1. GPCR/G Protein
  2. CXCR
    Virus Protease
  3. Plerixafor octahydrochloride

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

Cat. No.: HY-50912 Purity: >98.0%
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 24 publication(s) in Google Scholar

Other Forms of Plerixafor octahydrochloride:

Top Publications Citing Use of Products

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

    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.

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

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

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

    IC50 & Target[1][5]


    44 nM (IC50)




    1-10 nM (EC50)


    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].

    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.

    Clinical Trial
    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

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

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

    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.
    Cell Assay

    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

    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.
    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.


    Purity: >98.0%

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    Plerixafor octahydrochlorideAMD3100 octahydrochlorideJM3100 octahydrochlorideSID791 octahydrochlorideCXCRHIVVirus ProteaseCXC chemokine receptorsC-X-C motif chemokine receptorsHuman immunodeficiency virusInhibitorinhibitorinhibit

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