1. Metabolic Enzyme/Protease
    Autophagy
  2. Nampt
    Autophagy

FK866 (Synonyms: Daporinad; APO866)

Cat. No.: HY-50876 Purity: 99.91%
Handling Instructions

FK866 is an effective inhibitor of nicotinamide phosphoribosyltransferase (NMPRTase) with IC50 of 0.09 nM.

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

FK866 Chemical Structure

FK866 Chemical Structure

CAS No. : 658084-64-1

Size Price Stock Quantity
Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 81 In-stock
Estimated Time of Arrival: December 31
5 mg USD 74 In-stock
Estimated Time of Arrival: December 31
10 mg USD 132 In-stock
Estimated Time of Arrival: December 31
50 mg USD 468 In-stock
Estimated Time of Arrival: December 31
100 mg USD 708 In-stock
Estimated Time of Arrival: December 31
200 mg   Get quote  
500 mg   Get quote  

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Customer Review

    FK866 purchased from MCE. Usage Cited in: Mol Med Rep. 2017 Oct;16(4):5121-5128.

    Effects of Emodin, FK866 and DEX on PMN apoptosis in SAP rats. Protein expression levels of Fas, FasL, Bax, cleaved caspase 3 and Bcl xL are detected by western blotting. β actin served as an internal control. Data are presented as the mean±standard deviation.

    FK866 purchased from MCE. Usage Cited in: J Cell Physiol. 2018 Sep 7.

    SW620 and HCT116 cells are seeded into a six-well plate for 72 hr, followed by treatment with different concentrations (100 nM and 10 μM) of FK866 for 24 hr.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    FK866 is an effective inhibitor of nicotinamide phosphoribosyltransferase (NMPRTase) with IC50 of 0.09 nM.

    IC50 & Target

    IC50: 0.09 nM (NMPRTase)

    In Vitro

    Nampt inhibition with FK866 induces significant NAD+ intracellular reduction and selectively kills MM cells. FK866-induced cell death is associated with inhibition of Nampt activity, rather than protein expression, and higher NAD+ baseline levels in MM cells than normal PBMCs confer FK866 sensitivity. FK866 abrogates the survival advantage conferred by the bone marrow microenvironment[1]. FK866 prevents the [Ca2+]i increase induced by different mitogens and reduces the Ca2+ content of TG-responsive Ca2+ stores in Jurkat and in activated PBLs. FK866 reduces the Ca2+ content of TG-responsive Ca2+ stores in Jurkat cells but not in Bcl2-Jurkat cells[2]. Inhibition of NAMPT by FK866, or inhibition of SIRT by nicotinamide decreases proliferation and triggered death of 293T cells involving the p53 acetylation pathway[3].

    In Vivo

    FK866 (30 mg/kg, i.p.) decreases the tumor burden in CB17-SCID mice, and the tumor tissue demonstrates a significant decrease in ERK phosphorylation and proteolytic cleavage of LC3[1].

    Clinical Trial
    Solvent & Solubility
    In Vitro: 

    10 mM in DMSO

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.5542 mL 12.7711 mL 25.5421 mL
    5 mM 0.5108 mL 2.5542 mL 5.1084 mL
    10 mM 0.2554 mL 1.2771 mL 2.5542 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References
    Cell Assay
    [1]

    MM1S cells (2×104 cells/well) are cultured for 72 and 96 hours in BMSC-coated 96-well plates in the presence or absence of drug. DNA synthesis is measured by (3H)-thymidine uptake, with (3H)-thymidine added (0.5 μCi/well) during the last 8 hours of cultures.

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

    Animal Administration
    [1]

    CB17-SCID mice (28-35 days old) are irradiated (200 cGy), and then inoculated subcutaneously in the right flank with 3×106 MM1S cells in 100 μL RPMI 1640. After detection of tumor (2 weeks after the injection), 7 mice are treated intraperitoneally with either vehicle or FK866 (30 mg/kg body weight) twice a day for 4 days, repeated weekly over 3 weeks. Caliper measurements of the longest perpendicular tumor diameters are performed twice a week to estimate the tumor volume using the following formula: length×width2×0.5. Tumor growth inhibition (TGI) is calculated. Animals are killed when tumors reach 2 cm3 or the mice appear moribund. Survival is evaluated from the first day of treatment until death.

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

    References
    Molecular Weight

    391.51

    Formula

    C₂₄H₂₉N₃O₂

    CAS No.

    658084-64-1

    SMILES

    O=C(C1=CC=CC=C1)N(CC2)CCC2CCCCNC(/C=C/C3=CC=CN=C3)=O

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Purity: 99.91%

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    Product Name:
    FK866
    Cat. No.:
    HY-50876
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    Cat. No.: HY-50876