COMPOSITION
Azithromycin 500 mg tab
DESCRIPTION
Azithromycin is a semi-synthetic macrolide antibiotic chemically related to erythromycin and clarithromycin .It is effective against a wide variety of bacteria organisms, such as Hemophilus influenzae, Streptococcus pneumoniae, Mycoplasma pneumoniae, Staphylococcus aureus, and mycobacterium avium, and many others. It is unusual in that it stays in the body for quite a while, allowing for once a day dosing and for shorter treatment courses for most infections.
MODE OF ACTION
Tablet: 500 mg
INDICATION
Azithromycin is effective against susceptible bacteria causing infections of the middle ear, tonsillitis, throat infections, laryngitis, bronchitis, pneumonia and sinuses. It is also effective against certain sexually transmitted infectious diseases, such as gonococcal & nongonococcal urethritis and cervicitis
DOSAGE & ADMINISTRATION
Azithromycin should be taken at least one hour before or two hours after meals since it may bind to food and not be absorbed from the intestine. For most infections, azithromycin is taken once daily for a relatively short course of treatment (usually five days). The first dose is often a "double dose," twice as much as the remainder of the doses given. For acute bacterial sinusitis, azithromycin way be taken once daily for three days
INTERACTION
Unlike erythromycin and clarithromycin, azithromycin is generally considered free of interactions with most other medicines. It is recommended that azithromycin not be taken at the same time as aluminum- or magnesium- based antacids because antacids will bind the azithromycin and prevent it from being absorbed from the intestine.
PREGNANCY INSTRUCTIONS
There are no adequate studies of azithromycin in pregnant women. However, studies in animals suggest no important effects on the fetus. Azithromycin therefore can be used in pregnancy if the physician feels that it is clearly necessary.
NURSING MOTHERS
It is not known if azithromycin is secreted in breast milk.
SIDE EFFECTS
Azithromycin is generally well tolerated. The most common side effects are diarrhea or loose stools, nausea, abdominal pain, and vomiting, each of which may occur in fewer than one in twenty persons who receive azithromycin. Rarer side effects include abnormal liver tests, allergic reactions, and nervousness

COMPOSITION
Flupentioxl-------0.5mg Melitracen-------10mg
DESCRIPTION
Preclinical studies have shown advantages of the combined effect of the two Psychotropic’s flupenthixol and melitracen over the effect of each compound when tested individually .The findings indicate advantages of Depsure in clinical use due to synergism of the therapeutic efficacy and antagonism to the adverse effects of the two compounds. Flupenthixol is a well known and well proven compound with anxiolytic and antidepressant properties when given in low doses. Melitracen- a tricyclic antidepressant -was chosen because of its antidepressant and anticholinergic qualities. The purpose was to increase the antidepressant effect of flunaxol while minimizing the risk of side effectsFlupenthixol:- C23H25F3N2OS Melitracen:- C21H25N Melitracen-A tricyclic antidepressant-:Melitracen is a bipolar thymoleptic with activating properties in low doses Melitracen – As all other tricyclic acts by potentiating the actions of biogenic amines (noradernaline and serotonin (5-HT)) in the CNS by blockage of the reuptake at the nerve terminals (Goodman and Gilman’s 1985). The reuptake mechanism is the major means of physiological inactivation of neurotransmitters . Melitracen has a rather low antiserotonergic (5-HT2) and antiadrenergic effect; whereas the anticholinergic and antihistaminergic effects are rather strong. Flupenthixol an Anxiolytic -: Flupenthixol is thioxanthene derivative , given in daily doses up to 3 mg possesses antidepressant anxiolytic and activating properties which have been shown in many controlled , clinical trials with antidepressant action flupenthixol has antidepressant properties at low dosages but without anticholinergic side- effects, or indeed gastrointestinal effects .
MODE OF ACTION
Studies demonstrate the favorable action of a combination of a low dose of flupenthixol , and an equally low dose of a tricyclic antidepressant melitracen in the treatment of mild and moderate depressive states. The antidepressant activity of melitracen is due to its interference with the presynaptic reuptake of noradrenaline. As regards flupenthixol , a neuroleptic ,when prescribed in low doses , it facilitates the serotonin release by influencing the presylaptic 5HT2A receptors . This again favours the physiological action of the noradrenergic system. Flupenthixol and melitracen in Depsure the synergistic combination for better therapeutic efficacy and antagonism of the adverse effects.
