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

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CD7-H525b-100ug
$360.00
In Stock - Delivery in 1-2 business days
CD7-H525b-1mg
$2,615.00
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CD7-H525b
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Product Details
Performance Data
Reviews & Citations
Resources
  • Product Details
  • Performance Data
  • Reviews & Citations
  • Important Statement
  • Resources
Synonyms

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
Other Tags and Version Biotin & Other Labeled Version

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.

Shipping and Storage

This product is shipped at ambient temperature.

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:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.
ACRO Quality Management System

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.