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Książki na temat „Inhibitor Activity”

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Data publikacji: 6 września 2023

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1

Roué, Gael. Activity of the Novel BCR Kinase Inhibitor IQS019 in B-NHL. Saarbrücken: LAP LAMBERT Academic Publishing, 2017.

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2

G, Cory Joseph, i Cory Ann H, red. Inhibitors of ribonucleoside diphosphate reductase activity. New York: Pergamon Press, 1989.

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3

Merton, Sandler, i Smith H. J. 1930-, red. Design of enzyme inhibitors as drugs. Oxford: Oxford University Press, 1994.

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4

Merton, Sandler, i Smith H. J. 1930-, red. Design of enzyme inhibitors as drugs. Oxford [England]: Oxford University Press, 1989.

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5

Gupta, Satya Prakash. Matrix metalloproteinase inhibitors: Specificity of binding and structure-activity relationships. Basel: Springer, 2012.

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6

1935-, Tipper Donald J., red. Antibiotic inhibitors of bacterial cell wall biosynthesis. Oxford [Oxfordshire]: Pergamon Press, 1987.

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7

Kiss, S., i M. Simihăian. Improving Efficiency of Urea Fertilizers by Inhibition of Soil Urease Activity. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-017-1843-1.

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8

Atwell, Mark M. Inhibition of secretary activity in cells isolated from the rat stomach. Birmingham: Aston University, Department of Pharmaceutical Sciences, 1990.

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9

M, Simihǎian, red. Improving efficiency of urea fertilizers by inhibition of soil urease activity. Dordrecht: Kluwer Academic Publishers, 2002.

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10

J, Cragoe Edward, Kleyman Thomas R i Simchowitz Louis, red. Amiloride and its analogs: Unique cation transport inhibitors. New York, N.Y: VCH, 1992.

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11

service), ScienceDirect (Online, red. Constitutive activity in receptors and other proteins. Amsterdam: Elsevier/Academic, 2010.

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12

Salehi, Sebastian Albert. Insulin secretion: Modulation of islet acid glucan-1,4-gas-glucosidase activity by selective inhibitors, Ca2+ and nitric oxide. Lund [Sweden]: Department of Pharmacology, Lund University, 1995.

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13

Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.

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14

P, Braquet, red. CRC handbook of PAF and PAF antagonists. Boca Raton, Fla: CRC Press, 1991.

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15

Mayhew, Christopher N. Evaluation of the anti-retroviral activity and bone marrow toxicity of the novel ribonucleotide reductase inhibitors trimidox and didox and comparison with hydroxyurea in murine acquired immunodeficiency syndrome. Wolverhampton: University of Wolverhampton, 2001.

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16

1935-, Tipper Donald J., red. Antibiotic inhibitorsof bacterial cell wall biosynthesis. Oxford: Pergamon, 1987.

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17

Takao, Kumazawa, Kruger Lawrence i Mizumura Kazue, red. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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18

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Streszczenie:
Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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19

Majid, Adrian, i Bruce L. Gilliam. Future Antiretrovirals, Immune-Based Strategies, and Therapeutic Vaccines. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0023.

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Highly active antiretroviral therapy remains the mainstay of treatment for patients chronically infected with HIV. Novel drugs, both within existing classes and new ones, are in various stages of development and testing. New medications within existing classes of antiretroviral agents are in clinical trials and will likely offer activity against resistant HIV-1 strains and provide alternatives for combination pill therapy. Novel therapeutics including oral attachment inhibitors and monoclonal antibody treatments continue to show efficacy against HIV-1 and progress in clinical trials. Tenofovir alafenamide is a prodrug that produces higher intracellular levels of tenofovir diphosphate with likely less renal and bone toxicity. Among traditional classes of HIV treatment, both doravirine (a non-nucleoside reverse transcriptase inhibitor) and cabotegravir (an integrase strand inhibitor) are newer agents with activity against resistant virus. Maturation inhibitors are a new class of treatment that block protease cleavage, leading to the release of an immature virion.
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20

Trus, Michael. Altering retinoid sensitivity in acute myeloblastic leukemia cells by treatment with the histone deacetylase inhibitor, valproic acid, and the inhibitor of DNA methyltransferase activity, 5-aza-2'-deoxycytidine. 2006.

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21

Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.

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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.
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22

Keshav, Satish, i Palak Trivedi. Genetic liver disease. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0214.

