1.

Venlafaxine Mechanism of action Venlafaxine is a bicyclic antidepressant, and is usually categorized as a serotonin-norepinephrine reuptake inhibitor (SNRI), but it has been referred to as a serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI).[58][59] It works by blocking the transporter "reuptake" proteins for key neurotransmitters affecting mood, thereby leaving more active neurotransmitters in the synapse. The neurotransmitters affected are serotonin and norepinephrine. Additionally, in high doses it weakly inhibits the reuptake of dopamine,[60] with recent evidence showing that the norepinephrine transporteralso transports some dopamine as well, since dopamine is inactivated by norepinephrine reuptake in the frontal cortex, which largely lacks dopamine transporters, therefore venlafaxine can increase dopamine neurotransmission in this part of the brain.[61][62] Venlafaxine interacts with opioid receptors (mu-, kappa1- kappa3- and delta-opioid receptor subtypes) as well as alpha2-adrenergic receptor, and was shown to increase pain threshold in mice. When mice were tested with a hotplate analgesia meter, both venlafaxine and mirtazapine induced a dose-dependent, naloxone-reversible antinociceptive effect following ip administration. These findings suggest venlafaxine's seemingly superior efficacy in severe depression. 2. Levofloxacin Mechanism of action Levofloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. It functions by inhibiting DNA gyrase, a type II topoisomerase, and topoisomerase iv,[97]which is an enzyme necessary to separate replicated DNA, thereby inhibiting cell division. The fluoroquinolones interfere with DNA replication by inhibiting an enzyme complex called DNA gyrase. This can also affect mammalian cell replication. In particular, some congeners of this drug family display high activity not only against bacterial topoisomerases but also against eukaryotic topoisomerases, and are toxic to cultured mammalian cells and in vivo tumor models. Although the quinolone is highly toxic to mammalian cells in culture, its mechanism of cytotoxic action is not known. Quinolone-induced DNA damage was first reported in 1986. Recent studies have demonstrated a correlation between mammalian cell cytotoxicity of the quinolones and the induction of micronuclei. As such some fluoroquinolones may cause injury to the chromosome of eukaryotic cells. There continues to be debate as to whether or not this DNA damage is to be considered one of the mechanisms of action concerning the severe and non-abating adverse reactions experienced by some patients following fluoroquinolone therapy

3. Atorvastatin Mechanism of action Main article: Statin As with other statins, atorvastatin is a competitive inhibitor of HMG-CoA reductase. Unlike most others, however, it is a completely synthetic compound. HMG-CoA reductase catalyzes the reduction of3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) to mevalonate, which is the rate-limiting step in hepatic cholesterol biosynthesis. Inhibition of the enzyme decreases de novo cholesterol synthesis, increasing expression of low-density lipoprotein receptors (LDL receptors) on hepatocytes. This increases LDL uptake by the hepatocytes, decreasing the amount of LDLcholesterol in the blood. Like other statins, atorvastatin also reduces blood levels of triglycerides and slightly increases levels of HDL-cholesterol. In clinical trials, drugs that block cholesterol uptake like ezetimibe combine with and complement those that block biosynthesis like atorvastatin or simvastatin in lowering cholesterol or targeting levels of LDL. 4. Amlodipine Mechanism of action Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest

