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Journal articles on the topic 'Mechanism of action of drugs'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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1

Edwards, David I. "Nitroimidazole drugs-action and resistance mechanisms I. Mechanism of action." Journal of Antimicrobial Chemotherapy 31, no. 1 (1993): 9–20. http://dx.doi.org/10.1093/jac/31.1.9.

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2

Luciani, S., S. Bova, and G. Cargnelli. "Mechanism of action of antihypertensive drugs." Pharmacological Research 22 (September 1990): 278. http://dx.doi.org/10.1016/s1043-6618(09)80309-5.

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3

Yaqub, Farhat. "Mechanism of action of anthracycline drugs." Lancet Oncology 14, no. 8 (2013): e296. http://dx.doi.org/10.1016/s1470-2045(13)70118-9.

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4

Nakashima, Shigeru. "Mechanism of Action of Anti-Fungal Drugs." Nippon Ishinkin Gakkai Zasshi 40, no. 3 (1999): 119–23. http://dx.doi.org/10.3314/jjmm.40.119.

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5

Vane, J. R., and R. M. Botting. "Mechanism of Action of Anti-Inflammatory Drugs." Scandinavian Journal of Rheumatology 25, sup102 (1996): 9–21. http://dx.doi.org/10.3109/03009749609097226.

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6

Pleuvry, Barbara J. "Mechanism of action of general anaesthetic drugs." Anaesthesia & Intensive Care Medicine 5, no. 10 (2004): 352–53. http://dx.doi.org/10.1383/anes.5.10.352.52309.

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7

Vane, John R., and Renia M. Botting. "Mechanism of action of aspirin-like drugs." Seminars in Arthritis and Rheumatism 26 (June 1997): 2–10. http://dx.doi.org/10.1016/s0049-0172(97)80046-7.

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8

Samanin, Rosario, and Silvio Garattini. "Neurochemical Mechanism of Action of Anorectic Drugs." Pharmacology & Toxicology 73, no. 2 (1993): 63–68. http://dx.doi.org/10.1111/j.1600-0773.1993.tb01537.x.

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9

Pleuvry, Barbara J. "Mechanism of action of general anaesthetic drugs." Anaesthesia & Intensive Care Medicine 9, no. 4 (2008): 152–53. http://dx.doi.org/10.1016/j.mpaic.2007.08.004.

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10

Best, Sabine L., and Peter J. Sadler. "Gold drugs: Mechanism of action and toxicity." Gold Bulletin 29, no. 3 (1996): 87–93. http://dx.doi.org/10.1007/bf03214741.

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11

Kausar, Shamaila, Fahad Said Khan, Muhammad Ishaq Mujeeb Ur Rehman, et al. "A review: Mechanism of action of antiviral drugs." International Journal of Immunopathology and Pharmacology 35 (January 2021): 205873842110026. http://dx.doi.org/10.1177/20587384211002621.

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Antiviral drugs are a class of medicines particularly used for the treatment of viral infections. Drugs that combat viral infections are called antiviral drugs. Viruses are among the major pathogenic agents that cause number of serious diseases in humans, animals and plants. Viruses cause many diseases in humans, from self resolving diseases to acute fatal diseases. Developing strategies for the antiviral drugs are focused on two different approaches: Targeting the viruses themselves or the host cell factors. Antiviral drugs that directly target the viruses include the inhibitors of virus attachment, inhibitors of virus entry, uncoating inhibitors, polymerase inhibitors, protease inhibitors, inhibitors of nucleoside and nucleotide reverse transcriptase and the inhibitors of integrase. The inhibitors of protease (ritonavir, atazanavir and darunavir), viral DNA polymerase (acyclovir, tenofovir, valganciclovir and valacyclovir) and of integrase (raltegravir) are listed among the Top 200 Drugs by sales during 2010s. Still no effective antiviral drugs are available for many viral infections. Though, there are a couple of drugs for herpesviruses, many for influenza and some new antiviral drugs for treating hepatitis C infection and HIV. Action mechanism of antiviral drugs consists of its transformation to triphosphate following the viral DNA synthesis inhibition. An analysis of the action mechanism of known antiviral drugs concluded that they can increase the cell’s resistance to a virus (interferons), suppress the virus adsorption in the cell or its diffusion into the cell and its deproteinisation process in the cell (amantadine) along with antimetabolites that causes the inhibition of nucleic acids synthesis. This review will address currently used antiviral drugs, mechanism of action and antiviral agents reported against COVID-19.

