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Tumor inhibitors

H Hydroxamic acids High chelating power Histone deacetylase inhibitors Matrix metalloproteinases inhibitors Tumor necrosis factor a converting enzyme Almquist et aV Massa el Lu el al. Remiszewski et al., Plumb et a(., Kelly et Buggy et al. Hanessian et al. Aranapakam et Noe et al. Duan et... [Pg.306]

MoAb, Pa no rex) Signal Pathway Inhibitors tumor-specific glycoprotein located on colorectal tumor cells antitumor activity via antibody-dependent cellular cytotoxicity (ADCC) vomiting, infusion-related reactions (fever, chills) ... [Pg.2401]

Tumor inhibitor TUMOR INHIBITOR Divinyl —MEDICINAL United States 3,244,943 1965 Hercules Powder... [Pg.647]

Diacetylphloroglucinol and its homologues have been prepared and found to be inhibitors of the herpes vims (188). Syzygiol (50), a skin tumor promotion inhibitor, has been prepared from phloroglucinol (189). The first natural morphogen (cell-differentiation agent) (51) has also been identified as a phloroglucinol derivative (190). [Pg.385]

W. R. Hanson, Prostaglandin Inhibitors in Tumor Immunology andimmunotherapj, CRC Press, Inc., Boca Raton, 1994, pp. 171—186. [Pg.502]

Folic acid deficiency Hyperthermia Phenylketonuria Rheumatic disease Virilizing tumors Drugs and chemicals Androgenic chemicals Angiotensin-converting enzyme inhibitors Captopril, enalapril Antibiotics... [Pg.314]

Farnesyl transferase from rat cells is a heterodimer consisting of a 48 kD u-snbnnit and a 46 kD /3-snbnnit. In the structure shown here, helices 2 to 15 of the u-snbnnit are folded into seven short coiled coils that together form a crescent-shaped envelope partially surrounding the /3-snbnnit. Twelve helices of the /3-snl> nnit form a novel barrel motif that creates the active site of the enzyme. Farnesyl transferase inhibitors, one of which is shown here, are potent suppressors of tumor growth in mice, but their value in humans has not been established. [Pg.278]

The structure of 1-739,749, a farnesyl transferase inhibitor that is a potent tumor growth suppressor. [Pg.278]

Heterocycles as inhibitors of tumor necrosis a-factor 99JMC2295. [Pg.232]

Antineoplastic agents that cannot be grouped under subheadings 1-9 include miltefosine which is an alkylphosphocholine that is used to treat skin metastasis of breast cancer, and crispantase which breaks down asparagine to aspartic acid and ammonia. It is active against tumor cells that lack the enzyme asparaginase, such as acute lymphoblastic leukemia cells. Side effects include irritation of the skin in the case of miltefosine and anaphylactic reactions in the case of crispantase. Another recent development is the proteasome inhibitor bortezomib which is used to treat multiple myeloma. [Pg.156]

Calpain inhibition may represent an important mechanism for future drug development. Control of calpain activity may limit the invasive properties of cells and thereby provides a possible mechanism to limit the invasiveness of tumors or inhibits the development of chronic inflammation. For the moment, pharmacological inhibitors of calpains are still not capable of differentiating among different calpain isoforms in cellular systems or in vivo. The importance of calpains in diseases will continue to stimulate the development of new and better inhibitors. [Pg.313]

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. [Pg.334]

Inhibition of hematopoietic growth factors Imatinib (Glivec ) is applied to treat chronic myeloid leukemia in Philadelphia-chromosome positive patients. In these patients, translocation of parts of chromosomes 9 and 22 results in the expression of a fusion protein with increased tyrosine kinase activity, called Bcr-Abl. Imatinib is a small Mw inhibitor selective for the tyrosine kinase activity of Bcr-Abl. Thereby, it inhibits the Bcr-Abl induced cell cycle progression and the uncontrolled proliferation of tumor cells. [Pg.411]


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See also in sourсe #XX -- [ Pg.94 ]




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Drugs tumor inhibitors

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Ovarian tumor inhibitors of tubulin

Proton pump inhibitors, tumors

Tumor necrosis factor inhibitors

Tumor necrosis factor-a inhibitor

Tumor suppressor genes cyclin dependent kinase inhibitors

Tumor-associated trypsin inhibitor

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