2375823-45-1
Chemical Structure
RP-832c
- CAS. Nr.: 2375823-45-1
- Formula:C68H94N20O11
- Molecular Weight:1367.60
InChIKey: WKTQRKPNEMGWEX-OWBGLTAMSA-N
SMILES: O=C(N[C@@H](CC1=CNC2=CC=CC=C12)C(N[C@@H](CCCCN)C(N[C@@H](CC3=CC=CC=C3)C(NCC(NCC(N[C@@H](CC4=CC=CC=C4)C(N[C@@H](CCCCN)C(N[C@@H](CC5=CNC6=CC=CC=C56)C(N[C@@H](CCCNC(N)=N)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CCCNC(N)=N)N
Biological Activity: RP-832c is a synthetic analogue of host defense peptides (HDP), targeting the mannose receptor CD206 on the surface of M2 polarized macrophages (Kd = 3.5 μM). RP-832c binding to CD206 induces a significant conformational change in the receptor, activating signaling pathways that lead to rapid apoptosis and repolarization of CD206-positive M2 macrophages to an M1 phenotype. RP-832c treatment significantly reduces CD206 gene expression in M2 macrophages while transiently increasing expression of TNF-α, a marker for M1 macrophages. RP-832c is used for the studies of T-cell lymphoma (CTCL) and idiopathic pulmonary fibrosis (IPF)[1][2].
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RP-832c | 99.90% | RP-832c is a synthetic analogue of host defense peptides (HDP), targeting the mannose receptor CD206 on the surface of M2 polarized macrophages (Kd = 3.5 μM). RP-832c binding to CD206 induces a significant conformational change in the receptor, activating signaling pathways that lead to rapid apoptosis and repolarization of CD206-positive M2 macrophages to an M1 phenotype. RP-832c treatment significantly reduces CD206 gene expression in M2 macrophages while transiently increasing expression of TNF-α, a marker for M1 macrophages. RP-832c is used for the studies of T-cell lymphoma (CTCL) and idiopathic pulmonary fibrosis (IPF). | ||||||||||||||||||||
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References
- [1]. Carla Portocarrero, et al; Targeting Immunosuppressive Macrophages in the Cutaneous T-Cell Lymphoma Microenvironment. Blood 2022; 140 (Supplement 1): 3146–3147.
- [2]. Ghebremedhin A, et al. A Novel CD206 Targeting Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice. Cells. 2023 Apr 26;12(9):1254. [Content Brief]
