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CAS No: 1390630-22-4
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Emapticap pegol is a inhibitor of pro-inflammatory chemokine C-C motif-ligand 2 (CCL2). Emapticap pegol is a 40-nucleotide oligonucleotide aptamer, displays different Spiegelmers (L-RNA aptamer) isform in human (NOX-E36) and mouse (mNOX-E36).
体内研究：
Emapticap pegol (14.4 mg/kg, mNOX-E36; s.c.; three times per week, for 3 weeks) interferes the infiltration of M2-like macrophages into spleens of leukemia-bearing mice.Emapticap pegol (20 mg/kg, mNOX-E36; s.c.; three times per week, for 4 weeks) reduces albuminuria and restores the glomerular endothelial glycocalyx in diabetic mice.Animal Model:Non-irradiated immunocompetent C57BL/6 mice injected with syngeneic AML1/ETO9a-expressing primary murine leukemia cells
Dosage:14.4 mg/kg (mNOX-E36, Emapticap pegol of the mouse-specific CCL2 Spiegelmer)
Administration:Subcutaneous injection; three times per week for 3 weeks
Result:Abrogated this macrophage infiltration within the leukemia microenvironment.
Animal Model:Male?Apoe?KO C57BL/6J mice rendered diabetic (6-week-old)
Dosage:20 mg/kg (mNOX-E36, Emapticap pegol of the mouse-specific CCL2 Spiegelmer)
Administration:Subcutaneous injection; three times per week for 4 weeks
Result:Reduced albumin/creatinine ratio without affecting blood glucose level and weight of mice.Reduced heparanase and cathepsin L expression.
体外研究：
Spiegelmers are RNA-like molecules built from L-ribose units that are able to bind molecules such as peptides and proteins. NOX-E36, is human-specific CCL2 Spiegelmer; and mNOX-E36, is the mouse-specific CCL2 Spiegelmer. NOX-E36 (1 nM) significantly inhibits CCL2-mediated migration in human monocytic leukemia cell line THP-1. NOX-E36 inhibits monocyte chemotactic protein-1 (MCP-1), and blocks the inflammatory cell recruitment and differentiation of macrophages mediated by MCP-1.mNOX-E36 inhibits the migration and signaling pathway activation in murine hematopoietic cells, and blocks CCL2 receptor expressing Ba/F3 cells (Ba/F3-CCR2) migration (~2000 fold than normal migration) in a dose-dependent manner.mNOX-E36 abrogates the phosphorylation induced by CCL2 of AKT, ERK, p35-MAPK, respectively in mCCL2-stimulated cells (30 min).
Emapticap pegol is a inhibitor of pro-inflammatory chemokine C-C motif-ligand 2 (CCL2). Emapticap pegol is a 40-nucleotide oligonucleotide aptamer, displays different Spiegelmers (L-RNA aptamer) isform in human (NOX-E36) and mouse (mNOX-E36).
体内研究：
Emapticap pegol (14.4 mg/kg, mNOX-E36; s.c.; three times per week, for 3 weeks) interferes the infiltration of M2-like macrophages into spleens of leukemia-bearing mice.Emapticap pegol (20 mg/kg, mNOX-E36; s.c.; three times per week, for 4 weeks) reduces albuminuria and restores the glomerular endothelial glycocalyx in diabetic mice.Animal Model:Non-irradiated immunocompetent C57BL/6 mice injected with syngeneic AML1/ETO9a-expressing primary murine leukemia cells
Dosage:14.4 mg/kg (mNOX-E36, Emapticap pegol of the mouse-specific CCL2 Spiegelmer)
Administration:Subcutaneous injection; three times per week for 3 weeks
Result:Abrogated this macrophage infiltration within the leukemia microenvironment.
Animal Model:Male?Apoe?KO C57BL/6J mice rendered diabetic (6-week-old)
Dosage:20 mg/kg (mNOX-E36, Emapticap pegol of the mouse-specific CCL2 Spiegelmer)
Administration:Subcutaneous injection; three times per week for 4 weeks
Result:Reduced albumin/creatinine ratio without affecting blood glucose level and weight of mice.Reduced heparanase and cathepsin L expression.
体外研究：
Spiegelmers are RNA-like molecules built from L-ribose units that are able to bind molecules such as peptides and proteins. NOX-E36, is human-specific CCL2 Spiegelmer; and mNOX-E36, is the mouse-specific CCL2 Spiegelmer. NOX-E36 (1 nM) significantly inhibits CCL2-mediated migration in human monocytic leukemia cell line THP-1. NOX-E36 inhibits monocyte chemotactic protein-1 (MCP-1), and blocks the inflammatory cell recruitment and differentiation of macrophages mediated by MCP-1.mNOX-E36 inhibits the migration and signaling pathway activation in murine hematopoietic cells, and blocks CCL2 receptor expressing Ba/F3 cells (Ba/F3-CCR2) migration (~2000 fold than normal migration) in a dose-dependent manner.mNOX-E36 abrogates the phosphorylation induced by CCL2 of AKT, ERK, p35-MAPK, respectively in mCCL2-stimulated cells (30 min).
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