1. Apoptosis
  2. Apoptosis TNF Receptor
  3. RP-832c

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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RP-832c

RP-832c Chemical Structure

CAS No. : 2375823-45-1

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Description

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].

In Vitro

RP-832c (0-100 μM) shows dose-dependent inhibition on M2 polarized bone marrow-derived macrophages (BMDM), with an IC50 value of 6.184 μM, producing minimal cytotoxicity on M1 polarized macrophages and has no cytotoxicity towards two different human fetal lung fibroblast cell lines, MRC5 and IMR9[2].
RP-832c (10 μM, 24 h) significantly reduces the expression of CD206 in M2 macrophages, and briefly increases the expression of TNF-α[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

RT-PCR[2]

Cell Line: M2 macrophages
Concentration: 10 μM
Incubation Time: 0, 2, 8 and 24 h
Result: Decreased CD206 gene expression.
Resulted in an initial increase in TNF-α gene expression.
In Vivo

RP-832c (i.p., once daily for 10 days) in the CTCL tumor microenvironment inhibits tumor growth by inducing a phenotypic shift from immunosuppressive M2-like to anti-tumor M1-like macrophages[1].
RP-832c (5-10 mg/kg, s.c., once daily for 21 days) demonstrates significant preventive and therapeutic effects in the mouse model of pulmonary fibrosis[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Bleomycin (HY-108345) induced lung fibrosis model models established in 6-8-week-old C57BL/6 mice[2]
Dosage: 5 and 10 mg/kg for prevention group and 10 mg/kg for treatment group
Administration: Subcutaneous injection (s.c.), once daily for 21 days
Result: significantly reduced collagen deposition in a dose-dependent manner with the alveolar structure well-preserved and the degree of fibrosis mild in prevention group.
Significantly reduces the degree of already formed fibrosis , reduced TNF-α, IL-6, IL-10, IFN-γ, CXCL1/2, etc and the expression of TGF-β1 and MMP-13 in treatment group.
Observed no significant toxicity at a dose of up to 50 mg/kg.
Molecular Weight

1367.60

Formula

C68H94N20O11

CAS No.
Sequence

Arg-Trp-Lys-Phe-Gly-Gly-Phe-Lys-Trp-Arg

Sequence Shortening

RWKFGGFKWR

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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RP-832c
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HY-P11107
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