that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects can be detected in vitro but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa=8.6), and its kinetic interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect. Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure. The precise mechanisms by which amlodipine relieves angina have not been fully delineated, but are thought to include the following: Exertional angina In patients with exertional angina, amlodipine reduces the total peripheral resistance (afterload) against which the heart works and reduces the rate pressure product, and thus lowers myocardial oxygen demand, at any given level of exercise. Vasospastic angina Amlodipine has been demonstrated to block constriction and restore blood flow in coronary arteries and arterioles in response to calcium, potassium epinephrine, serotonin, and thromboxane A2 analog in experimental animal models and in human coronary vessels in vitro. This inhibition of coronary spasm is responsible for the effectiveness of amlodipine in vasospastic (Prinzmetal's or variant) angina. 5. Venlafaxine Mechanism of action Venlafaxine is a bicyclic antidepressant, and is usually categorized as a serotonin-norepinephrine reuptake inhibitor (SNRI), but it has been referred to as a serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI).[58][59] It works by blocking the transporter "reuptake" proteins for key neurotransmitters affecting mood, thereby leaving more active neurotransmitters in the synapse. The neurotransmitters affected are serotonin and norepinephrine. Additionally, in high doses it weakly inhibits the reuptake of dopamine,[60] with recent evidence showing that the norepinephrine transporteralso transports some dopamine as well, since dopamine is inactivated by norepinephrine reuptake in the frontal cortex, which largely lacks dopamine transporters, therefore venlafaxine can increase dopamine neurotransmission in this part of the brain.[61][62] Venlafaxine interacts with opioid receptors (mu-, kappa1- kappa3- and delta-opioid receptor subtypes) as well as alpha2-adrenergic receptor, and was shown to increase pain threshold in mice. When mice were tested with a hotplate analgesia meter, both venlafaxine and mirtazapine induced a dose-dependent, naloxone-reversible antinociceptive effect following ip administration. These findings suggest venlafaxine's seemingly superior efficacy in severe depression.[63] 6. Enoxaparin sodium Mechanism of action Enoxaparin binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and IIa. The anticoagulant effect of enoxaparin can be directly correlated to its ability to inhibit factor Xa. Factor Xa catalyzes the conversion of prothrombin to thrombin, so enoxaparins inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation. 7. Imatinib Mechanism of action

Imatinib is a 2-phenylaminopyrimidine derivative that functions as a specific inhibitor of a number of tyrosine kinase enzymes. It occupies the TK active site, leading to a decrease in activity. There are a large number of TK enzymes in the body, including the insulin receptor. Imatinib is specific for the TK domain inabl (the Abelson proto-oncogene), c-kit and PDGF-R (platelet-derived growth factor receptor). In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of abl with bcr (breakpoint cluster region), termed bcr-abl. As this is now a constitutively active tyrosine kinase, imatinib is used to decrease bcrabl activity. The active sites of tyrosine kinases each have a binding site for ATP. The enzymatic activity catalyzed by a tyrosine kinase is the transfer of the terminal phosphate from ATP to tyrosine residues on its substrates, a process known as protein tyrosine phosphorylation. Imatinib works by binding close to the ATP binding site of bcr-abl, locking it in a closed or self-inhibited conformation, and therefore inhibiting the enzyme activity of the protein semicompetitively.[22] This fact explains why many BCR-ABL mutations can cause resistance to imatinib by shifting its equilibrium toward the open or active conformation.[23] Imatinib is quite selective for bcr-abl it does also inhibit other targets mentioned above (c-kit and PDGF-R), but no other known tyrosine kinases. Imatinib also inhibits the abl protein of non-cancer cells but cells normally have additional redundant tyrosine kinases which allow them to continue to function even if abl tyrosine kinase is inhibited. Some tumor cells, however, have a dependence on bcr-abl.[5] Inhibition of the bcr-abl tyrosine kinase also stimulates its entry in to the nucleus, where it is unable to perform any of its normal anti-apoptopic functions.[24] 8. Zolpidem Mechanism of action Due to its selective binding, Zolpidem has very weak anxiolytic, myorelaxant, and anticonvulsant properties but very strong hypnotic properties.[44] Zolpidem binds with high affinity and acts as a full agonist at the 1containing GABAA receptors, about 10-fold lower affinity for those containing the 2- and 3GABAA receptorsubunits, and with no appreciable affinity for 5 subunit-containing receptors.[45][46] 1 type GABAA receptors are the 1-containing GABAA receptors and 2GABAA receptors are the 2-, 3-, 4-, 5-, and 6-containing GABAA receptors. 1 GABAA receptors are found primarily in the brain, whereas 2 receptors are found primarily in the spine. Thus, zolpidem has a preferential binding for the GABAAbenzodiazepine receptor complex in the brain but a low affinity for the GABAA-benzodiazepine receptor complex in the spine.[47] Like the vast majority of benzodiazepine-like molecules, zolpidem has no affinity for 4 and 6 subunitcontaining receptors.[48] Zolpidem positively modulates GABAAreceptors, it is presumed by increasing the GABAA receptor complexes apparent affinity for GABA, without affecting desensitization or peak current.[49] Zolpidem increases slow wave sleep and caused no effect on stage 2 sleep in laboratory tests.[50] A meta-analysis of the randomised controlled clinical trials that compared benzodiazepines against Zdrugs such as zolpidem has shown that there are few consistent differences between zolpidem and benzodiazepines in terms of sleep onset latency, total sleep duration, number of awakenings, quality of sleep, adverse events, tolerance, rebound insomnia, and daytime alertness.[51] Oxaliplatin Mechanism of action The cytotoxicity of platinum compounds is thought to result from inhibition of DNA synthesis in cancer cells. In vivo studies showed that Oxaliplatin has anti-tumor activity against colon carcinoma through its (nontargeted) cytotoxic effects. Bupropion Mechanism of action Bupropion is a dopamine and norepinephrine reuptake inhibitor and releaser.[125] It is about twice as potent an inhibitor of dopamine reuptake than of norepinephrine reuptake.[126] As bupropion is rapidly converted in the body into

