Cevimeline is a cholinergic agonist, which binds to muscarinic receptors. Muscarinic agonists in sufficient dosage can increase secretion of exocrine glands, such as salivary and sweat glands and increase tone of the smooth muscle in the gastrointestinal and urinary tracts. Cevimeline is indicated for the treatment of symptoms of dry mouth in patients with Sjögren’s Syndrome. Known side effects include nausea, vomiting, diarrhea, excessive sweating, rash, headache, runny nose, cough, drowsiness, hot flashes, blurred vision, and difficulty sleeping. Cevimeline should be administered with caution to patients taking beta adrenergic antagonists, because of the possibility of conduction disturbances. Drugs with para-sympathomimetic effects administered concurrently with cevimeline can be expected to have additive effects. Cevimeline might interfere with desirable antimuscarinic effects of drugs used concomitantly.

Pantoprazole is a proton pump inhibitor that inhibits gastric acid secretion and used for short-term treatment of erosive esophagitis associated with gastroesophageal reflux disease. Pantoprazole suppresses the final step in gastric acid production by covalently binding to the (H+, K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. The binding to the (H+, K+)-ATPase results in a duration of antisecretory effect that persists longer than 24 hours. Pantoprazole is used for short-term treatment of erosion and ulceration of the esophagus for adults and pediatric patients 5 years of age and older caused by gastroesophageal reflux disease. It can be used as a maintenance therapy for long-term use after initial response is obtained, but there have not been any controlled studies about the use of pantoprazole past a duration of 12 months. Pantoprazole may also be used in combination with antibiotics to treat ulcers caused by Helicobacter pylori. Use of pantoprazole may increase the chance of developing infections such as pneumonia, particularly in hospitalized patients.

Pantoprazole is a proton pump inhibitor that inhibits gastric acid secretion and used for short-term treatment of erosive esophagitis associated with gastroesophageal reflux disease. Pantoprazole suppresses the final step in gastric acid production by covalently binding to the (H+, K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. The binding to the (H+, K+)-ATPase results in a duration of antisecretory effect that persists longer than 24 hours. Pantoprazole is used for short-term treatment of erosion and ulceration of the esophagus for adults and pediatric patients 5 years of age and older caused by gastroesophageal reflux disease. It can be used as a maintenance therapy for long-term use after initial response is obtained, but there have not been any controlled studies about the use of pantoprazole past a duration of 12 months. Pantoprazole may also be used in combination with antibiotics to treat ulcers caused by Helicobacter pylori. Use of pantoprazole may increase the chance of developing infections such as pneumonia, particularly in hospitalized patients.

Alosetron, marketed under the brand name Lotronex, is a 5-HT3 antagonist used for the management of severe diarrhea-predominant irritable bowel syndrome (IBS) in women only. Alosetron is a potent and selective 5-HT3 receptor antagonist. 5-HT3 receptors are nonselective cation channels that are extensively distributed on enteric neurons in the human gastrointestinal tract, as well as other peripheral and central locations. Activation of these channels and the resulting neuronal depolarization affect the regulation of visceral pain, colonic transit and gastrointestinal secretions, processes that relate to the pathophysiology of irritable bowel syndrome (IBS). 5-HT3 receptor antagonists such as alosetron inhibit activation of non-selective cation channels which results in the modulation of the enteric nervous system. Alosetron is used for the treating women with severe irritable bowel syndrome (IBS) accompanied by severe diarrhea (usually lasting for 6 months or more). It is only prescribed to women who do not respond to other medicines and is not to be used by women whose main IBS problem is constipation.

Cevimeline is a cholinergic agonist, which binds to muscarinic receptors. Muscarinic agonists in sufficient dosage can increase secretion of exocrine glands, such as salivary and sweat glands and increase tone of the smooth muscle in the gastrointestinal and urinary tracts. Cevimeline is indicated for the treatment of symptoms of dry mouth in patients with Sjögren’s Syndrome. Known side effects include nausea, vomiting, diarrhea, excessive sweating, rash, headache, runny nose, cough, drowsiness, hot flashes, blurred vision, and difficulty sleeping. Cevimeline should be administered with caution to patients taking beta adrenergic antagonists, because of the possibility of conduction disturbances. Drugs with para-sympathomimetic effects administered concurrently with cevimeline can be expected to have additive effects. Cevimeline might interfere with desirable antimuscarinic effects of drugs used concomitantly.

