2. GPCR/G Protein Immunology/Inflammation
  3. CXCR
  4. Peptide R

Peptide R is a cyclic peptide and a specific CXCR4 antagonist. Peptide R exhibits excellent ability to effectively remodel tumor stroma. Peptide R has potential for use in tumor research.

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Synthèse de peptides personnalisée

Peptide R

Peptide R Chemical Structure

CAS No. : 1318232-11-9

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Peptide R Related Antibodies

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CXCR CXCR1 CXCR2 CXCR3 CXCR4 CXCR7 CXCR6

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Description

Peptide R is a cyclic peptide and a specific CXCR4 antagonist. Peptide R exhibits excellent ability to effectively remodel tumor stroma. Peptide R has potential for use in tumor research[1][2].

IC50 & Target

CXCR4

 

Cellular Effect
Cell Line Type Value Description References
HT-29 IC50
5.2 3
Compound: 2
Inhibition of 12G5 anti-CXCR4 antibody binding to CXCR4 in human HT29 cells preincubated for 30 mins followed by antibody addition by FACS Canto II cytofluorometric analysis
Inhibition of 12G5 anti-CXCR4 antibody binding to CXCR4 in human HT29 cells preincubated for 30 mins followed by antibody addition by FACS Canto II cytofluorometric analysis
[PMID: 27571038]
In Vitro

Peptide R (10 μM; 48-72 h) stably reduces CXCR4 membrane and total CXCR4 protein expression in human glioblastoma U87MG cells over 48 to 72 h of treatment[2].
Peptide R (10 μM; 72 h) reduces proliferation of human glioblastoma U87MG cells by 35% relative to CXCL12-stimulated cells after 72 h of treatment[2].
Peptide R (10 μM; 72 h) significantly reduces the metabolic viability of human glioblastoma U87MG cells after 72 h of treatment[2].
Peptide R (10 μM; 20 h) significantly reduces CXCL12-induced migration of human glioblastoma U87MG cells in a 20 h Transwell assay[2].

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

Peptide R Related Antibodies

Cell Proliferation Assay[2]

Cell Line: human glioblastoma U87MG cells
Concentration: 10 μM
Incubation Time: 72 h
Result: Reduced cell number by 35% compared to CXCL12-stimulated cells at 72 h.
Reduced cell number by 20% compared to unstimulated cells at 72 h.
Showed no significant effects at 24 or 48 h.

Cell Viability Assay[2]

Cell Line: human glioblastoma U87MG cells
Concentration: 10 μM
Incubation Time: 72 h
Result: Caused a significant reduction in metabolic activity of U87MG cells at 72 h.

Cell Migration Assay[2]

Cell Line: human glioblastoma U87MG cells
Concentration: 10 μM
Incubation Time: 20 h
Result: Significantly reduced the percentage of area occupied by migrating U87MG cells.
Hampered cell migration through membrane pores, with very few cells visible on the lower side of the filter compared to CXCL12-stimulated cells.
In Vivo

Peptide R (i.p.) accesses intracranial human glioblastoma xenografts, remodels the tumor stroma via macrophage polarization, and significantly slows neoplastic progression[1].
Peptide R (2 mg/kg; i.p.; twice per day; 23 days) reduces tumor cellularity and abrogates distant glioblastoma cell dissemination, promotes M1 polarization of GAMs, and impairs intra-tumor vasculature in orthotopic U87MG xenografts in CD1 nude mice[2].

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

Animal Model: CD1 nude mice (6-week-old)[2]
Dosage: 2 mg/kg
Administration: i.p.; twice per day; 23 days (starting on cell implantation day)
Result: Reduced tumor cellularity via decreased vimentin expression.
Abrogated dissemination of glioblastoma cells to distant cerebral sites, with no vimentin-positive cells detected in the contralateral hemisphere.
Decreased accumulation of CD11b+ and CD68+ glioma-associated microglia/macrophages (GAMs) at the tumor edge, with mean CD11b fluorescence reduced by ~55% and mean CD68 fluorescence reduced by ~50% compared to vehicle-treated mice.
Promoted M1 pro-inflammatory features in GAMs, with a significant increase in mean inducible nitric oxide synthase (iNOS) fluorescence in the tumor core compared to vehicle-treated mice, and a 2-fold increase in the percentage of CD11b-iNOS colocalized area.
Induced stronger astrogliosis (glial fibrillary acidic protein expression) in tumor tissue.
Masse moléculaire

900.08

Formule

C39H57N13O8S2
CAS No.
Appearance

Solid

Color

White to off-white

Sequence

Arg-Ala-Cys-Arg-Phe-Phe-Cys (disulfide bridge:Cys3-Cys7)
Sequence Shortening

RACRFFC (disulfide bridge:Cys3-Cys7)
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Pureté et documentation
Références
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Peptide R Related Classifications

  • Calculateur de molarité

  • Calculateur de dilution

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
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:

Peptide R1318232-11-9CXCRCXC chemokine receptorsC-X-C motif chemokine receptorsCD1 nude miceCXCL12human glioblastoma U87MG cellsmicroglia reactivityM2 glioma-associated macrophageshuman glioblastoma xenograftsglioma-induced astrogliosisblood-brain barrierCXCR4M1 phenotypeInhibitorinhibitorinhibit

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