2. GPCR/G Protein
    Immunology/Inflammation
    Anti-infection
  3. CXCR
    HIV
    Virus Protease
  4. Plerixafor octahydrochloride

Plerixafor octahydrochloride  (Synonyms: AMD3100 octahydrochloride; JM3100 octahydrochloride; SID791 octahydrochloride)

Cat. No.: HY-50912 Purity: ≥98.0%
COA Handling Instructions

Plerixafor octahydrochloride (AMD3100 octahydrochloride) is a selective CXCR4 antagonist with an IC50 of 44 nM.

For research use only. We do not sell to patients.

Plerixafor octahydrochloride Chemical Structure

Plerixafor octahydrochloride Chemical Structure

CAS No. : 155148-31-5

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Customer Review

Based on 63 publication(s) in Google Scholar

Other Forms of Plerixafor octahydrochloride:

Top Publications Citing Use of Products

51 Publications Citing Use of MCE Plerixafor octahydrochloride

RT-PCR
WB
IF
Proliferation Assay
IHC

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Cancer Lett. 2022 Oct 7;551:215944.  [Abstract]

    Immunohistochemical staining of proliferation-related protein, Ki-67, in breast cancer after treatment with control, AMD3100 (2.5 mg/kg), Olaparib, or a combination of AMD3100 and Olaparib.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Cancer Lett. 2022 Oct 7;551:215944.  [Abstract]

    Viability of cells treated with combinations different concentrations of AMD3100 and Olaparib for 24 h.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Cell Death Dis. 2022 Feb 4;13(2):118.  [Abstract]

    PGK1 induced the CXCR4-mediated phosphorylation of AKT (p-AKT) and ERK (p-ERK), and blockade of CXCR4 signaling by AMD3100 (48 h) treatment did not alter cellular PGK1 expression in KIRC cells.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Bioact Mater. 2021 Jan 7;6(7):2039-2057.  [Abstract]

    Western blot analysis of the expression of CXCR4, integrin αvβ3, p-Jak2, Jak2, p-FAK, FAK, p-STAT3 and STAT3 in MSCs (pretreated with a CXCR4 inhibitor (AMD3100; 20 μM; pretreated with 1 h) and an integrin αvβ3 inhibitor (cyclo(-RGDfK))) after the addition of 152RM for 24 h.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Theranostics. 2021 Jan 1;11(6):2612-2633.  [Abstract]

    Caco-2 cells are incubated with vehicle or AMD3100 (1 µg/ml, 24 hours) after lentivirus transfection (LV-HOXB5), then Western blotting assays are conducted to measure the protein levels of CXCL12, HOXB5, CXCR4, p-ERK and p-ETS1 in the indicated cell lines.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Theranostics. 2021 Jan 1;11(6):2612-2633.  [Abstract]

    Transwell assays indicated that AMD3100 treatment (1 µg/ml, 24 hours) significantly decreases the migration and invasion of Caco-2-HOXB5 cells.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Adv Funct Mater. 2020, 2000309.

    NOD/SCID mice were i.p. injected with AMD3100 (4 mg/kg). After 1 h, the mice are i.v. injected with iFluor 647-labeled [email protected] At 12 h after nanoparticle injection, the mouse craniums are excised for the observation of nanoparticle bone marrow niches targeting under CLSM. Pre-treatment with AMD3100 significantly declined the bone marrow niches targeting of the nanoparticles.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Cell Mol Immunol. 2020 Mar;17(3):283-299.  [Abstract]

    ELISA of IL-1β in supernatants of BV2 cells stimulated with gp120 LAV (0.5 μg/mL) for 24 h in the presence of increasing doses of a CXCR4-specific inhibitor (AMD3100, 0.1-10 μM; prestimulated with 30 min-2 h).

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Oncogene. 2019 Jun;38(25):5021-5037.  [Abstract]

    Additional EMT-related proteins (Snail and Slug) are downregulated by AMD3100 (5 mg/kg or 3.5 mg/kg) in tumor samples from both diet groups, as quantified by immunoblotting.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Oncogene. 2019 Jun;38(25):5021-5037.  [Abstract]

    IF staining of the tumor tissue sections showed decreased Ki67 and a reversal of EMT markers indicated by increased E-cadherin and decreased N-cadherin expression in the AMD3100 (5 mg/kg or 3.5 mg/kg) treated groups.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Cell Physiol Biochem. 2018;46(3):890-906.  [Abstract]

    The protein expression of LRRC4, SDF-1, CXCR4, ERK, Slit2 and VEGF in the brain tissue of rats is determined by Western blotting.