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12

Woroń, Jarosław. "Drugs containing extracts from Ruscus in chronic venal disease therapy – what's new we know about their effects?" Polish Journal of Surgery 94, no. 1 (2022): 75–78. http://dx.doi.org/10.5604/01.3001.0015.7954.

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Pharmacotherapy of venous insufficiency is based on the use of drugs which, through their mechanism of action, contribute to the complex pathomechanism of this disease. One of the drugs used in the treatment of CVD are extracts of Ruscus. Numerous studies have demonstrated a multidirectional mechanism of action involving the effect of the drug on the adrenergic and cholinergic systems and the intracellular calcium metabolism. All these mechanisms are responsible for the multidirectional mechanism of action of the drug.

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13

Sills, Graeme J., and Martin J. Brodie. "Update on the mechanisms of action of antiepileptic drugs." Epileptic Disorders 3, no. 4 (2001): 165–72. http://dx.doi.org/10.1684/j.1950-6945.2001.tb00392.x.

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ABSTRACT After a hiatus of almost 20 years, nine new antiepileptic drugs were licensed during the last decade of the 20th century. Expansion of the range of drug treatments for epilepsy complicates selection of the most suitable drug, or combination of drugs, for individual patients. Clinical experience suggests that mechanism of action may become an important criterion in this decision‐making process. At the cellular level, three major pharmacological actions are recognised: modulation of voltage‐dependent ion channels, enhancement of inhibitory neurotransmission, and attenuation of excitatory transmission. This review provides an update on the principal mechanisms of action of a range of established and modern antiepileptic drugs.

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14

Lyu, Weichen. "Antiviral Resistance in Influenza Virus: Mechanism of Action." Theoretical and Natural Science 4, no. 1 (2023): 634–38. http://dx.doi.org/10.54254/2753-8818/4/20220671.

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The "Spanish flu" pandemic caused by H1N1 virus in 1918 caused 50 million deaths. The best-known drugs for treating influenza viruses are antiviral drugs, including amantadine, rimantadine, zanamivir, and oseltamivir. Amantadine and rimantadine are excellent prophylactic drugs against influenza A. Whereas, Zanamivir and oseltamivir have comparable efficacy against influenza A and B viruses. This paper reviews antiviral drugs, approved for clinical use. This review evaluates neuraminidase inhibitors (NAIs), focusing on their mechanism of action and the emergence of resistance to them. The results showed that the viruses mutated and developed resistance during the treatment with NAIs for seasonal, pandemic, and avian influenza

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15

Kuzmanova, R., and I. Stefanova. "Basic Mechanisms of Action of the Antiepileptic Drugs." Acta Medica Bulgarica 44, no. 2 (2017): 52–58. http://dx.doi.org/10.1515/amb-2017-0020.

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AbstractAvailable antiepileptic drugs interact with a variety of different molecular targets. The mechanism of action of most anticonvulsants is most often complex with a number of affected regions. The combination of mechanisms of action of drugs in particular proportions can possibly determine the showcase of its antiepileptic activity. The common factor between the different supposed mechanisms for a number of drugs includes the possibility for modulating the excitatory and inhibitory neurotransmission through effects upon the voltage-gated ion channels, synaptic plasticity, heterogeneous receptors, and metabolism of neurotransmitters. There are controversial data on the extent to which a specific action can be the reason for the wholesome anticonvulsive characteristics of various medications, as well as the relation with the presence of undesired drug effects. The complexity of the action of some antiepileptic drugs creates conditions for optimal choice during therapy. In many cases, the insufficient familiarity with individual genetic differences and the disease related receptor damages can hinder defining a particular drug action. Characterizing the mechanisms of action of the present antiepileptic medications would increase the understanding for the pathophysiological mechanisms of epileptic seizures, as well as the development of new therapeutic strategies. The development of novel antiepileptic drugs and the ongoing research regarding the mechanism of action of established antiepileptic drugs, are continuously increasing the level of complexity in the spectrum of molecular targets relevant for epilepsy therapy. The current state of knowledge as well as the limitations in our understanding should guide future research aiming for a more detailed elucidation of the impact of genetics and pathophysiological mechanisms on interindividual differences in expression and function of antiepileptic drug targets.