several metabolites with differing activity, its action cannot be understood without reference to its metabolism. The occupancy of dopamine transporter (DAT) by bupropion and its metabolites in the human brain as measured by positron emission tomography was 622% in an independent study[127] and 1235% according to GlaxoSmithKline researchers.[128]Based on analogy with serotonin reuptake inhibitors, higher than 50% inhibition of DAT would be needed for the dopamine reuptake mechanism to be a major mechanism of the drug's action. By contrast, approximately 65% occupancy or greater of DAT is required to achieve euphoria and reach abuse potential.[129] However recent research indicates that dopamine is inactivated by norepinephrine reuptake in the frontal cortex, which largely lacks dopamine transporters, therefore bupropion can increase dopamine neurotransmission in this part of the brain, and this may be one possible explanation for any additional dopaminergic effects.[130] Bupropion does not inhibit monoamine oxidase or serotonin reuptake. However, it has been shown to indirectly enhance the firing of serotonergic neurons, via activation of downstream norepinephrine flow. Bupropion has also been shown to act as a noncompetitive nicotinic antagonist.[125] The degree of inhibition of 34 receptors correlates well with the decrease in self-administration of morphine and methamphetamine in rats,[131] and may be relevant to the effect of bupropion on nicotine addiction. The drug is supplied as aracemic mixture, and the activities of the individual enantiomers were not found to differ.[132] Two SAR studies date from 2009[133] and 2010.[134] Lamotrigine Mechanism of action Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.[18] Early studies of lamotrigine's mechanism of action examined its effects on the release of endogenous amino acids from rat cerebral cortex slices in vitro. As is the case for antiepileptic drugs that act on voltage-dependent sodium channels, lamotrigine inhibited the release of glutamate and aspartate evoked by the sodium-channel activator veratrine and was less effective in the inhibition of acetylcholine or GABA release. At high concentrations, it had no effect on spontaneous or potassium evoked amino acid release. These studies suggested that lamotrigine acts presynaptically on voltage-gated sodium channels to decrease glutamate release. Several electrophysiological studies have investigated the effects of lamotrigine on voltage-dependent sodium channels. For example, lamotrigine blocked sustained repetitive firing in cultured mouse spinal cord neurons in a concentration-dependent manner at concentrations therapeutic in the treatment of human seizures. In cultured hippocampal neurons, lamotrigine reduced sodium currents in a voltagedependent manner, and at depolarized potentials showed a small frequency-dependent inhibition. These and a variety of other results indicate that the antiepileptic effect of lamotrigine, like that of phenytoin and carbamazepine, is at least in part due to use- and voltage-dependent modulation of fast voltage-dependent sodium currents. However, lamotrigine has a broader clinical spectrum of activity than phenytoin and carbamazepine and is recognized to be protective against generalized absence epilepsy and other generalized epilepsy syndromes, including primary generalized tonicclonic seizures, juvenile myoclonic epilepsy, and Lennox-Gastaut syndrome. The basis for the broader spectrum of activity of lamotrigine is unknown, but could relate to actions of the drug on voltage-activated calcium channels. Lamotrigine blocks T-type calcium channels weakly, if at all. However, it does inhibit native and recombinant high-voltageactivated calcium channels (N- and P/Q/R-types) at therapeutic concentrations. Whether this activity on calcium channels accounts for lamotrigine's broader clinical spectrum of activity in comparison with phenytoin and carbamazepine remains to be determined. Valaciclovir Mechanism of action Valaciclovir is a prodrug, an esterified version of aciclovir that has greater oral bioavailability (about 55%) than aciclovir (1020%). It is converted by esterases to the active drug aciclovir, as well as the amino acid valine, via hepatic first-pass metabolism. Acyclovir is selectively converted into a monophosphate form by viral thymidine kinase, which is far more effective (3000 times) in phosphorylation than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into the active triphosphate form, aciclo-GTP, by cellular kinases. Aciclo-GTP is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination.