    Plerixafor octahydrochloride purchased from MCE. Usage Cited in: Int J Biol Sci. 2017 May 5;13(5):604-614.  [Abstract]

    Epithelial cells with or without AMD3100 pretreatment are cultured in conditioned medium (CM) from LPS-treated NFs or LTA-treated NFs for 3 days, and the secretion of TNF-α in the supernatant of culture is detected by ELISA. Epithelial cells cultured in MSM are used as control. Both LPS-treated NFs and LTA-treated NFs enhanced the section of TNF-α by epithelial cells compared with control. Pretreatment of epithelial cells with AMD3100 significantly attenuates the increase of TNF-α.

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    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review

    Description

    Plerixafor octahydrochloride (AMD3100 octahydrochloride) is a selective CXCR4 antagonist with an IC50 of 44 nM.

    IC50 & Target

    125I-CXCL12-CXCR4

    44 nM (IC50)

    125I-CXCL12-CXCR7

     

    HIV-1

    1-10 nM (EC50)

    HIV-2

    1-10 nM (EC50)

    In Vitro

    The CXCR4 inhibitor Plerixafor (AMD3100) is a potent inhibitor of CXCL12-mediated chemotaxis (IC50, 5.7 nM) with a potency slightly better than its affinity for CXCR4. Treating the cells with CCX771 or CXCL11 has no effect on CXCL12-mediated MOLT-4 or U937 TEM. In contrast, 10 μM Plerixafor inhibits CXCL12-mediated TEM in both cells lines[1]. Plerixafor (10 μM)-treated cells show a moderate reduction in cell proliferation compared to CXCL12-stimulated cells, which do not reach statistical significance[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.
    In Vivo

    Plerixafor (2 mg/kg) administration to UUO mice exacerbates renal interstitial T cell infiltration, resulting in increased production of the pro-inflammatory cytokines IL-6 and IFN-γ and decreased expression of the anti-inflammatory cytokine IL-10[3]. Both perivascular and interstitial fibrosis are significantly reduced by the CXCR4 antagonist, Plerixafor (AMD3100) at 8 weeks[4]. LD50, mouse, SC: 16.3 mg/kg; LD50, rat, SC: >50 mg/kg; LD50, mouse and rat, IV injection: 5.2 mg/kg.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.
    Clinical Trial
    Molecular Weight

    794.47

    Appearance

    Solid

    Formula

    C28H62Cl8N8
    CAS No.
    SMILES

    [H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.[H]Cl.N1(CCCNCCNCCCNCC1)CC2=CC=C(C=C2)CN3CCCNCCNCCCNCC3
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    4°C, sealed storage, away from moisture

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

    H2O : 100 mg/mL (125.87 mM; Need ultrasonic)

    DMSO : < 1 mg/mL (insoluble or slightly soluble)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.2587 mL 6.2935 mL 12.5870 mL
    5 mM 0.2517 mL 1.2587 mL 2.5174 mL
    10 mM 0.1259 mL 0.6294 mL 1.2587 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  PBS

      Solubility: 120 mg/mL (151.04 mM); Clear solution; Need ultrasonic

    *All of the co-solvents are available by MCE.
    Purity & Documentation

    Purity: ≥98.0%

    COA (255 KB) HNMR (179 KB)

    Handling Instructions (2659 KB)
    References
    Cell Assay
    [2]

    U87MG cells are seeded in 96-well plates at the density of 6×103 cells in 200 μL/well and treated with CXCL12, Plerixafor or with peptide R, as described in the previous “Treatments” section. MTT (5 μg/mL) is added at each time point (24, 48, 72 h) during the final 2 h of treatment. After removing cell medium, 100 μL DMSO are added and optical densities measured at 595 nm with a LT-4000MS Microplate Reader. Measurements are made in triplicates from three independent experiments[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.
    Animal Administration
    [3][4]

    Mice[3]
    Male C57bl/6 mice (6-7 weeks old, weighing 20 g) are used. The animals are acclimated to the housing environment, which is SPF and had a temperature of 22°C and a 12h/12h light/dark cycle for a week. Then, they are randomly divided into following experimental groups, with 8 mice in each group: normal (no specific intervention), UUO+AMD3100 (mice received UUO surgery and 2 mg/kg AMD3100), and UUO+PBS (mice received UUO surgery and the same volume of PBS). AMD3100 and PBS are administered via intraperitoneal injection every day until sacrifice.
    Rats[4]
    The CXCR4 antagonist, AMD3100 dissolved in H2O, is delivered in the type 2 diabetic sand rat model at a dose of 6 mg/kg per day for 8 weeks. In complementary studies, the effect of CXCR4 antagonism (AMD3100 6mg/kg/d) on regulatory T cell numbers is examined. For these studies, AMD3100 or vehicle is delivered via minipump for a period of one week.

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

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    Keywords:

    Plerixafor octahydrochloride155148-31-5AMD3100 octahydrochlorideJM3100 octahydrochlorideSID791 octahydrochlorideCXCRHIVVirus ProteaseCXC chemokine receptorsC-X-C motif chemokine receptorsHuman immunodeficiency virusInhibitorinhibitorinhibit

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