Tumor Necrosis Factor alpha, Mutant, Recombinant, Human (TNFa)

TNF is secreted by macrophages, monocytes, neutrophils, T-cells, NK-cells following their stimulation by bacterial LPS . Cells expressing CD4 secrete TNF-alpha while CD8 cells secrete little or no TNF-alpha. The synthesis of TNF-alpha is induced by many different stimuli including interferons, IL2 , GM-CSF.\n\nDescription: \nThe clinical use of the potent anti-tumor activity of TNF-alfa has been limited by the proinflammatory side effects including fever, dose-limiting hypotension, hepatotoxicity, intravascular thrombosis, and hemorrhage. Designing clinically applicable TNF-a mutants with low systemic toxicity has been an intense pharmacological interest. Human TNF- , which binds to the murine TNF-R55 but not to the mouse TNF-R75, exhibits retained anti-tumor activity and reduced systemic toxicity in mice compared with murine TNF-a, which binds to both murine TNF receptors. Based on these results, many TNF- mutants that selectively bind to TNF-R55 have been designed. These mutants displayed cytotoxic activities on tumor cell lines in vitro, and exhibited lower systemic toxicity in vivo. Recombinant Human TNF-alfa Variant/Mutant compared with the wild-type, has an amino acid sequence deletion from a.a. 1-7, and the following a.a. substitutes Arg8, Lys9, Arg10 and Phe157 which is proven to have more activity and with less inflammatory side effect in vivo. Recombinant Human TNF-a Variant produced in E.Coli is a single, non-glycosylated, polypeptide chain containing 151 amino acids and having a molecular mass of 16598 Dalton. The Human TNF-alpha Variant is purified by standard chromatographic techniques.\n\nAA Sequence: \nMRKRKPVAHV VANPQAEGQL QWLNRRANAL LANGVELRDN QLVVPSEGLY LIYSQVLFKG QGCPSTHVLL THTISRIAVS YQTKVNLLSA IKSPCQRETP EGAEAKPWYE PIYLGGVFQL EKGDRLSAEI NRPDYLDFAE SGQVYFGIIAF.\n\nBiological Activity: \nThe ED50 as determined by the cytolysis of murine L929 cells in the presence of Actinomycin D is < 0.05ng/ml, corresponding to a Specific Activity of 2.0x10e7 U/mg.\n\nStorage and Stability:\nLyophilized powder may be stored at -20 degrees C. Stable for 12 months at -20 degrees C. Reconstitute with sterile ddH2O, 0.1% HSA or BSA. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

T9160-10M

Size

10ug

Form

Supplied as a lyophilized powder in 0.5X PBS pH 7.0. Reconstitute with sterile dH2O to (same/more than)0.1mg/ml.

Purity

(same/more than) 95% as determined by RP-HPLC, anion-exchange FPLC and/or reducing and non-reducing SDS-PAGE Silver Stained gel. Endotoxin: (same/less than)0.1ng/ug (IEU/ug))

References

1. Who might be predisposed to the development of serious side effects when treated with TNF-alpha antagonist?\n\nClin Exp Rheumatol 2006 Mar-Apr;24(2):211; author reply 211\n\n2. The effect of periodontal therapy on TNF-alpha, IL-6 and metabolic control in type 2 diabetics.\n\nJ Dent Hyg 2006 Spring;80(2):7\n\n3. Cell to cell contact through ICAM-1-LFA-1 and TNF-alpha synergistically contributes to GM-CSF and subsequent cytokine synthesis in DBA/2 mice induced by 1,3-beta-D-Glucan SCG.\n\nJ Interferon Cytokine Res 2006 Apr;26(4):235-47\n\n4. TNF-alpha is necessary for induction of coronary artery inflammation and aneurysm formation in an animal model of Kawasaki disease.\n\nJ Immunol 2006 May 15;176(10):6294-301\n\n5. Interleukin-17 acts i ndependently of TNF-alpha under arthritic conditions.\n\nJ Immunol 2006 May 15;176(10):6262-9\n\n6. Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J.\n\nJ Am Coll Surg 2006 May;202(5):788-96