INDICATION
Psychosomatic disorders, Psychogenic depression, Depressive neurosis, Masked depression, Psychosomatic affections accompanied by Anxiety and Apathy, Menopausal depression, Dysphoria and Depression in alcoholic and drugs addicts
DOSAGE & ADMINISTRATION
Adults: Usually 2 tablets in the morning for the first week followed by one tablet as maintenance for the subsequent weeks. Elderly patients: 1tablet in the morning. Maintenance dose: Usually 1 tablet in the morning.
INTERACTION
PREGNANCY INSTRUCTIONS
Depsure should preferably not be given during pregnancy and lactation.
NURSING MOTHERS
Depsure should preferably not be given during pregnancy and lactation.
SIDE EFFECTS
“Treatment with Melitracen was accompanied by side effects which were qualitatively similar to those produced by Amitriptyline but less intense not so frequent, so that toleration was better leading to a grater therapeutic index. Because of these characteristics ,,Elitracen appears particularly useful for the treatment of depressive syndrome in out-patient who require well tolerated drugs with rapid action”

COMPOSITION
Fluconazole.................................150mg. Excipients........................................q.s.
DESCRIPTION
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
DESCRIPTION
Ebastine is a long-acting and selective H1-histamine receptor antagonist. After repeated administration, inhibition of peripheral receptors remain at a constant level. Ebastine is rapidly absorbed and undergoes extensive first pass metabolism following oral administration. Ebastine is almost totally converted to the pharmacologically active acid metabolite, carebastine. After a single 10 mg oral dose, peak plasma levels of carebastine occur at 2,6 to 4 hours and achieve levels of 80 to 100 ng/mL. The half-life of carebastine is between 15 and 19 hours with 66% of the medicine being excreted in the urine mainly as conjugated metabolites. Following repeated administration of 10 mg once daily, steady state is achieved in 3 to 5 days with peak plasma levels ranging from 130 to 160 ng/mL. In vitro studies with human liver microsomes show that ebastine is metabolised to carebastine predominantly via the CYP3A4 pathway. Concurrent administration of ebastine with ketoconazole or erythromycin (both CYP3A4 inhibitors) to healthy volunteers was associated with significantly increased plasma concentration and elimination half-life of ebastine and carebastine. With ketoconazole the Cmax and AUC were 15 times and 40 times respectively increased, with erythromycin the values were doubled. Both ebastine and carebastine are highly protein bound, >95%. In elderly subjects, no statistically significant changes were observed in the pharmacokinetics compared to those of young adult volunteers. In patients with renal insufficiency the elimination half-life of carebastine was increased to 23-26 hours. Similarly, in patients with hepatic insufficiency, the half-life increased to 27 hours.
MODE OF ACTION
INDICATION
Ebastine is indicated for the symptomatic treatment of: • Seasonal and perennial allergic rhinitis • Idiopathic chronic urticaria
DOSAGE & ADMINISTRATION
Allergic rhinitis 10 mg (one tablet) once a day Idiopathic chronic urticaria 10 mg (one tablet) once a day. Ebastine may be taken with or without food.
INTERACTION
The interaction of ebastine in combination with either ketoconazole or erythromycin (both known to prolong the QTc interval) has been evaluated. A significant pharmacokinetic and pharmacodynamic interaction has been observed with these combination; an 18-19 msec (4,7% - 5%) increase in QTc has been reported with either combination. Ebastine does not interact with the kinetics of theophylline, warfarin, cimetidine, diazepam or alcohol. The sedation effect of alcohol and diazepam may be enhanced. When ebastine is administered with food, there is a 1,5 to 2,0 fold increase in the plasma levels and the AUC of the main active acid metabolite of ebastine. This increase does not alter the Tmax. The administration of ebastine with food does not cause a modification in its clinical effect. Ebastine lacks significant sedative effects. Patients should, however, be warned that a small number of individuals may experience sedation. It is therefore advisable to determine individual response before driving or performing complicated tasks. This effect may be compounded by the simultaneous intake of alcohol or other central nervous system depressants.
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS
The most common side-effects are headache, dry mouth and drowsiness. