1mg

Molecular Formula : 13C2 C6 H13 15N O3

Molecular Formula : C12H18D3NO4

Molecular Formula : C41 H71 N3 O8

Molecular Formula : C41H61D10N3O8

Molecular Formula : C17 H23 N O2 . Cl H

Molecular Formula : C17 2H6 H17 N O2 . Cl H

Molecular Formula : C20H19N3O2

Molecular Formula : C7H2D5ClNa2O6P2S

T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation. TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer, and tumor-infiltrating T cells that co-express PD-1 and TIM-3 exhibit the most severe exhausted phenotype. Tumor-infiltrating dendritic cells also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells. Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced antitumor responses in a mouse model of colorectal cancer. Its binding to Galectin-9 induces a range of immunosuppressive functions which enhance immune tolerance and inhibit anti-tumor immunity. TIM-3 ligation attenuates CD8+ and Th1 cell responses and promotes the activity of Treg and myeloid derived suppressor cells. In addition, dendritic cell-expressed TIM-3 dampens inflammation by enabling the phagocytosis of apoptotic cells and the cross-presentation of apoptotic cell antigens.

Molecular Formula : C22H20D4FN3OS

Molecular Formula : C4 D4 H3 N O2 S

Molecular Formula : C19 H22 N O4 S2 . Br

Molecular Formula : C19H16D6BrNO4S2

Molecular Formula : C29H38O7S

Molecular Formula : C31 H33 F3 N2 O5 S

Molecular Formula : C9H4D4ClN5S

Molecular Formula : C9H5D4Cl2N5S

Molecular Formula : C10H3D4N3O4S

Molecular Formula : C16 D4 H10 N3 O10 S . Na

Molecular Formula : C13 H19 N O3 . H2 S O4

Molecular Formula : C17H16N6O2

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseasesuch as Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-α) plays a major role in regulating growth, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells. In addition to inducing hemorrhagic necrosis of tumors, studies indicate TNF is involved in tumor igenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, Crohn’s disease, rheumatoid arthritis and graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been 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. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. Besides inducing hemorrhagic necrosis of tumors, TNF has been 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.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. Besides inducing hemorrhagic necrosis of tumors, TNF has been 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. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn’s disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

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. TNF-β is a potent mediator of inflammatory and immune responses. It belongs to the TNF family of ligands, and signals through TNFR1 and TNFR2. TNF-β is produced by activated T and B lymphocytes, and has similar activities to TNF-α. It mediates a large variety of inflammatory, immunostimulatory, and antiviral responses.

Molecular Formula : C19H28ClNO6

Molecular Formula : C19H38N6O10 xC2H4O2

Molecular Formula : C18H37N5O9 for undeuterated

Molecular Formula : C18H36DN5O8¹⁸O . (xCH3COOH)

Molecular Formula : C13H19N5

Molecular Formula : C17 H21 N O . Cl H

Molecular Formula : C17H18D4ClNO

Molecular Formula : C14H7D4NO5

Molecular Formula : 13C6 C8 H12 Cl N O2

Molecular Formula : C21 H23 N O9

Molecular Formula : C15 D3 H12 N O3

Molecular Formula : C16 2H10 H13 N O . Cl H

Molecular Formula : C18 2H3 H11 F3 N3 O4 S

Molecular Formula : C10H6D7Cl2FN2O2S2

Molecular Formula : C50 H83 N O21

Molecular Formula : C18 D11 H15 O

Molecular Formula : C36H51BF2N2O