2. NF-κB Apoptosis
  3. NF-κB Apoptosis TNF Receptor Caspase
  4. RP-182

RP-182 is a synthetic immunomodulatory peptide that exerts anti-tumor effects by targeting the mannose receptor CD206 (Kd = 8 μM) on the surface of tumor-associated macrophages (TAMs). RP-182 induces a conformational switch of the CD206 receptor, which activates NF-κB signaling and phagocytosis in CD206high TAMs. RP-182 has dual function: activation of canonical NF-κB signaling, triggering TNFα secretion and autocrine activation of the TNF receptor 1 (TNFR1), leading to activation of caspase 8, apoptosis, and cell death. RP-182 is used in pancreatic cancer and melanoma research.

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RP-182

RP-182 Chemical Structure

CAS No. : 1895883-60-9

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RP-182 Related Antibodies

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Description

RP-182 is a synthetic immunomodulatory peptide that exerts anti-tumor effects by targeting the mannose receptor CD206 (Kd = 8 μM) on the surface of tumor-associated macrophages (TAMs). RP-182 induces a conformational switch of the CD206 receptor, which activates NF-κB signaling and phagocytosis in CD206high TAMs. RP-182 has dual function: activation of canonical NF-κB signaling, triggering TNFα secretion and autocrine activation of the TNF receptor 1 (TNFR1), leading to activation of caspase 8, apoptosis, and cell death. RP-182 is used in pancreatic cancer and melanoma research[1][2].

IC50 & Target[1][2]

Caspase-8

 

NF-κB

 

In Vitro

RP-182 (1 nM-1 mM, 48 h) increases cell killing of CD206high M2-like macrophages with an IC50 of 17.6 μM through the MyD88/NF-κB pathway[1][2].
RP-182 (0.1 μM, 2-24 h) internalizes CD206, activated NF-κB, and increased IRF7 phosphorylation in IL-4-polarized M2 bone marrow-derived macrophages[1][2].
RP-182 (3-30 μM, 24 h) increases levels of inflammatory factors secreted by macrophages, indicating immune reprogramming[1][2].

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

RP-182 Related Antibodies

ELISA Assay[1]

Cell Line: Macrophages
Concentration: 3, 10 and 30 μM
Incubation Time: 24 h
Result: Increased the levels of TNFα and IFNγ.
In Vivo

RP-182 (20 mg/kg, i.p., every other day for 2 weeks) significantly inhibits tumor growth B16 melanoma and KP16 pancreatic model and improves mice immunogenicity[1][2].
RP-182 (20 mg/kg, i.p., once daily for 18 days) significantly alleviates pulmonary fibrosis in mice[2].

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

Animal Model: B16 melanoma allograft and KP16 pancreatic model established in eight- to twelve-week old C57B/L6 mice[1]
Dosage: 20 mg/kg
Administration: Intraperitoneal injection (i.p.), every other day for 2 weeks
Result: Inhibited tumor growth and prolonged median survival in mice
Increased CD8+ T cell infiltration.
Significantly increased IFN-γ secretion by CD8+ T cells in tumors.
Animal Model: Bleomycin (HY-108345) induced pulmonary fibrosis model established in BALB/c mice[2]
Dosage: 20 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 18 days
Result: Prolonged survival and reduced pulmonary fibrosis in mice.
Reduced CD206+ alveolar macrophages.
Molecular Weight

1374.68

Formula

C69H103N19O11
CAS No.
Sequence

Lys-Phe-Arg-Lys-Ala-Phe-Lys-Arg-Phe-Phe
Sequence Shortening

KFRKAFKRFF
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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RP-182 Related Classifications

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Help & FAQs
  • 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.

Keywords:

RP-1821895883-60-9RP182RP 182NF-κBApoptosisTNF ReceptorCaspaseNuclear factor-κBNuclear factor-kappaBTumor Necrosis Factor ReceptorTNFR?Pancreatic CancerInhibitorinhibitorinhibit

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