This product is freeze dried. All water molecules have been removed.
Every lot is tried & tested in a relevant biological assay.
0.1 EU per 1 µg of the protein by the LAL method & lyophilized from a 0.2 µm filtered solution.
- Ware, C. et al. (1998) Thomson, A.W. ed. The Cytokine Handbook 3rd ed., San Diego, CA, 549.
- Alomone Labs Recombinant human TNF-alpha protein induces cytolysis in HeLa cells.Cells were incubated with increasing Recombinant human TNF-alpha protein (#T-100) concentrations in the presence of 1µg/ml actinomycin D. Cell death was determined after 24 h by the XTT methods and plotted against Recombinant human TNF-alpha protein concentrations (ED50 = 12.5 pg/ml).
TNF-α is a cytokine that binds to TNFR-55 and TNFR-75 receptors which are expressed on all somatic cells. It is derived from several types of cells but especially by activated monocytes1-2 and can induce cell death of certain tumor cell lines3. It is a potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia. Under certain conditions it can stimulate cell proliferation and induce cell differentiation.
The secretion of the acute phase protein TNF-α initiates a cascade of cytokines and increases vascular permeability, thereby recruiting macrophages and neutrophils to a site of bacterial, fungal, viral or parasitic infection. Without TNF-α, mice infected with gram negative bacteria experience septic shock4.
The cytokine possesses both growth stimulating properties and growth inhibitory processes, and it appears to have self-regulatory properties as well. For instance, TNF-α induces neutrophil proliferation during inflammation, but it also induces neutrophil apoptosis upon binding to the TNF-R55 receptor5.
TNF-α participates in both inflammatory disorders of inflammatory and non-inflammatory origin6. Originally, sepsis was believed to result directly from the invading bacteria itself, but it was later recognized that host system proteins, such as TNF-α induced sepsis in response.
TNF-α seems to serve as a mediator in various pathologies. A few such examples include: septic shock, cancer, AIDS, transplantation rejection, multiple sclerosis, diabetes, rheumatoid arthritis, trauma, malaria, meningitis, ischemia-reperfusion injury, adult respiratory distress syndrome, ankylosing spondylitis, inflammatory bowel disease, psoriasis, hidradenitis suppurativa and refractory asthma. Since TNF-α plays a role in several diseases, a substantial amount of research has been conducted concerning TNF-α and anti-TNF-α therapies. TNF-α inhibition can be achieved with a monoclonal antibody or with a circulating receptor fusion protein. Clinical experience so far concludes that it is safe to give TNF antagonists to cancer patients since TNF antagonist treatment results in a period of disease stabilization or better in 20% of patients with advanced cancer7-10.