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This chapter discusses three of the major inherited forms of liver disease (all autosomal recessive): hereditary haemochromatosis, Wilson’s disease, and alpha-1-antitrypsin deficiency. Hereditary haemochromatosis is characterized by excessive absorption of dietary iron, with a pathological increase in total body iron that accumulates in tissues and organs, disrupting their function. Wilson’s disease (hepatolenticular degeneration) is an autosomal recessive genetic disorder in which copper accumulates in tissues. Alpha-1-antitrypsin deficiency is characterized by reduced circulating levels of alpha-1-antitrypsin, a liver-derived protease inhibitor, and accumulation within the hepatocytes of the abnormal, poorly degraded protein; the consequent excessive activity of proteases such as elastase in pulmonary alveoli, unopposed by protease inhibitors, leads to emphysema, and the accumulation of alpha-1-antitrypsin in hepatocytes causes liver dysfunction.
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23

(Editor), Merton Sandler, i H. John Smith (Editor), red. Design of Enzyme Inhibitors As Drugs: Volume 2 (Design of Enzyme Inhibitors as Drugs). Oxford University Press, USA, 1994.

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24

Gupta, Satya Prakash. Matrix Metalloproteinase Inhibitors: Specificity of Binding and Structure-Activity Relationships. Springer, 2014.

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25

Böldicke, Thomas. Protein Targeting Compounds: Prediction, Selection and Activity of Specific Inhibitors. Springer, 2016.

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26

Böldicke, Thomas. Protein Targeting Compounds: Prediction, Selection and Activity of Specific Inhibitors. Springer, 2018.

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27

Böldicke, Thomas. Protein Targeting Compounds: Prediction, Selection and Activity of Specific Inhibitors. Springer London, Limited, 2016.

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28

Borgnis, Ramie Lynn. Latent inhibition of multiple unit activity and EEG in rabbit hippocampus. 1993.

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29

Kiss, S., i M. Simihaian. Improving Efficiency of Urea Fertilizers by Inhibition of Soil Urease Activity. Springer, 2002.

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30

Kiss, S., i M. Simihaian. Improving Efficiency of Urea Fertilizers by Inhibition of Soil Urease Activity. Springer, 2013.

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31

Kiss, S. Improving Efficiency of Urea Fertilizers by Inhibition of Soil Urease Activity. Springer, 2010.

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32

Kiss, S., i M. Simihaian. Improving Efficiency of Urea Fertilizers by Inhibition of Soil Urease Activity. Springer London, Limited, 2013.

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33

Castellanos, Madeleine M. Female Sexual Biochemistry (DRAFT). Redaktor Madeleine M. Castellanos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190225889.003.0001.

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“Female Sexual Biochemistry” reviews the key hormones and neurotransmitters that have a major role in female sexuality. Estrogens—estradiol, estrone, and estriol—as well as major androgens, such as testosterone and dihydrotestosterone (DHT), are presented with a discussion of their role in the support of the reproductive organs and genitals as well as their actions on the central nervous system to affect sexual desire, arousal, and responsiveness. The interaction and regulation of estrogen by progesterone and thyroid hormone is included. A review of the dual-control model of sexual responsiveness is presented, including excitatory and inhibitory factors, as well as a summary of major neurotransmitters that work to enhance sexual arousal or inhibit it. The sexual response cycle is reviewed and relevant changes in pregnancy, childbirth, perimenopause, and menopause are presented. Finally, there is mention of how synthetic hormones and environmental toxins with hormone activity may alter a woman’s sexual response.
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34

Eisen, Tim. The patient with renal cell cancer. Redaktor Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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35

Cragoe, Edward J., i Thomas R. Kleyman. Amiloride and Its Analogs: Unique Cation Transport Inhibitors. John Wiley & Sons, 1993.

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36

Zhen, Liping. Hydrogen cyanamide on triphenyltetrazolium chloride reduction, sulfhydryl group binding, and catalase activity in bromegrass (Bromus inermis Leyss) cells. 1988.

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37

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2013.

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38

Modulation of oscillatory activity in inhibitory neuronal networks by anesthetics: The role of receptor desensitization. Ottawa: National Library of Canada, 2001.

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39

Herman, James P. Limbic Pathways to Stress Control. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.

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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.
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40

Test No. 224: Determination of the Inhibition of the Activity of Anaerobic Bacteria. OECD, 2007. http://dx.doi.org/10.1787/9789264067332-en.

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41

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2007.

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42

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley-Interscience, 2005.

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43

Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists (Methods of Biochemical Analysis). Wiley-Interscience, 2005.

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44

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2013.

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45

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2013.

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46

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Limited, John, 2013.

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47

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2005.

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48

Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery: A Guide for Medicinal Chemists and Pharmacologists. Wiley & Sons, Incorporated, John, 2013.

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49

Watson, Catherine J. Urease Activity and Inhibition - Principles and Practice (Proceedings of the International Fertiliser Society S.). International Fertiliser Society, 2000.

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50

Ali, Anmar K. M. Quantitative structure-activity relationship analysis of nuclear substituted pargylines as competitive inhibitors of MAO-A and MAO-B. 1987.

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