Boc-MLF TFA is a tripeptide compound with FPR1 antagonistic activity. Boc-MLF TFA blocks fMLF binding to FPR1 and inhibits neutrophil chemotaxis, superoxide production, and primary granule exocytosis. Boc-MLF TFA inhibits FPRL1-mediated calcium response. Boc-MLF TFA is used for research on neutrophil inflammation, infection-related inflammation, and premature rupture of membranes[1-4].
In vitro, pretreatment of Neuro2a cells with 5μM Boc-MLF TFA for 30min followed by FPRa14 treatment for 48h reduced FPRa14-induced Neuro2a cell differentiation[5]. Incubation of fMLF-stimulated human neutrophils with 5-10μM Boc-MLF TFA for 5min inhibited neutrophil superoxide production[6]. Pretreatment of U87 cells with 5μM Boc-MLF TFA for 30min followed by 0.1μM fMLF stimulation for 24h. Boc-MLF TFA attenuated fMLF-induced tumorigenic chemotaxis and migration of U87 cells[7].
In vivo, intraperitoneal injection of 25mg/kg Boc-MLF TFA for 8 days in a CT26 cell xenograft BALB/c mouse model treated with neoadjuvant chemoradiotherapy reduced tumor-infiltrating CD8α+ T cells, CD8α+CD44+ T cells, and CD8α+GzmB+ TILs, and weakened the antitumor efficacy of CCRT[8]. Intraperitoneal injection of 5mg/kg Boc-MLF TFA for 2 days in a pregnant SD rat fetal membrane inflammation model promoted an increase in fetal membrane collagen, inhibited amniotic epithelial-mesenchymal transition, and repaired fetal membrane epithelial cell structure[9].
References:[1] Stenfeldt AL, Karlsson J, Wennerås C, et al. Cyclosporin H, Boc-MLF TFA and Boc-FLFLF are antagonists that preferentially inhibit activity triggered through the formyl peptide receptor. Inflammation. 2007 Dec;30(6):224-9.
[2] Xu XW, Zhang Y, Zhao CW, et al. Lenvatinib-resistant liver cancer-derived HSP90α-containing extracellular vesicles enhance drug resistance via macrophage CXCL8 secretion. Immunol Lett. 2026 Apr;278:107122.
[3] Gong Z, Yang C, Dai W, et al. Annexin A1 exerts analgesic effect in a mouse model of medication overuse headache. iScience. 2023 Nov 17;26(11):108153.
[4] Chiu I M, Heesters B A, Ghasemlou N, et al. Bacteria activate sensory neurons that modulate pain and inflammation. Nature. 2013 Sep 5;501(7465):52-57.
[5] Cussell P J G, Howe M S, Illingworth T A, et al. The formyl peptide receptor agonist FPRa14 induces differentiation of Neuro2a mouse neuroblastoma cells into multiple distinct morphologies which can be specifically inhibited with FPR antagonists and FPR knockdown using siRNA. PLoS ONE. 2019 Jun;14(6):e0217815.
[6] Stenfeldt A L, Karlsson J, Wenneras C, et al. Cyclosporin H, Boc-MLF TFA and Boc-FLFLF are antagonists that preferentially inhibit activity triggered through the formyl peptide receptor. Inflammation. 2007 Dec;30(6):224-229.
[7] Bao Z, Chen K, Krepel S, et al. High glucose promotes human glioblastoma cell growth by increasing the expression and function of chemoattractant and growth factor receptors. Transl Oncol. 2019 Sep;12(9):1155-1163.
[8] Chiang S, Huang K, Chen W, et al. Polymorphism of formyl peptide receptor 1(FPR1) reduces the therapeutic efficiency and antitumor immunity after neoadjuvant chemoradiotherapy(CCRT) treatment in locally advanced rectal cancer. Cancer Immunol Immunother. 2021;70(12):2937-2950.
[9] Huang X, Liao E, Liao J, et al. FPR1 antagonist(Boc-MLF TFA) inhibits amniotic epithelial-mesenchymal transition. Current Medical Science. 2024 Feb;44(1):187-194.
