Rivastigmine (sold under the trade name Exelon) is a parasympathomimetic or cholinergic agent for the treatment of mild to moderate dementia of the Alzheimer's type and dementia due to Parkinson's disease. Rivastigmine, an acetylcholinesterase inhibitor, inhibits both butyrylcholinesterase and acetylcholinesterase (unlike donepezil, which selectively inhibits acetylcholinesterase). It is thought to work by inhibiting these cholinesterase enzymes, which would otherwise break down the brain neurotransmitter acetylcholine. Rivastigmine capsules, liquid solution, and patches are used for the treatment of mild to moderate dementia of the Alzheimer's type and for mild to moderate dementia related to Parkinson's disease. Rivastigmine has demonstrated treatment effects on the cognitive (thinking and memory), functional (activities of daily living) and behavioral problems commonly associated with Alzheimer's and Parkinson's disease dementia. In people with either type of dementia, rivastigmine has been shown to provide meaningful symptomatic effects that may allow patients to remain independent and ‘be themselves’ for longer. In particular, it appears to show marked treatment effects in patients showing a more aggressive course of the disease, such as those with younger-onset ages, poor nutritional status, or those experiencing symptoms such as delusions or hallucinations. Side effects may include nausea and vomiting, decreased appetite and weight loss.

Oxcarbazepine and its active metabolite (10,11-dihydro-10-hydroxy-carbazepine, MHD) have been effective in animal models of epilepsy that generally predict efficacy in generalized tonic-clonic seizures and partial seizures in humans. The pharmacokinetic profile of oxcarbazepine is less complicated than that of carbamazepine, with less metabolism by the cytochrome P450 system, no production of an epoxide metabolite, and lower plasma protein binding. The clinical efficacy and tolerability of oxcarbazepine have been demonstrated in trials in adults, children, and the elderly. The pharmacological activity of oxcarbazepine is primarily exerted through the 10-monohydroxy metabolite (MHD) of oxcarbazepine. The precise mechanism by which oxcarbazepine and MHD exert their antiseizure effect is unknown; however, in vitro electrophysiological studies indicate that they produce blockade of voltage-sensitive sodium channels, resulting in stabilization of hyperexcited neural membranes, inhibition of repetitive neuronal firing, and diminution of propagation of synaptic impulses. These actions are thought to be important in the prevention of seizure spread in the intact brain. In addition, increased potassium conductance and modulation of high-voltage activated calcium channels may contribute to the anticonvulsant effects of the drug.

Gatifloxacin is a recently developed antibacterial agent differing from earlier fluoroquinolones by the presence of a methoxy group at the C-8 position. The presence of the methoxy group has conferred improved antibacterial activity against both Gram-positive and Gram-negative organisms, making gatifloxacin a broad-spectrum antimicrobial agent applicable in many clinical settings. Gatifloxacin is sold under the brand Zymar and is indicated for the treatment of bacterial conjunctivitis caused by susceptible strains of the following organisms: Aerobic Gram-Positive Bacteria: Cornyebacterium propinquum, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mitis, Streptococcus pneumoniae and Aerobic Gram-Negative Bacteria: Haemophilus influenza. The antibacterial action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. In addition, Gatifloxacin inhibits bacterial topoisomerase IV. This enzyme is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division. The mechanism of action of fluoroquinolones including gatifloxacin is different from that of aminoglycoside, macrolide, and tetracycline antibiotics. Therefore, gatifloxacin may be active against pathogens that are resistant to these antibiotics and these antibiotics may be active against pathogens that are resistant to gatifloxacin. There is no cross-resistance between gatifloxacin and the aforementioned classes of antibiotics. Cross-resistance has been observed between systemic gatifloxacin and some other fluoroquinolones.

Gatifloxacin is a recently developed antibacterial agent differing from earlier fluoroquinolones by the presence of a methoxy group at the C-8 position. The presence of the methoxy group has conferred improved antibacterial activity against both Gram-positive and Gram-negative organisms, making gatifloxacin a broad-spectrum antimicrobial agent applicable in many clinical settings. Gatifloxacin is sold under the brand Zymar and is indicated for the treatment of bacterial conjunctivitis caused by susceptible strains of the following organisms: Aerobic Gram-Positive Bacteria: Cornyebacterium propinquum, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mitis, Streptococcus pneumoniae and Aerobic Gram-Negative Bacteria: Haemophilus influenza. The antibacterial action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. In addition, Gatifloxacin inhibits bacterial topoisomerase IV. This enzyme is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division. The mechanism of action of fluoroquinolones including gatifloxacin is different from that of aminoglycoside, macrolide, and tetracycline antibiotics. Therefore, gatifloxacin may be active against pathogens that are resistant to these antibiotics and these antibiotics may be active against pathogens that are resistant to gatifloxacin. There is no cross-resistance between gatifloxacin and the aforementioned classes of antibiotics. Cross-resistance has been observed between systemic gatifloxacin and some other fluoroquinolones.

Dalfopristin is a pristinamycin-like component of anti-bacterial drug called Synercid which also containes quinupristin (quinupristin:dalfopristin ratio is 30:70 (w/w)). The drug was approved by FDA and used for the treatment of skin diseases caused by Staphylococcus aureus or Streptococcus pyogenes. Dalfopristin binds to the RNA of the 50S ribosomal subunit and thus inhibits the late phase of protein synthesis.