It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolised within the cell, possibly by cellular phosphatases. Fentanyl Mechanism of action Fentanyl provides some of the effects typical of other opioids through its agonism of the opioid receptors. Its strong potency in relation to that of morphine is largely due to its high lipophilicity. Because of this, it can more easily penetrate the CNS.[18] Meloxicam Mechanism of action Meloxicam inhibits cyclooxygenase (COX), the enzyme responsible for converting arachidonic acid into prostaglandin H2the first step in the synthesis of prostaglandins, which are mediators of inflammation. Meloxicam has been shown, especially at its low therapeutic dose, selectively to inhibit COX-2 over COX-1.[2] Meloxicam concentrations in synovial fluid range from 40% to 50% of those in plasma. The free fraction in synovial fluid is 2.5 times higher than in plasma, due to the lower albumin content in synovial fluid as compared to plasma. The significance of this penetration is unknown,[1] but it may account for the fact that it performs exceptionally well in treatment of arthritis in animal models. Clarithromycin Mechanism of action Clarithromycin prevents bacteria from growing by interfering with their protein synthesis. Clarithromycin binds to the subunit 50S of the bacterial ribosomeand thus inhibits the translation of peptides. Clarithromycin has similar antimicrobial spectrum as erythromycin but is more effective against certain gram-negative bacteria, particularly Legionella pneumophila. Besides this bacteriostatic effect, clarithromycin also has bactericidal effect on certain strains such as Haemophilus influenzae, Streptococcus pneumoniae and Neisseria gonorrhoeae. Bosentan Mechanism of action Bosentan is a competitive antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors. Under normal conditions, endothelin-1 binding of ET-A or ET-B receptors causes pulmonary vasoconstriction. By blocking this interaction, bosentan decreases pulmonary vascular resistance. Bosentan has a slightly higher affinity for ET-A than ET-B. Diclofenac Mechanism of action The exact mechanism of action is not entirely known, but it is thought that the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is inhibition of prostaglandinsynthesis by inhibition of cyclooxygenase (COX). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.[16] Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid.[citation needed] This is also the main side-effect of diclofenac. Diclofenac has a low to moderate preference to block the COX2-isoenzyme (approximately 10-fold) and is said to have, therefore, a somewhat lower incidence of gastrointestinal complaints than noted with indomethacin and aspirin.[citation needed] The action of one single dose is much longer (6 to 8 hours) than the very short half-life that the drug indicates.[citation
needed]

This could be partly because it persists for over 11 hours in synovial fluids.[17]

