Inhibitor tumor necrosis factor

Jones RE, Moreland LW Tumor necrosis factor inhibitors for rheumatoid arthritis. Bull Rheum Dis 1999 48 14. 

Weinberg JM et al Biologic therapy for psoriasis An update on the tumor necrosis factor inhibitors infliximab, etanercept, and adalimumab, and the T-cell-targeted therapies efalizumab and alefacept. J Drugs Dermatol 2005 4 544. [PMID 16167412]... 

Drug Anakinra Trade Name Kineret Usual Dosage Subcutaneous injection 100 mg/d. Special Considerations Can be used alone or with other antiarthritic agents, but should not be used with tumor necrosis factor inhibitors. 

Anderson, P.J. 2005. Tumor necrosis factor inhibitors clinical implications of their different immunogenicity profiles. Semin. Arthritis Rheum. 34 19-22. 

The oxazolidinone-based compounds are the most common (Figure 23.1), and examples include antibacterial,27-28 adhesion receptor antagonists,29-30 tumor necrosis factor inhibitors,31 platelet aggregation inhibitors,32 antimigraine drugs,33 and monoamine oxidase inhibitors.3435 In one case, an oxazolidinone has been used as a transdermal drug delivery agent.36... 

Krueger, G. and K. Callis, Potential of tumor necrosis factor inhibitors in psoriasis and psoriatic arthritis. Arch. Dermatol., 2004, 140 218-25. 

Chakravarty EF, Michaud K, Wolfe F. Skin cancer, rheumatoid arthritis and tumor necrosis factor inhibitors. J Rheumatol 2005 32 2130-215. 

Gomez-Reino JJ, CarmonaL, Valverde VR, et al. Treatment of rheumatoid arthritis with tumor necrosis factor inhibitors may predispose to significant increase in tuberculosis risk A multicenter active-surveillance report. Arthritis Rheum 2003 48 2122-2127. 

Calabrese L. The yin and yang of tumor necrosis factor inhibitors. Cleveland Chnic J Med 2006 73 251-256. 

Erythropoietin has remained the best-selling human medicine for the past 3 years, followed by Lipitor (Atorvastatin), and both of these had over 12 billion in sales [20-22]. The sales of erythropoietin in Japan were over 1 billion. Tumor necrosis factor inhibitors, interferons, and insulins with, respectively, sales of 8.6 billion, 7.3 billion, and 6.5 billion in 2005 were the third, fourth, and fifth bestselling products after EPO and Lipitor (Table 1.5-8) [20-22, 24, 25]. The time taken to reach 1 billion annual sales for monoclonal antibodies has varied and was much faster for follow up and cancer products (Fig. 1.5-1). Rituxan is the leading antibody since 2003 by sales. The growth of Avastin and Erbitux has been much faster as compared to Herceptin and took only two years to reach 1 billion sales. 

Naguwa SM. Tumor necrosis factor inhibitor therapy for rheumatoid arthritis. N Y Acad Sci 2005 1051 709-715. 

Mohan AK, Cote TR, Block JA, et al. Tuberculosis following the use of etanercept, a tumor necrosis factor inhibitor. Clin Infect Dis 2004 39 295-299. 

HBV, hepatitis B HCV, hepatitis C IAP, inhibitor of apoptosis protein DBM, IAP binding motifs INCA, inhibitory CARD NASH, non-alcoholic steatohepatitis PCD, programmed cell death PCI, pan-caspase inhibitor OA, osteoarthritis RA, rheumatoid arthritis Smac, second mitochondria-derived activator of caspases TRAIL, tumor necrosis factor-related apoptosis-inducing ligand. 

Etanercept is a fully human dimeric fusion protein composed of human TNF-a p75 receptor fused to the Fc portion of human IgG 1.41 It acts as a tumor necrosis factor-a (TNF-a) inhibitor by binding to and inactivating TNF-a, thus preventing interactions with its cell surface receptors.41 This agent is useful for chronic moderate to severe plaque psoriasis and for psoriatic... 

Compounds 674-676 are potent orally bioavailable inhibitors of tumor necrosis factor-a (TNF-a) production <2004BML4267, 2004JME2724>. 

Liu, H. et al., Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin, Mol. Cell. Biol., 20, 2198, 2000. 

NO acts as an autocrine factor that mediates HIV-1 replication as at the molecular level, NO seems to stimulate long-terminal repeat-mediated transcription [125]. It was noted that exogenous NO increases replication of HIV-1 T-tropic isolates in primary T cells or T-cell lines, and inhibitors of iNOS partly block HIV-1 replication, especially that induced by tumor necrosis factor a [125]. The contrasting effects of exogenous NO, particularly NO donors, may depend on the type of NO donors, their releasing kinetics, and the dose used in the study design. 

Matthews, N., Neale, M.L., Jackson, S.K., and Stark, J.M., 1987, Tumor cell kilhng by tumor necrosis factor inhibition by anearobiotic condition, free-radical scavengers and inhibitors of arachidonate metabolism. Immunology 62 153-155 Miller, M.G., Rodgers, A., and Cohen, G.M., 1986, Mechanisms oftoxicity of naphthoquinones to isolated hepatocytes. Biochem. Pharmacol. 35 1177-1184 Minko, T., Kopeckova, P., and Kopecek, J., 1999, Comparison ofthe anticancer effect of free and HPMA copolymer-bound adtiamycin in human ovarian carcinoma cells. Pharmaceut. Res. 16 986-996... 

Higuchi, M., Singh, S., Chan, H., and Aggarwal, B. B., 1995, Protease inhibitors differentially regulate tumor necrosis factor-induced apoptosis, nuclear factor -kB activation, cytotoxicity, and differentiation. Blood 86 2248-2256. 

Kobayashi D, Watanabe N, Yamauchi N, Tsuji N, Sato T, Sasaki H, Okamoto T, Niitsu Y (1997) Protein kinase C inhibitors augment tumor-necrosis-factor-induced apoptosis in normal human diploid cells. Chemotherapy 43 415-423... 

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