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16

KAMIYA, KOICHIRO. "Simulation of the action mechanism of antiarrhythmic drugs." Japanese Journal of Electrocardiology 10, no. 2 (1990): 163–67. http://dx.doi.org/10.5105/jse.10.163.

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17

Yaksh, Tony L., David M. Dirig, and Annika B. Malmberg. "Mechanism of Action of Nonsteroidal Anti-inflammatory Drugs." Cancer Investigation 16, no. 7 (1998): 509–27. http://dx.doi.org/10.3109/07357909809011705.

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18

Bruera, Eduardo. "Mechanism of Action of Nonsteroidal Anti-inflammatory Drugs." Cancer Investigation 16, no. 7 (1998): 538–39. http://dx.doi.org/10.3109/07357909809011707.

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19

VAGHY, PAL L., KIYOSHI ITAGAKI, KUNIHISA MIWA, EDWARD McKENNA, and ARNOLD SCHWARTZ. "Mechanism of Action of Calcium Channel Modulator Drugs." Annals of the New York Academy of Sciences 522, no. 1 Calcium Antag (1988): 176–86. http://dx.doi.org/10.1111/j.1749-6632.1988.tb33353.x.

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20

Agambar, Lindsay, and Rod Flower. "Anti-inflammatory Drugs: History and mechanism of action." Physiotherapy 76, no. 4 (1990): 198–202. http://dx.doi.org/10.1016/s0031-9406(10)62174-8.

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21

Scholz, H. "Classification and mechanism of action of antiarrhythmic drugs." Fundamental & Clinical Pharmacology 8, no. 5 (1994): 385–90. http://dx.doi.org/10.1111/j.1472-8206.1994.tb00817.x.

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22

Livingston, Alexander. "Mechanism of Action of Nonsteroidal Anti-Inflammatory Drugs." Veterinary Clinics of North America: Small Animal Practice 30, no. 4 (2000): 773–81. http://dx.doi.org/10.1016/s0195-5616(08)70006-8.

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23

Vane, John R., and Regina M. Botting. "Mechanism of Action of Nonsteroidal Anti-inflammatory Drugs." American Journal of Medicine 104, no. 3 (1998): 2S—8S. http://dx.doi.org/10.1016/s0002-9343(97)00203-9.

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24

Luethi, Dino, and Matthias E. Liechti. "Designer drugs: mechanism of action and adverse effects." Archives of Toxicology 94, no. 4 (2020): 1085–133. http://dx.doi.org/10.1007/s00204-020-02693-7.

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25

Casucci, Gerardo, Veronica Villani, and Fabio Frediani. "Central mechanism of action of antimigraine prophylactic drugs." Neurological Sciences 29, S1 (2008): 123–26. http://dx.doi.org/10.1007/s10072-008-0902-9.

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26

Frediani, Fabio, Veronica Villani, and Gerardo Casucci. "Peripheral mechanism of action of antimigraine prophylactic drugs." Neurological Sciences 29, S1 (2008): 127–30. http://dx.doi.org/10.1007/s10072-008-0903-8.

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27

Palumbo, Manlio, Barbara Gatto, Giuseppe Zagotto, and Giorgio Palù. "On the mechanism of action of quinolone drugs." Trends in Microbiology 1, no. 6 (1993): 232–35. http://dx.doi.org/10.1016/0966-842x(93)90138-h.

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28

Meltzer, H. Y. "The Mechanism of Action of Novel Antipsychotic Drugs." Schizophrenia Bulletin 17, no. 2 (1991): 263–87. http://dx.doi.org/10.1093/schbul/17.2.263.

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29

Reedijk, J. "The mechanism of action of platinum antitumor drugs." Pure and Applied Chemistry 59, no. 2 (1987): 181–92. http://dx.doi.org/10.1351/pac198759020181.