Diclofenac may also be a unique member of the NSAIDs. There is some evidence that diclofenac inhibits the lipoxygenase pathways,[citation needed] thus reducing formation of the leukotrienes (also pro-inflammatory autacoids). There is also speculation[by whom?] that diclofenac may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain the high potency of diclofenac it is the most potent NSAID on a broad basis.{Scholer. Pharmacology of Diclofenac Sodium. Am J of Medicine Volume 80 April 28, 1986}

There are marked differences among NSAIDs in their selective inhibition of the two subtypes of cyclooxygenase, COX-1 and COX-2.[citation needed] Much pharmaceutical drug design has attempted to focus on selective COX-2 inhibition as a way to minimize the gastrointestinal side-effects of NSAIDs like aspirin. In practice, use of some COX-2 inhibitors with their adverse effects has led to massive numbers of patient family lawsuits alleging wrongful death by heart attack, yet other significantly COX-selective NSAIDs such as diclofenac have been welltolerated by most of the population.[citation needed] Besides the well-known and often-cited COX-inhibition, a number of other molecular targets of diclofenac that could contribute to its pain-relieving actions have recently been identified. These include:

Blockage of voltage-dependent sodium channels (after activation of the channel, diclofenac inhibits its reactivation also known as phase inhibition)[citation needed] Blockage of acid-sensing ion channels (ASICs)[citation needed] Positive allosteric modulation of KCNQ- and BK-potassium channels (diclofenac opens these channels, leading

to hyperpolarization of the cell membrane) Imiquimod Mechanism of action The exact mechanism of action in which imiquimod and its analogs activate the immune system is not yet known. Nevertheless, it is known that imiquimod activates immune cells through the toll-like receptor 7 (TLR7), commonly involved in pathogen recognition.[5] Cells activated by imiquimod via TLR-7 secretecytokines (primarily interferon (IFN-), interleukin-6 (IL-6) and tumor necrosis factor- (TNF-)).[6] There is evidence that imiquimod, when applied to skin, can lead to the activation of Langerhans cells, which subsequently migrate to local lymph nodes to activate the adaptive immune system.[7] Other cell types activated by imiquimod include natural killer cells, macrophages and B-lymphocytes.[7] New research has shown that imiquimod has anti-proliferative effects in vitro that are independent of immune system activation or function. Imiquimod exerts its effect by increasing levels of the opioid growth factor receptor (OGFr). Blocking OGFr function with siRNA technology resulted in loss of any antiproliferative effect of imiquimod.[8] Zalcitabine Mechanism of action Zalcitabine is an analog of pyrimidine. It is a derivative of the naturally existing deoxycytidine, made by replacing the hydroxyl group in position 3' with ahydrogen. It is phosphorylated in T cells and other HIV target cells into its active triphosphate form, ddCTP. This active metabolite works as a substrate for HIV reverse transcriptase, and also by incorporation into the viral DNA, hence terminating the chain elongation due to the missing hydroxyl group. Since zalcitabine is areverse transcriptase inhibitor it possess activity only against retroviruses. Butorphanol Mechanism of action Butorphanol exhibits partial agonist and antagonist activity at the opioid receptor and agonist activity at the opioid receptor.[2] Stimulation of these receptors on central nervous system neurons causes an intracellular inhibition of adenylate cyclase, closing of influx membrane calcium channels, and opening of membrane potassium channels. This leads to hyperpolarization of the cell membrane potential and suppression of action potential transmission of ascending pain pathways. Because of its -agonist activity, at analgesic doses butorphanol increases pulmonary arterial pressure and cardiac work. Additionally, -agonism can cause dysphoria at therapeutic or supertherapeutic doses; this gives butorphanol a lower potential for abuse than other opioid drugs.

10 RIGHTS OF DRUG ADMINISTRATION

1. Right Drug 2. Right Patient 3. Right Dose 4. Right Route 5. Right Time & Frequency 6. Right Documentation 7. Right History and Assessment (Complete patient drug/relevant history) 8. Drug approach and Right to Refuse 9. Right Drug-Drug Interaction and Evaluation (drug-food incompatibilities/interaction) 10. Right Education and Information (Teach pt about the drug he is taking)