NMDA-evoked currents[4]. Treatment of HT-29 and HCT-116 colorectal cancer cells with 2-BFI hydrochloride (250μM; 24-48h) significantly potentiated hydroxychloroquine cytotoxicity, elevated ROS, increased early/late apoptosis, and blocked autophagic flux[5].
In vivo, 2-BFI hydrochloride (3mg/kg; i.p.; 3 days) reduced cerebral infarct volume, improved motor deficits in distal middle cerebral artery occlusion (dMCAO) rats, inhibited mTOR phosphorylation and shifted cytokine balance toward anti-inflammation[6]. 2-BFI hydrochloride (10mg/kg; i.p.; twice daily for 7 days) reversed CCI-induced mechanical and thermal hypersensitivity, and reduced spinal Iba-1 and GFAP expression and TNF-α levels in neuropathic pain rats[7].
References:
[1] Carpéné C, Collon P, Remaury A, et al. Inhibition of amine oxidase activity by derivatives that recognize imidazoline I2 sites. J Pharmacol Exp Ther. 1995;272(2):681-688.
[2] Li JX. Imidazoline I2 receptors: An update. Pharmacol Ther. 2017;178:48-56.
[3] Ni H, Rui Q, Lin X, Li D, Liu H, Chen G. 2-BFI Provides Neuroprotection Against Inflammation and Necroptosis in a Rat Model of Traumatic Brain Injury. Front Neurosci. 2019;13:674.
[4] Xu S, Chen J, Xu C, et al. 2-BFI protects against ischemic stroke by selectively acting on NR2B-containing NMDA receptors. Brain Res. 2024;1845:149284.
[5] Kowalski S, Wityk P, Raczak-Gutknecht J, Olszewska A, Zmijewski M, Kocic I. The imidazoline I2 receptor agonist 2-BFI enhances cytotoxic activity of hydroxychloroquine by modulating oxidative stress, energy-related metabolism and autophagic influx in human colorectal adenocarcinoma cell lines. Eur J Pharmacol. 2025;996:177590.
[6] Cheng Y, Zhang W, Cao W, et al. 2-BFI attenuates ischemic injury by modulating mTOR signaling and neuroinflammation in rats. Neurosci Lett. 2021;750:135766.
[7] Siemian JN, LaMacchia ZM, Spreuer V, et al. The imidazoline I2 receptor agonist 2-BFI attenuates hypersensitivity and spinal neuroinflammation in a rat model of neuropathic pain. Biochem Pharmacol. 2018;153:260-268.
2-BFI hydrochloride是高亲和力、选择性的咪唑啉I2受体(I2R)激动剂,Ki值为70.1nM[1]。I2R是单胺氧化酶B上的变构结合位点,可调节神经递质代谢和神经保护[2]。2-BFI hydrochloride常用于神经保护、抗炎和创伤性脑损伤(TBI)等研究[3]。
在体外,2-BFI hydrochloride(30-1000µM;2-3分钟)可选择性抑制培养大鼠皮层神经元中NMDA诱发的电流[4]。2-BFI hydrochloride(250µM;24-48小时)显著增强HT-29和HCT-116结肠癌细胞中羟氯喹的细胞毒性,升高活性氧(ROS)水平,增加早期/晚期凋亡,并阻断自噬通量[5]。
在体内,2-BFI hydrochloride(3mg/kg;腹腔注射;连续3天)可减少远端大脑中动脉闭塞(dMCAO)大鼠的脑梗死体积,改善运动功能缺陷,抑制mTOR磷酸化,并使细胞因子平衡向抗炎方向转变[6]。2-BFI hydrochloride(10mg/kg;腹腔注射;每日两次,连续7天)可逆转慢性缩窄性损伤(CCI)诱导的机械性和热痛觉过敏,并降低神经病理性疼痛大鼠脊髓中Iba-1和GFAP的表达及TNF-α水平[7]。
















