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Cell proliferation inhibitor

Kurogi Y, Miyata K, Okamura T, Hashimoto K, Tsutsumi K, Nasu M, Moriyasu M. Discovery of novel mesangial cell proliferation inhibitors using a three-dimensional database searching method. J Med Chem 2001 44 2304-7. [Pg.423]

IFN-y THi,Tc, NK Various cells including macrophages Inhibitor of viral replication. Inhibitor of cell proliferation. Inhibitor of IL-4-induced isotype switching... [Pg.47]

Andrews (3) and Tang (4) prepared VEGF receptor tyrosine kinase antagonists consisting of l,3-dihydro-2H-indol-2-one derivatives, (I) and (II), respectively, which were effective as abnormal cell proliferation inhibitors. [Pg.508]

Thienopyridazinones derivatives, (VI), prepared by Cooper (6) were effective as T-cell proliferation inhibitors and used in treating psoriasis, atopical dermatitis, contact dermatitis, and related disorders. [Pg.638]

Addition of the terpene, famesol, to cysteine residues near the end of protein chains is a cmcial process for transporting some proteins to the intended membrane compartment. This process thus plays an important role in cell proliferation. Inhibitors of the enzyme that catalyzes farnesyla-tion, famesyl transferase, provide yet one more mechanism for interrupting the multiplication of malignant cells. One of several synthesis of this agent... [Pg.171]

Chen, Z., Liang, H., Liu, Y. Qin, Q. (2013). 1-Azabenzanthrone-platinum (11) complex, and synthetic method and application thereof as cell proliferation inhibitor. Faming Zhuanli Shenqing, CN 103450281 A20131218. [Pg.245]

Mesangial cell proliferation inhibitors Catalyst/HipHop 7 features N/A... [Pg.275]

Cell proliferation inhibitor Ellipticine Indole alkaloid 1039... [Pg.1082]

Eflornithine (difluoromethylornithine, DFMO) inhibits the ornithine decarboxylase of the polyamine pathway, in both the trypanosome and the mammalian cell, by acting as an irreversible competitor of the natural substrate ornithine. Inhibition of ornithine decarboxylase results in depletion of the polyamines, putrescine, spermidine and spermine, which are essential for cell proliferation. Eflornithine selectively harms the parasite and not the mammalian cells, despite acting as an ornithine decarboxylase inhibitor in both cell types. This selectivity is explained by the lower rate of ornithine decarboxylase production in the parasite, as compared to mammalian cells. Due to the high turnover rate, mammalian cells are capable of quickly replenishing inhibited ornithine decarboxylase by newly... [Pg.179]

PTKs have been implicated in the regulation of a variety of biological responses such as cell proliferation, migration, differentiation, and survival. They have been demonstrated to play significant roles in the development of many disease states, including immunodeficiency, atherosclerosis, psoriasis, osteoporosis, diabetes, and cancer. In recent clinical trials impressive antitumor effects of PTK inhibitors have been observed. In future, PTK inhibitors may therefore become important drugs for the treatment of specific cancers. [Pg.1258]

ATLURU s, ATLURU D (1991) Evidence that genistein, a protein-tyrosine kinase inhibitor, inhibits CD28 monoclonal antibody stimulated human T-cell proliferation. Transplantation. 51 448-50. [Pg.81]

These agents generally are considered to be adjuvant to the calcineurin inhibitors or possibly sirolimus. The antiproliferatives azathioprine and the mycophenolic acid (MPA) derivatives inhibit T cell proliferation. [Pg.840]

Azathioprine was originally approved by the FDA in 1968 as an adjunct immunosuppressant for use in renal transplant recipients. It is available in oral and IV dosage forms.11 Prior to the advent of cyclosporine, the combination of azathioprine and corticosteroids was the mainstay of immunosuppressive therapy. Over the past 10 years, the use of azathioprine has declined markedly due in large part to the success of the MPA derivatives, which are more specific inhibitors of T cell proliferation. [Pg.840]

Gleevec ) is a tyrosine kinase inhibitor used as first-line therapy in the majority of patients with CML. As a potent tyrosine kinase inhibitor, imatinib inhibits phosphorylation of various proteins involved in cell proliferation. Imatinib works by binding to the ATP-binding pocket of BCR-ABL.7 The drug induces complete hematologic responses in more than 95% of patients and complete cytogenetic responses in about 80% of patients in chronic phase.8 Most patients have traces of the disease when measured by RT-PCR and are not cured of their disease. [Pg.1417]

Graham GJ, Wright EG, Hewick R, et al. Identification and characterization of an inhibitor of haemopoietic stem cell proliferation. Nature 1990 344(6265) 442-444. [Pg.131]

Receptor tyrosine kinases are critical components of signaling pathways that control cell proliferation and differentiation. Enhanced RTK activity due to activating mutations or overexpression has been implicated in human cancers. Thus, selective inhibitors of RTKs have considerable value. Although a number of compounds have been identified as effective inhibitors of RTKs,... [Pg.148]

Kondo T, Raff M 2000b Oligodendrocyte precursor cells reprogrammed to become multipotential CNS stem cells. Science 289 1754-1757 Lane ME, Sauer K, Wallace K, Jan YN, Lehner CF, Vaessin H 1996 Dacapo, a cyclin-dependent kinase inhibitor, stops cell proliferation during Drosophila development. Cell 87 1225-1235... [Pg.106]


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See also in sourсe #XX -- [ Pg.5 , Pg.30 ]

See also in sourсe #XX -- [ Pg.5 ]




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