Anti-IL11RA Antibody (X209) (EnX209) is a human-derived IgG4, κ-type antibody inhibitor targeting IL11RA, with a K D of 6 nM. Anti-IL11RA Antibody (X209) blocks the IL11RA signaling pathway, inhibits ERK-dependent activation, and reduces the activation level of ERK1/2. Anti-IL11RA Antibody (X209) exerts a protective effect against fibrosis. Anti-IL11RA Antibody (X209) is applicable to studies related to liver fibrosis, cardiac fibrosis and other related conditions. Recommended isotype control: Human IgG4 kappa, Isotype Control [1] [2].
In Vivo, Anti-IL11RA Antibody (X209) (10 mg/kg; s.c.; bi-weekly; 4 weeks) abolishes ERK activation, alleviates liver fibrosis and hepatocellular injury, and regulates the expression of profibrotic genes in mice with established NASH[1]. Anti-IL11RA Antibody (X209) (10 mg/kg; i.p.; three times weekly; 7 weeks) reduces liver fibrosis levels and inflammatory gene expression in mice with advanced non-alcoholic steatohepatitis (NASH) induced by Streptozotocin [1]. Anti-IL11RA Antibody (X209) (20 mg/kg; i.p.; bi-weekly; 2 weeks) significantly attenuates AAC-induced cardiac fibrosis and ERK1/2 activation in male C57BL/6J mice[2].
In Vitro, Anti-IL11RA Antibody (X209) (24 h) inhibits the secretion of profibrotic proteins by primary human hepatic stellate cells (HSCs), with an IC50 of 5.4 pM[1]. Anti-IL11RA Antibody (X209) (2 μg/mL; 24 h) inhibits the transformation of primary human hepatic stellate cells (HSCs) into myofibroblasts induced by various NASH-related stimuli[1]. Anti-IL11RA Antibody (X209) (2 μg/mL; 15 min pre-incubation, 48 h co-incubation) potently inhibits Matrigel invasion of primary human hepatic stellate cells (HSCs) induced by PDGF and CCL2[1]. Anti-IL11RA Antibody (X209) (24 h) potently inhibits the secretion of MMP2 and TIMP1 by mouse and human cardiac fibroblasts stimulated with TGFβ1, with an IC50 in the low nM range[2].
References:
[1]. Widjaja A A, et al. IL-11 neutralising therapies target hepatic stellate cell-induced liver inflammation and fibrosis in NASH. bioRxiv, 2018: 470062.
[2]. Lim WW, et al. Antibody-mediated neutralization of IL11 signalling reduces ERK activation and cardiac fibrosis in a mouse model of severe pressure overload. Clin Exp Pharmacol Physiol. 2021;48(4):605-613.
In Vivo, Anti-IL11RA Antibody (X209) (10 mg/kg; s.c.; bi-weekly; 4 weeks) abolishes ERK activation, alleviates liver fibrosis and hepatocellular injury, and regulates the expression of profibrotic genes in mice with established NASH[1]. Anti-IL11RA Antibody (X209) (10 mg/kg; i.p.; three times weekly; 7 weeks) reduces liver fibrosis levels and inflammatory gene expression in mice with advanced non-alcoholic steatohepatitis (NASH) induced by Streptozotocin [1]. Anti-IL11RA Antibody (X209) (20 mg/kg; i.p.; bi-weekly; 2 weeks) significantly attenuates AAC-induced cardiac fibrosis and ERK1/2 activation in male C57BL/6J mice[2].
In Vitro, Anti-IL11RA Antibody (X209) (24 h) inhibits the secretion of profibrotic proteins by primary human hepatic stellate cells (HSCs), with an IC50 of 5.4 pM[1]. Anti-IL11RA Antibody (X209) (2 μg/mL; 24 h) inhibits the transformation of primary human hepatic stellate cells (HSCs) into myofibroblasts induced by various NASH-related stimuli[1]. Anti-IL11RA Antibody (X209) (2 μg/mL; 15 min pre-incubation, 48 h co-incubation) potently inhibits Matrigel invasion of primary human hepatic stellate cells (HSCs) induced by PDGF and CCL2[1]. Anti-IL11RA Antibody (X209) (24 h) potently inhibits the secretion of MMP2 and TIMP1 by mouse and human cardiac fibroblasts stimulated with TGFβ1, with an IC50 in the low nM range[2].
References:
[1]. Widjaja A A, et al. IL-11 neutralising therapies target hepatic stellate cell-induced liver inflammation and fibrosis in NASH. bioRxiv, 2018: 470062.
[2]. Lim WW, et al. Antibody-mediated neutralization of IL11 signalling reduces ERK activation and cardiac fibrosis in a mouse model of severe pressure overload. Clin Exp Pharmacol Physiol. 2021;48(4):605-613.