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30

Vane, J. R., and R. M. Botting. "Anti-inflammatory drugs and their mechanism of action." Inflammation Research 47 (December 3, 1998): 78–87. http://dx.doi.org/10.1007/s000110050284.

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31

Muralinath, E., Devi Pooja, Chbukdhara Prasanta, et al. "Understanding the Mechanism of Action of Antitussive Drugs." Journal of Advances in Experimental Therapeutics and Neurotherapeutics 2, no. 1 (2024): 17–20. https://doi.org/10.5281/zenodo.10795828.

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<em>Coughing is a natural reflex that assists in clearing the airways of irritants and mucus. Opioid have been used as an effective antitussive compounds namely codeine and hydro condone are helpful in stopping coughing in a wide manner. By binding with mu Opioid receptors, opioid ms stop the release of neurotransmitters particularly participated I'm the cough reflex and decrease the urge to cough. Dextro methorphin ( DXM) is a non_ Opioid derivative that participates in the over the counter cough medications. If performs centrally by blocking N_ methyl_D_ asparate (NMDA) receptors and stopping the transmission of signals in the cough centers. Sodium benzoate and benzonatate are examples of antitussives that act in a peripheral manner. Benzonatate performs by anesthetizing the stretch receptors particularly in the respiratory passages and decrease the sensitivity of the cough reflex. Expectorants namely guaifenesin play major role particularly I'm cough management by thinning mucus and enhancing it's removal. Gaifenesin enhances the volume and decreases the viscosity of respiratory tract secretions and makes cough more productive and less frequent.</em><em> </em><em>Cannbinoids namely cannabidiol </em><em>(</em><em>CBD) shows promise particularly in pre-clinical studies for their antitussive effects. Anti histamines namely dephenhydramine consist of anti tudsive properties. Drugs such as cromolyn sodium and nedocromil show their action peripheral ly by stabilizing mast cells and inhibiting the release of inflammatory mediators. Finally, it is concluded that antitussive drugs encompass a diverse array of compounds that target different aspects of the cough reflex.</em>

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32

Thomas, Charlotte M., and David J. Timson. "The Mechanism of Action of Praziquantel: Can New Drugs Exploit Similar Mechanisms?" Current Medicinal Chemistry 27, no. 5 (2020): 676–96. http://dx.doi.org/10.2174/0929867325666180926145537.

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Praziquantel (PZQ) is the drug of choice for treating infection with worms from the genus Schistosoma. The drug is effective, cheap and has few side effects. However, despite its use in millions of patients for over 40 years its molecular mechanism of action remains elusive. Early studies demonstrated that PZQ disrupts calcium ion homeostasis in the worm and the current consensus is that it antagonises voltage-gated calcium channels. It is hypothesised that disruption of these channels results in uncontrolled calcium ion influx leading to uncontrolled muscle contraction and paralysis. However, other experimental studies have suggested a role for myosin regulatory light chains and adenosine uptake in the drug’s mechanism of action. Assuming voltage-gated calcium channels do represent the main molecular target of PZQ, the precise binding site for the drug remains to be identified. Unlike other commonly used anti-parasitic drugs, there are few definitive reports of resistance to PZQ in the literature. The lack of knowledge about PZQ’s molecular mechanism(s) undermines our ability to predict how resistance might arise and also hinder our attempts to develop alternative antischistosomal drugs which exploit the same target(s). Some PZQ derivatives have been identified which also kill or paralyse schistosomes in culture. However, none of these are in widespread clinical use. There is a pressing need for fundamental research into the molecular mechanism( s) of action of PZQ. Such research would enable new avenues for antischsistosomal drug discovery.

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33

Ayyad, Rezk R., Ahmed M. Nejm, Yasser Abdel Allem Hassan, and Ahmed R. Ayyad. "Mechanism of Action of Many Drugs Depend on Enzyme Inhibition." Current Research in Medical Sciences 2, no. 4 (2023): 1–9. http://dx.doi.org/10.56397/crms.2023.12.01.

