Human TNF-alpha Protein, His Tag, active trimer (MALS verified)
Synonym
DIF, TNF-alpha, TNFA, TNFSF2, cachexin, cachectin, TNFα
Source
Human TNF-alpha Protein, His Tag (TNA-H5228) is expressed from human 293 cells (HEK293). It contains AA Val 77 - Leu 233 (Accession # NP_000585.2).
Predicted N-terminus: Val 77
Molecular Characterization

This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 18.3 kDa. The protein migrates as 17-19 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.
>95% 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:
-20°C to -70°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.



Background
Tumor necrosis factor alpha (TNFα) is a cytokine produced primarily by monocytes and macrophages. It is found in synovial cells and macrophages in the tissues.The primary role of TNFα is in the regulation of immune cells. TNFα is able to induce apoptotic cell death, to induce inflammation, and to inhibit tumorigenesis and viral replication. Dysregulation of TNFα production has been implicated in a variety of human diseases, including major depression, Alzheimer's disease and cancer. Recombinant TNFα is used as an immunostimulant under the INN tasonermin. TNFα can be produced ectopically in the setting of malignancy and parallels parathyroid hormone both in causing secondary hypercalcemia and in the cancers with which excessive production is associated.