Lovastatin acid is an active metabolite of hypolipidemic drug Lovastatin. Lovastatin acid inhibits HMG-CoA reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol. Lovastatin has been shown to reduce both normal and elevated low-density lipoprotein cholesterol (LDL-C). Lovastatin in approved for prevention of cardiovascular events and hypercholesterolemia. Off-label use of lovastatin includes treatmetn of diabetic dyslipidemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia, or nephrotic hyperlipidemia. Lovastatin was tested in clinical trials agains radioation injury during therapy of prostate cancer.

Mesna is an organosulfur compound used as an adjuvant in cancer chemotherapy involving cyclophosphamide and ifosfamide. No clinical drug interaction studies have been conducted with mesna. Mesna concentrates in the bladder where acrolein accumulates after administration of chemotherapy and through a Michael addition, forms a conjugate with acrolein and other urotoxic metabolites. This conjugation reaction inactivates the urotoxic compounds to harmless metabolites. The most common adverse reactions (> 10%) when MESNEX is given with ifosfamide are nausea, vomiting, constipation, leukopenia, fatigue, fever, anorexia, thrombocytopenia, anemia, granulocytopenia, diarrhea, asthenia, abdominal pain, headache, alopecia, and somnolence.

Mometasone is a medium-potency synthetic corticosteroid with antiinflammatory, antipruritic, and vasoconstrictive properties. Studies in asthmatic patients have demonstrated that mometasone provides a favorable ratio of topical to systemic activity due to its primary local effect along with the extensive hepatic metabolism and the lack of active metabolites. Though effective for the treatment of asthma, glucocorticoids do not affect asthma symptoms immediately. Maximum improvement in symptoms following inhaled administration of mometasone furoate may not be achieved for 1 to 2 weeks or longer after starting treatment. When glucocorticoids are discontinued, asthma stability may persist for several days or longer. Mometasone has been shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor which is approximately 12 times that of dexamethasone, 7 times that of triamcinolone acetonide, 5 times that of budesonide, and 1.5 times that of fluticasone. Mometasone inhaler is indicated for the maintenance treatment of asthma as prophylactic therapy. The nasal spray is indicated for the treatment of the nasal symptoms of seasonal allergic and perennial allergic rhinitis. ELOCON Lotion (Mometasone) is indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses.

Lisinopril is a potent, competitive inhibitor of angiotensin-converting enzyme (ACE). Lisinopril is marketed under the brand name ZESTRIL. ZESTRIL is indicated for the treatment of hypertension. It may be used alone as initial therapy or concomitantly with other classes of antihypertensive agents. It is also indicated as adjunctive therapy in the management of heart failure in patients who are not responding adequately to diuretics and digitalis. Lisinopril inhibits angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. The beneficial effects of lisinopril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. Inhibition of ACE results in decreased plasma angiotensin II which leads to decreased vasopressor activity and to decreased aldosterone secretion. While the mechanism through which ZESTRIL lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, ZESTRIL is antihypertensive even in patients with low-renin hypertension.

Fluoxetine hydrochloride is the first agent of the class of antidepressants known as selective serotonin-reuptake inhibitors (SSRIs). Fluoxetine is a racemic mixture of the R- and S- enantiomers and are of equivalent pharmacologic activity. Despite distinct structural differences between compounds in this class, SSRIs possess similar pharmacological activity. As with other antidepressant agents, several weeks of therapy may be required before a clinical effect is seen. SSRIs are potent inhibitors of neuronal serotonin reuptake. They have little to no effect on norepinephrine or dopamine reuptake and do not antagonize α- or β-adrenergic, dopamine D2 or histamine H1 receptors. During acute use, SSRIs block serotonin reuptake and increase serotonin stimulation of somatodendritic 5-HT1A and terminal autoreceptors. Fluoxetine is marketed under the trade names Prozac and Sarafem among others. It is also marketed for the treatment of premenstrual dysphoric disorder (Sarafem®, fluoxetine hydrochloride). PROZAC is a selective serotonin reuptake inhibitor indicated for: • Acute and maintenance treatment of Major Depressive Disorder (MDD) in adult and pediatric patients aged 8 to 18 years • Acute and maintenance treatment of Obsessive Compulsive Disorder (OCD) in adult and pediatric patients aged 7 to 17 years • Acute and maintenance treatment of Bulimia Nervosa in adult patients • Acute treatment of Panic Disorder, with or without agoraphobia, in adult patients. Studies at clinically relevant doses in man have demonstrated that fluoxetine blocks the uptake of serotonin into human platelets. Studies in animals also suggest that fluoxetine is a much more potent uptake inhibitor of serotonin than of norepinephrine. Antagonism of muscarinic, histaminergic, and α1-adrenergic receptors has been hypothesized to be associated with various anticholinergic, sedative, and cardiovascular effects of classical tricyclic antidepressant (TCA) drugs. Fluoxetine binds to these and other membrane receptors from brain tissue much less potently in vitro than do the tricyclic drugs.