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Enzyme inhibition is an important process in the mode of action of many drugs used in the treatment of various diseases. Antibiotics, anti-hypertensive agents, anti-hyperlipidaemic, anti-glaucoma, and anti-malarial drugs act on specific enzymes, leading to bacteriostatic or bactericidal effects, lower blood pressure, reduce cholesterol levels, and cause smooth muscle relaxation of blood vessels. Understanding the mode of action of these drugs and how they affect enzymes is crucial for the development of new drugs and the optimization of existing therapies. This article highlights some various drugs that act through enzyme inhibition and their mechanisms of action.

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34

Wang, Feng, Robert Langley, Gulcin Gulten, et al. "Mechanism of thioamide drug action against tuberculosis and leprosy." Journal of Experimental Medicine 204, no. 1 (2007): 73–78. http://dx.doi.org/10.1084/jem.20062100.

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Thioamide drugs, ethionamide (ETH) and prothionamide (PTH), are clinically effective in the treatment of Mycobacterium tuberculosis, M. leprae, and M. avium complex infections. Although generally considered second-line drugs for tuberculosis, their use has increased considerably as the number of multidrug resistant and extensively drug resistant tuberculosis cases continues to rise. Despite the widespread use of thioamide drugs to treat tuberculosis and leprosy, their precise mechanisms of action remain unknown. Using a cell-based activation method, we now have definitive evidence that both thioamides form covalent adducts with nicotinamide adenine dinucleotide (NAD) and that these adducts are tight-binding inhibitors of M. tuberculosis and M. leprae InhA. The crystal structures of the inhibited M. leprae and M. tuberculosis InhA complexes provide the molecular details of target–drug interactions. The purified ETH-NAD and PTH-NAD adducts both showed nanomolar Kis against M. tuberculosis and M. leprae InhA. Knowledge of the precise structures and mechanisms of action of these drugs provides insights into designing new drugs that can overcome drug resistance.

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35

Palko, N., V. Potemkin, and M. Grishina. "Decision Tree for Mechanism of Antitumor Drugs Action Prediction." Bulletin of the South Ural State University series "Chemistry" 11, no. 1 (2019): 18–24. http://dx.doi.org/10.14529/chem190102.

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36

Zeng, Daina, Dmitri Debabov, Theresa L. Hartsell, et al. "Approved Glycopeptide Antibacterial Drugs: Mechanism of Action and Resistance." Cold Spring Harbor Perspectives in Medicine 6, no. 12 (2016): a026989. http://dx.doi.org/10.1101/cshperspect.a026989.

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37

Lieberman, Jeffrey A. "Understanding the Mechanism of Action of Atypical Antipsychotic Drugs." British Journal of Psychiatry 163, S22 (1993): 7–18. http://dx.doi.org/10.1192/s0007125000292544.

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The thrust of development of new antipsychotic drugs has been to identify new compounds that have enhanced antipsychotic efficacy and have lesser side-effects than standard neuroleptic compounds. Drug development strategies no longer concentrate on D2 receptor antagonism but aim to produce novel compounds. The following have been pursued: (a) selective dopamine receptor antagonists; (b) serotonin receptor agonists and antagonists (5-HT1a,e, 5-HT2, 5-HT3) or mixed 5-HT2 - D2 receptor antagonist; (c) selective dopamine agonists or partial agonists; and (d) sigma-site and excitatory amino-acid antagonists. Such compounds are at various stages of development. The only drug which has truly distinguished itself as ‘atypical’ is clozapine. Its mechanism of action is unknown and the search for it, in large part, has been the impetus for development of the compounds listed above.

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38

Sulser, F., J. Watts, and Bernard B. Brodie. "ON THE MECHANISM OF ANTIDEPRESSANT ACTION OF IMIPRAMINELIKE DRUGS." Annals of the New York Academy of Sciences 96, no. 1 (2006): 279–88. http://dx.doi.org/10.1111/j.1749-6632.1962.tb50122.x.

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39

CROOKE, STANLEY T. "Evaluating the Mechanism of Action of Antiproliferative Antisense Drugs." Antisense and Nucleic Acid Drug Development 10, no. 2 (2000): 123–26. http://dx.doi.org/10.1089/oli.1.2000.10.123.

