3-Aminopropionitrile fumarate 2:1 is an irreversible lysyl oxidase (LOX) inhibitor [1]. 3-Aminopropionitrile fumarate 2:1 reduces the stability of the fibril network by inhibiting LOX-catalyzed collagen-elastin cross-linking [2]. 3-Aminopropionitrile fumarate 2:1 is used to study fibrosis, scar formation, metabolic disorders, and tumor invasion [3-4].
In MT6 cells, pretreatment with 3-Aminopropionitrile fumarate 2:1 (625μM; 48h) reduces the cytotoxicity of chemotherapeutic drugs. [5]. In Caco2 PLEKHA7 KO cells, 3-Aminopropionitrile fumarate 2:1 (150μM; 14d) treatment inhibits cell invasion [6].
In thoracic Alzheimer's disease (TAD) mice model, 3-Aminopropionitrile fumarate 2:1 (0.25% wt/vol; po; 28d) induced a significant upregulation of aortic gene expression and plasma MMP8 levels in mice [7]. In C56BL/6 mice, oral 3-Aminopropionitrile fumarate 2:1 (0.25% wt/vol; po; 100d) combined with periaortic elastase can induce chronic late abdominal aortic aneurysm [8].
References:
[1]. Wilk A, Grajkowski A, Phillips L R, et al. The 4-[N-methyl-N-(2, 2, 2-trifluoroacetyl) amino] butyl group as an alternative to the 2-cyanoethyl group for phosphate protection in the synthesis of oligodeoxyribonucleotides[J]. The Journal of Organic Chemistry, 1999, 64(20): 7515-7522.
[2]. Martínez-Martínez E, Rodríguez C, Galán M, et al. The lysyl oxidase inhibitor (β-aminopropionitrile) reduces leptin profibrotic effects and ameliorates cardiovascular remodeling in diet-induced obesity in rats[J]. Journal of molecular and cellular cardiology, 2016, 92: 96-104.
[3]. Lata A, Gowri C, Dhar S C, et al. Topical β-aminopropionitrile and biochemistry of granuloma tissue[J]. Journal of Surgical Research, 1988, 44(1): 67-72.
[4]. Halsey G. Cellular Mechanism of Pentagalloyl Gucose-Mediated Prevention and Reversal of Abdominal Aortic Aneurysms[D]. Clemson University, 2023.
[5]. Schütze F, Röhrig F, Vorlová S, et al. Inhibition of lysyl oxidases improves drug diffusion and increases efficacy of cytotoxic treatment in 3D tumor models[J]. Scientific reports, 2015, 5(1): 17576.
[6]. Daulagala A C, Cetin M, Nair-Menon J, et al. The epithelial adherens junction component PLEKHA7 regulates ECM remodeling and cell behavior through miRNA-mediated regulation of MMP1 and LOX[J]. bioRxiv, 2024.
[7]. Zhang C, Niu K, Ren M, et al. Targeted inhibition of matrix metalloproteinase-8 prevents aortic dissection in a murine model[J]. Cells, 2022, 11(20): 3218.
[8]. Lu G, Su G, Davis J P, et al. A novel chronic advanced stage abdominal aortic aneurysm murine model[J]. Journal of vascular surgery, 2017, 66(1): 232-242. e4.
3-Aminopropionitrile fumarate 2:1是一种不可逆赖氨酰氧化酶（LOX）抑制剂 [1]。3-Aminopropionitrile fumarate 2:1通过抑制LOX催化的胶原-弹性蛋白交联来降低纤维网络的稳定性 [2]。3-Aminopropionitrile fumarate 2:1用于研究纤维化、瘢痕形成、代谢紊乱和肿瘤侵袭 [3-4]。
在MT6细胞中，用3-Aminopropionitrile fumarate 2:1（625μM；48h）预处理可降低化疗药物的细胞毒性 [5]。在Caco2 PLEKHA7 KO细胞中，用3-Aminopropionitrile fumarate 2:1（150μM；14d）治疗抑制细胞的侵袭 [6]。
在胸腔阿尔茨海默病（TAD）小鼠模型中，3-Aminopropionitrile fumarate 2:1（0.25% wt/vol；po；28d）诱导小鼠主动脉基因表达和血浆MMP8水平显著上调 [7]。在C56BL/6小鼠中，口服3-Aminopropionitrile fumarate 2:1（0.25% wt/vol；po；100d）联合主动脉周围弹性蛋白酶可诱发慢性晚期腹主动脉瘤 [8]。