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Your Position: Home > Protein > CD117 > CD7-H525b

Human CD117 / c-kit Protein, Fc Tag (MALS verified)

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  • Synonym
    CD117, SCFR, c-Kit, KIT
  • Source
    Human CD117 Protein, Fc Tag(CD7-H525b) is expressed from human 293 cells (HEK293). It contains AA Val 308 - Thr 516 (Accession # P10721-2).
  • Molecular Characterization
    CD117 Structure

    This protein carries a human IgG1 Fc tag at the C-terminus.

    The protein has a calculated MW of 50.2 kDa. The protein migrates as 65-90 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

  • Endotoxin
    Less than 1.0 EU per μg by the LAL method / rFC method.
  • Purity

    >95% as determined by SDS-PAGE.

    >90% as determined by SEC-MALS.

  • Formulation

    Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

    Contact us for customized product form or formulation.

  • Reconstitution

    Please see Certificate of Analysis for specific instructions.

    For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

  • Storage

    For long term storage, the product should be stored at lyophilized state at -20°C or lower.

    Please avoid repeated freeze-thaw cycles.

    This product is stable after storage at:

    1. -20°C to -70°C for 12 months in lyophilized state;
    2. -70°C for 3 months under sterile conditions after reconstitution.
SDS-PAGE
CD117 SDS-PAGE

Human CD117 Protein, Fc Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95% (With Star Ribbon Pre-stained Protein Marker).

SEC-MALS
CD117 MALS images

The purity of Human CD117 Protein, Fc Tag (Cat. No. CD7-H525b) is more than 90% and the molecular weight of this protein is around 115-140 kDa verified by SEC-MALS.

  • Background
    c-KIT activation has been shown to have oncogenic activity in gastrointestinal stromal tumors (GISTs), melanomas, lung cancer, and other tumor types. The targeted therapeutics nilotinib and sunitinib have shown efficacy in treating KIT overactive patients, and are in late-stage trials in melanoma and GIST. KIT overactivity can be the result of many genomic events from genomic amplification to overexpression to missense mutations. Missense mutations have been shown to be key players in mediating clinical response and acquired resistance in patients being treated with these targeted therapeutics.
  • Clinical and Translational Updates

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Drug Development Status

  • Number of Launched Drugs:16 Details
  • Number of Drugs in Clinical Trials:24 Details
  • Latest Research Phase:Approved

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