1390630-22-4
1390630-22-4 structure
- Name: Emapticap pegol
- Chemical Name: Emapticap pegol
- CAS Number: 1390630-22-4
- Molecular Formula:
- Molecular Weight:
- Catalog: Research Areas Cancer
- Create Date: 2022-10-12 18:23:57
- Modify Date: 2024-04-09 06:45:50
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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)[1][2][3].
| Name | Emapticap pegol |
|---|
| Description | 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)[1][2][3]. |
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| Related Catalog | |
| Target |
chemokine C-C motif-ligand 2 (CCL2)[1]; MCP-1[3] |
| In Vitro | 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[2]. NOX-E36 (1 nM) significantly inhibits CCL2-mediated migration in human monocytic leukemia cell line THP-1[2]. NOX-E36 inhibits monocyte chemotactic protein-1 (MCP-1), and blocks the inflammatory cell recruitment and differentiation of macrophages mediated by MCP-1[3]. 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[2]. mNOX-E36 abrogates the phosphorylation induced by CCL2 of AKT, ERK, p35-MAPK, respectively in mCCL2-stimulated cells (30 min)[2]. |
| In Vivo | 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[2]. 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[3]. Animal Model: Non-irradiated immunocompetent C57BL/6 mice injected with syngeneic AML1/ETO9a-expressing primary murine leukemia cells[2] 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)[3] 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. |
| References |
[2]. Rodrigo, et al. Effects of CCL2/CCR2 Blockade in Acute Myeloid Leukemia. Blood. |
| No Any Chemical & Physical Properties |