Description: A competitive ELISA for quantitative measurement of Human True insulin in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.

Description: ELISA

Description: Tumor Necrosis Factor- alpha (TNF- alpha) is secreted by macrophages, monocytes, neutrophils, T-cells, and NK-cells following stimulation by bacterial LPS. Cells expressing CD4 secrete TNF- alpha while cells that express CD8 secrete little or no TNF- alpha. Synthesis of TNF- alpha can be induced by many different stimuli including interferons, IL2, and GM-CSF. The clinical use of the potent anti-tumor activity of TNF- alpha has been limited by the proinflammatory side effects such as fever, dose-limiting hypotension, hepatotoxicity, intravascular thrombosis, and hemorrhage. Designing clinically applicable TNF- alpha mutants with low systemic toxicity has been of intense pharmacological interest. Human TNF- alpha that binds to murine TNF-R55 but not murine TNF-R7, exhibits retained anti-tumor activity and reduced systemic toxicity in mice compared with murine TNF- alpha, which binds to both murine TNF receptors. Based on these results, many TNF- alpha mutants that selectively bind to TNF-R55 have been designed. These mutants displayed cytotoxic activities on tumor cell lines in vitro and have exhibited lower systemic toxicity in vivo. Recombinant Human TNF- alpha High Active Mutant differs from the wild-type by amino acid subsitution of amino acids 1-7 with Arg8, Lys9, Arg10 and Phe157. This mutant form has been shown to have increased activity with less inflammatory side effects in vivo.

Description: Tumor Necrosis Factor- alpha (TNF- alpha) is secreted by macrophages, monocytes, neutrophils, T-cells, and NK-cells following stimulation by bacterial LPS. Cells expressing CD4 secrete TNF- alpha while cells that express CD8 secrete little or no TNF- alpha. Synthesis of TNF- alpha can be induced by many different stimuli including interferons, IL2, and GM-CSF. The clinical use of the potent anti-tumor activity of TNF- alpha has been limited by the proinflammatory side effects such as fever, dose-limiting hypotension, hepatotoxicity, intravascular thrombosis, and hemorrhage. Designing clinically applicable TNF- alpha mutants with low systemic toxicity has been of intense pharmacological interest. Human TNF- alpha that binds to murine TNF-R55 but not murine TNF-R7, exhibits retained anti-tumor activity and reduced systemic toxicity in mice compared with murine TNF- alpha, which binds to both murine TNF receptors. Based on these results, many TNF- alpha mutants that selectively bind to TNF-R55 have been designed. These mutants displayed cytotoxic activities on tumor cell lines in vitro and have exhibited lower systemic toxicity in vivo. Recombinant Human TNF- alpha High Active Mutant differs from the wild-type by amino acid subsitution of amino acids 1-7 with Arg8, Lys9, Arg10 and Phe157. This mutant form has been shown to have increased activity with less inflammatory side effects in vivo.

Description: TNF alpha is a homotrimer with a subunit molecular mass of 17 kD and plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, autoimmune diseases and in viral, bacterial, fungal, and parasitic infections. Besides inducing hemorrhagic necrosis of tumors, TNF was found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Description: Tumor Necrosis Factor- alpha (TNF- alpha) is secreted by macrophages, monocytes, neutrophils, T-cells, and NK-cells following stimulation by bacterial LPS. Cells expressing CD4 secrete TNF- alpha while cells that express CD8 secrete little or no TNF- alpha. Synthesis of TNF- alpha can be induced by many different stimuli including interferons, IL2, and GM-CSF. The clinical use of the potent anti-tumor activity of TNF- alpha has been limited by the proinflammatory side effects such as fever, dose-limiting hypotension, hepatotoxicity, intravascular thrombosis, and hemorrhage. Designing clinically applicable TNF- alpha mutants with low systemic toxicity has been of intense pharmacological interest. Human TNF- alpha that binds to murine TNF-R55 but not murine TNF-R7, exhibits retained anti-tumor activity and reduced systemic toxicity in mice compared with murine TNF- alpha, which binds to both murine TNF receptors. Based on these results, many TNF- alpha mutants that selectively bind to TNF-R55 have been designed. These mutants displayed cytotoxic activities on tumor cell lines in vitro and have exhibited lower systemic toxicity in vivo. Recombinant Human TNF- alpha High Active Mutant differs from the wild-type by amino acid subsitution of amino acids 1-7 with Arg8, Lys9, Arg10 and Phe157. This mutant form has been shown to have increased activity with less inflammatory side effects in vivo.

Description: Tumor necrosis factor alpha (TNF alpha) is the prototypic ligand of the TNF superfamily. TNF alpha forms a homotrimer and functions by activating two types of receptors TNF-R1 (TNF receptor type 1,p55R) and TNF-R2 (TNF receptor type 2,p75R). TNF alpha is a pleiotropic cytokine that is capable to promote inflammation, to induce apoptotic cell death, and to inhibit tumorigenesis and viral replication. TNF alpha is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Description: TNF-alpha is a pleiotrophic pro-inflammatory cytokine secreted by various cells including adipocytes, activated monocytes, macrophages, B cells, T cells and fibroblasts. It belongs to the TNF family of ligands and signals through two receptors, TNFR1 and TNFR2. TNF-alpha is cytotoxic to a wide variety of tumor cells and is an essential factor in mediating the immune response against bacterial infections. TNF-alpha also plays a role in the induction of septic shock, auto immune diseases, rheumatoid arthritis, inflammation, and diabetes. Recombinant murine TNF-alpha is a soluble 156 amino acid protein (17.3 kDa) which corresponds to C-terminal extracellular domain of the full length transmembrane protein.

Description: TNF-alpha is a pleiotrophic pro-inflammatory cytokine secreted by various cells including adipocytes, activated monocytes, macrophages, B cells, T cells and fibroblasts. It belongs to the TNF family of ligands and signals through two receptors, TNFR1 and TNFR2. TNF-alpha is cytotoxic to a wide variety of tumor cells and is an essential factor in mediating the immune response against bacterial infections. TNF-alpha also plays a role in the induction of septic shock, auto immune diseases, rheumatoid arthritis, inflammation, and diabetes. Recombinant murine TNF-alpha is a soluble 156 amino acid protein (17.3 kDa) which corresponds to C-terminal extracellular domain of the full length transmembrane protein.

Description: TNF-β is a pleiotrophic pro-inflammatory cytokine secreted by various cells including adipocytes, activated monocytes, macrophages, B cells, T cells and fibroblasts. It belongs to the TNF family of ligands and signals through two receptors, TNFR1 and TNFR2. TNF-β is cytotoxic to a wide variety of tumor cells and is an essential factor in mediating the immune response against bacterial infections. TNF-β also plays a role in the induction of septic shock, auto immune diseases, rheumatoid arthritis, inflammation, and diabetes. Recombinant rat TNF-β is a soluble 157 amino acid protein (17.3 kDa) which corresponds to C-terminal extracellular domain of the full length transmembrane protein.

Description: TNF-β is a pleiotrophic pro-inflammatory cytokine secreted by various cells including adipocytes, activated monocytes, macrophages, B cells, T cells and fibroblasts. It belongs to the TNF family of ligands and signals through two receptors, TNFR1 and TNFR2. TNF-β is cytotoxic to a wide variety of tumor cells and is an essential factor in mediating the immune response against bacterial infections. TNF-β also plays a role in the induction of septic shock, auto immune diseases, rheumatoid arthritis, inflammation, and diabetes. Recombinant rat TNF-β is a soluble 157 amino acid protein (17.3 kDa) which corresponds to C-terminal extracellular domain of the full length transmembrane protein.