| Protein Name: | Tumor necrosis factor precursor (P01375) |
|---|---|
| Gene Name: | TNF |
| Description: | |
| PDB ID: | 1A8M |
| Protein Family: | PF00229, PS00251 |
| Protein Category: | Secreted Protein |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| 12-O-tetradecanoylphorbol-14-acetate (TPA) | Carcinogenesis | Topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) to the dorsal epidermis of Sencar mice induces synthesis of pro-inflammatory cytokines, including interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF-alpha),which leads to murine multistage carcinogenesis [ ADR Type 5 ] | Inhibition of pro-inflammatory cytokine gene expression and papilloma growth during murine multistage carcinogenesis by pentoxifylline |
| Amphotericin B | Neurotoxicity | Amphotericin B caused a dose-dependent increase of NO generation in interferon-gamma (IFN-gamma)-stimulated rat and mouse astrocytes, as well as in IFN-gamma + tumor necrosis factor-alpha (TNF-alpha)-activated rat astrocytoma cell line C6,which might be at least partly responsible for AMB neurotoxicity. [ ADR Type 1 ] | Amphotericin B potentiates the activation of inducible nitric oxide synthase and causes nitric oxide-dependent mitochondrial dysfunction in cytokine-treated rodent |
| diethylamine-NO | Inflammation | The NO donor diethylamine-NO (DETA-NO)reduced VCAM-1 gene expression induced by the cytokine tumor necrosis factor alpha (TNF-alpha) at the cell surface level by 65% and intracellular adhesion molecule 1 (ICAM-1) gene expression by 35%,Through this mechanism, NO may function as an immunomodulator of the vessel wall and thus mediate inflammatory events involved in the pathogenesis of atherosclerosis [ ADR Type 5 ] | Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells |
| Ibritumomab | Pathogenesis Of Side-Effects | Infusion of rituximab induced rapid complement activation, preceding the release of TNF-alpha, IL-6 and IL-8,which is correlated with pathogenesis of side-effects [ ADR Type 5 ] | Complement activation plays a key role in the side-effects of rituximab treatment |
| Indomethacin | Gastric Damage | TNF-alpha, acting via TNF-R1, is involved in indomethacin induced gastric damage and granulocyte infiltration. [ ADR Type 1 ] | Gastric damage and granulocyte infiltration induced by indomethacin in tumour necrosis factor receptor 1 (TNF-R1) or inducible nitric oxide synthase (iNOS) deficient mice |
| Indomethacin | Granulocyte Infiltration | TNF-alpha, acting via TNF-R1, is involved in indomethacin induced gastric damage and granulocyte infiltration. [ ADR Type 1 ] | Gastric damage and granulocyte infiltration induced by indomethacin in tumour necrosis factor receptor 1 (TNF-R1) or inducible nitric oxide synthase (iNOS) deficient mice |
| Ketoprofen | Intestinal Toxicity | A significant increase of tumor necrosis factor-alpha production and decreases in glutathione levels and glutathione reductase activity after treatment of the racemate and (R)-(-)-ketoprofen,suggesting induced intestinal toxicity could be correlated with a reduced oxidative damage characterized not only by a lack of changes in glutathione reductase activity but also by an absence of up-regulation of tumor necrosis factor-alpha production in intestinal mucosa. [ ADR Type 2 ] | Mechanisms involved in the attenuation of intestinal toxicity induced by (S)-(+)-ketoprofen in re-fed rats |
| METHYLENE BLUE | Mucosal Damage And The Mpo Activity | Methylene blue decreased TNF-alpha response to reperfusion injury but significantly increased the grade of the mucosal damage and the MPO activity. [ ADR Type 1 ] | Effects of the anti-ICAM-1 monoclonal antibody, allopurinol, and methylene blue on intestinal reperfusion injury |
| Pentoxifylline | Inflammation | Expression and production of TNF alpha and TNF beta were inhibited by PTX in a dose-dependent manner,which plays a key role in inflammation. [ ADR Type 1 ] | Differential regulation of TNF alpha, IL-1 beta, IL-6, IL-8, TNF beta, and IL-10 by pentoxifylline |
| Peplomycin (PLM) | Pulmonary Fibrosis | In vitro, peplomycin(PLM) up-regulated the release of interleukin-1 beta, interleukin-6, tumor necrosis factor alpha, and granulocyte-macrophage colony-stimulating factor both from human cells and from RAM and pulmonary fibroblasts,which are the causative factors of PLM-induced pulmonary fibrosis. [ ADR Type 2 ] | Contrasting influence of peplomycin and azelastine hydrochloride (Azeptin) on reactive oxygen generation in polymorphonuclear leukocytes, cytokine generation in lymphocytes, and collagen synthesis in fibroblasts |
| Sertraline | Photosensitivity Reaction | Not Available | Large-scale prediction and testing of drug activity on side-effect targets |
This panel provides information on drug category