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40

Amsterdam, E. A. "Mechanism of Action of Antianginal Drugs: What Is It?" Cardiology 74, no. 6 (1987): 425–26. http://dx.doi.org/10.1159/000174247.

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41

Forrest, Michael, and Peter M. Brooks. "Mechanism of action of non-steroidal anti-rheumatic drugs." Baillière's Clinical Rheumatology 2, no. 2 (1988): 275–94. http://dx.doi.org/10.1016/s0950-3579(88)80015-3.

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42

Meltzer, H. Y. "Mechanism of action of clozapine — like atypical antipsychotic drugs." European Neuropsychopharmacology 1, no. 3 (1991): 351. http://dx.doi.org/10.1016/0924-977x(91)90561-8.

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43

Reglinski, J., and W. E. Smith. "Mechanism of action of the gold drugs in arthritis." Journal of Inorganic Biochemistry 51, no. 1-2 (1993): 418. http://dx.doi.org/10.1016/0162-0134(93)85447-g.

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44

Gregori-Puigjane, E., V. Setola, J. Hert, et al. "Identifying mechanism-of-action targets for drugs and probes." Proceedings of the National Academy of Sciences 109, no. 28 (2012): 11178–83. http://dx.doi.org/10.1073/pnas.1204524109.

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45

Jackson, Richard T. "Mechanism of Action of Some Commonly Used Nasal Drugs." Otolaryngology–Head and Neck Surgery 104, no. 4 (1991): 433–40. http://dx.doi.org/10.1177/019459989110400403.

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46

Meldrum, Brian S. "Update on the Mechanism of Action of Antiepileptic Drugs." Epilepsia 37, s6 (1996): S4—S11. http://dx.doi.org/10.1111/j.1528-1157.1996.tb06038.x.

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47

Contreras-García, Itzel Jatziri, Noemí Cárdenas-Rodríguez, Antonio Romo-Mancillas, et al. "Levetiracetam Mechanisms of Action: From Molecules to Systems." Pharmaceuticals 15, no. 4 (2022): 475. http://dx.doi.org/10.3390/ph15040475.

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Epilepsy is a chronic disease that affects millions of people worldwide. Antiepileptic drugs (AEDs) are used to control seizures. Even though parts of their mechanisms of action are known, there are still components that need to be studied. Therefore, the search for novel drugs, new molecular targets, and a better understanding of the mechanisms of action of existing drugs is still crucial. Levetiracetam (LEV) is an AED that has been shown to be effective in seizure control and is well-tolerable, with a novel mechanism of action through an interaction with the synaptic vesicle protein 2A (SV2A). Moreover, LEV has other molecular targets that involve calcium homeostasis, the GABAergic system, and AMPA receptors among others, that might be integrated into a single mechanism of action that could explain the antiepileptogenic, anti-inflammatory, neuroprotective, and antioxidant properties of LEV. This puts it as a possible multitarget drug with clinical applications other than for epilepsy. According to the above, the objective of this work was to carry out a comprehensive and integrative review of LEV in relation to its clinical uses, structural properties, therapeutical targets, and different molecular, genetic, and systemic action mechanisms in order to consider LEV as a candidate for drug repurposing.

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48

Coulter, Douglas A. "Antiepileptic Drug Cellular Mechanisms of Action: Where Does Lamotrigine Fit In?" Journal of Child Neurology 12, no. 1_suppl (1997): S2—S9. http://dx.doi.org/10.1177/0883073897012001031.