Olsalazine is an anti-inflammatory drug used in the treatment of inflammatory bowel disease such as ulcerative colitis. Orally administered olsalazine is converted to mesalamine which is thought to be the therapeutically active agent in the treatment of ulcerative colitis. The mechanism of action of mesalamine (and sulfasalazine) is unknown but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyelcosatetraenoic acids (HETEs) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. After oral administration, olsalazine has limited systemic bioavailability. Based on oral and intravenous dosing studies, approximately 2.4% of a single 1.0 g oral dose is absorbed. Less than 1% of olsalazine is recovered in the urine. The remaining 98 to 99% of an oral dose will reach the colon, where each molecule is rapidly converted into two molecules of 5¬ aminosalicylic acid (5-ASA) by colonic bacteria and the low prevailing redox potential found in this environment. The liberated 5-ASA is absorbed slowly resulting in very high local concentrations in the colon. Olsalazine has been evaluated in ulcerative colitis patients in remission, as well as those with acute disease. Both sulfasalazine-tolerant and intolerant patients have been studied in controlled clinical trials. Overall, 10.4% of patients discontinued olsalazine because of an adverse experience compared with 6.7% of placebo patients. The most commonly reported adverse reactions leading to treatment withdrawal were diarrhea or loose stools (olsalazine 5.9%; placebo 4.8%), abdominal pain, and rash or itching (slightly more than 1% of patients receiving olsalazine).

Phenylacetic acid (abr. PAA and synonyms are: α-toluic acid, benzeneacetic acid, alpha tolylic acid, 2-phenylacetic acid, β-phenylacetic acid) is an organic compound containing a phenyl functional group and acarboxylic acid functional group. Because it is used in the illicit production of phenylacetone (used in the manufacture of substituted amphetamines), it is subject to controls in countries including the United States and China Phenylacetic acid is used in some perfumes, possessing a honey-like odor in low concentrations, and is also used in penicillin G production. It is also employed to treat type II hyperammonemia to help reduce the amounts of ammonia in a patient's bloodstream by forming phenylacetyl-CoA, which then reacts with nitrogen-rich glutamine to form phenylacetylglutamine. This compound is then secreted by the patient's body. In Phase 2 of clinical research it investigated in the treatment of Brain and Central Nervous System Tumors.

Misoprostol is a prostaglandin E1 (PGE1) analogue used for the treatment and prevention of stomach ulcers. When administered, misoprostol stimulates increased secretion of the protective mucus that lines the gastrointestinal tract and increases mucosal blood flow, thereby increasing mucosal integrity. It is sometimes co-prescribed with non-steroidal anti-inflammatory drugs (NSAIDs) to prevent the occurrence of gastric ulceration, a common adverse effect of the NSAIDs. Misoprostol seems to inhibit gastric acid secretion by a direct action on the parietal cells through binding to the prostaglandin receptor. The activity of this receptor is mediated by G proteins which normally activate adenylate cyclase. The indirect inhibition of adenylate cyclase by Misoprostol may be dependent on guanosine-5’-triphosphate (GTP). The significant cytoprotective actions of misoprostol are related to several mechanisms. These include: 1. Increased secretion of bicarbonate, 2. Considerable decrease in the volume and pepsin content of the gastric secretions, 3. It prevents harmful agents from disrupting the tight junctions between the epithelial cells which stops the subsequent back diffusion of H+ ions into the gastric mucosa, 4. Increased thickness of mucus layer, 5. Enhanced mucosal blood flow as a result of direct vasodilatation, 6. Stabilization of tissue lysozymes/vascular endothelium, 7. Improvement of mucosal regeneration capacity, and 8. Replacement of prostaglandins that have been depleted as a result of various insults to the area. Misoprostol has also been shown to increase the amplitude and frequency of uterine contractions during pregnancy via selective binding to the EP-2/EP-3 prostanoid receptors. Misoprostol is indicated for the treatment of ulceration (duodenal, gastric and NSAID induced) and prophylaxis for NSAID induced ulceration. Misoprostol is also indicated for other uses that are not approved in Canada, including the medical termination of an intrauterine pregnancy used alone or in combination with methotrexate, as well as the induction of labour in a selected population of pregnant women with unfavourable cervices. This indication is avoided in women with prior uterine surgery or cesarean surgery due to an increased risk of possible uterine rupture. Misoprostol is also used for the prevention or treatment of serious postpartum hemorrhage. Misoprostol is sold under the brandname Cytotec among others.

Sulbactam is a β-lactamase inhibitor given in combination with β-lactam antibiotics to inhibit β-lactamase, an enzyme produced by bacteria that destroys the antibiotics. Sulbactam in combination with semisynthetic antibiotic ampicillin sodium is indicated for the treatment of infections due to susceptible strains of the designated microorganisms: Skin and Skin Structure Infections caused by beta-lactamase producing strains of Staphylococcus aureus, Escherichia coli etc; Intra-Abdominal Infections caused by beta-lactamase producing strains of Escherichia coli, Klebsiella spp. (including K. Pneumoniae) tec; Gynecological Infections caused by beta-lactamase producing strains of Escherichia coli, and Bacteroides spp. (including B. fragilis).

Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin. Tranexamic acid is a competitive inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid. Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. Tranexamic acid in a concentration of 1 mg per mL does not aggregate platelets in vitro. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1). Tranexamic acid is used for use in patients with hemophilia for short term use (two to eight days) to reduce or prevent hemorrhage and reduce the need for replacement therapy during and following tooth extraction. It can also be used for excessive bleeding in menstruation, surgery, or trauma cases.