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Current frontline antiepileptic drugs tend to fall into several cellular mechanistic categories, and these categories often correlate with the clinical spectrum of action of the various antiepileptic drugs. Many antiepileptic drugs effective in control of partial and generalized tonic-clonic seizures are use- and voltage-dependent blockers of sodium channels. This mechanism selectively dampens pathologic activation of sodium channels, without interacting with normal sodium channel function. Examples include phenytoin, carbamazepine, valproic acid, and lamotrigine. Many antiepileptic drugs effective in control of generalized absence seizures block low threshold calcium currents. Low threshold calcium channels are present in high densities in thalamic neurons, and these channels trigger regenerative bursts that drive normal and pathologic thalamocortical rhythms, including the spike wave discharges of absence seizures. Examples include ethosuximide, trimethadione, and methsuximide. Several antiepileptic drugs that have varying clinical actions interact with the γ-aminobutyric acid (GABA)ergic system. Diazepam and clonazepam selectively augment function of a subset of GABA A receptors, and these drugs are broad-spectrum antiepileptic drugs. In contrast, barbiturates augment function of all types of GABAA receptors, and are ineffective in control of generalized absence seizures, but effective in control of many other seizure types. Tiagabine and vigabatrin enhance cerebrospinal levels of GABA by interfering with reuptake and degradation of GABA, respectively. These antiepileptic drugs are effective in partial seizures. Lamotrigine is effective against both partial and generalized seizures, including generalized absence seizures. Its sole documented cellular mechanism of action is sodium channel block, a mechanism shared by phenytoin and carbamazepine. These drugs are ineffective against absence seizures. Consequently, unless there are unique aspects to the sodium channel block by lamotrigine, it seems unlikely that this mechanism alone could explain its broad clinical efficacy. Therefore, lamotrigine may have as yet uncharacterized cellular actions, which could combine with its sodium channel blocking actions, to account for its broad clinical efficacy. (J Child Neurol 1997;12(Suppl 1):S2-S9).

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49

Asadi‐Pooya, Ali A., Maromi Nei, Ashwini D. Sharan, et al. "Antiepileptic drugs and relapse after epilepsy surgery." Epileptic Disorders 10, no. 3 (2008): 193–98. http://dx.doi.org/10.1684/epd.2008.0198.

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ABSTRACT Purpose To evaluate whether the postoperative, antiepileptic drug (AED) regimen influences seizure recurrence after anterior temporal lobectomy when considering the putative mechanism of action and possible neuroprotective effects. Methods This was a retrospective study. Patients who had an anterior temporal lobectomy for refractory epilepsy, whose preoperative MRI indicated mesial temporal sclerosis, were included. Postoperative AED regimens were compared with regard to seizure‐outcome, considering the putative mechanism of action (sodium channel blockers, non‐sodium channel blockers, and mixed mechanisms) or possible neuroprotective effect (levetiracetam, topiramate, tiagabine and zonisamide versus others). Time‐to‐event (first seizure after surgery) analysis was used to produce a Kaplan‐Meier estimate of seizure recurrence, and groups were compared using Cox proportional hazard analysis. Results 226 patients (103 males and 123 females; mean age 42 ± 11 years) were studied. The rates of postoperative seizure recurrence were not significantly different between the three groups regardless of the use of AEDs with different mechanisms of action (p = 0.23). Fifty patients were receiving possibly neuroprotective AEDs and 176 patients were not. Rates of seizure recurrence were not significantly different between these two groups either (p = 0.11). The differences between one‐year seizure‐free rates were not significant when we compared levetiracetam versus phenytoin or carbamazepine. Discussion There appeared to be no advantage or disadvantage to either prescribing drugs with different mechanisms of action or using drugs with possible neuroprotective effect after temporal lobectomy. Prospective studies with larger sample sizes may be of benefit to further explore this issue.

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Goodin, Susan, Michael P. Kane, and Eric H. Rubin. "Epothilones: Mechanism of Action and Biologic Activity." Journal of Clinical Oncology 22, no. 10 (2004): 2015–25. http://dx.doi.org/10.1200/jco.2004.12.001.

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Drugs that target microtubules are among the most commonly prescribed anticancer therapies. Although the mechanisms by which perturbation of microtubule function leads to selective death of cancer cells remain unclear, several new microtubule-targeting compounds are undergoing clinical testing. In part, these efforts focus on overcoming some of the problems associated with taxane-based therapies, including formulation and administration difficulties and susceptibility to resistance conferred by P-glycoprotein. Epothilones have emerged from these efforts as a promising new class of anticancer drugs. Preclinical studies indicate that epothilones bind to and stabilize microtubules in a manner similar but not identical to that of paclitaxel and that epothilones are effective in paclitaxel-resistant tumor models. Clinical phase I and early phase II data are available for BMS-247550, BMS-310705, EPO906, and KOS-862. The results suggest that these compounds have a broad range of antitumor activity at doses and schedules associated with tolerable side effects.

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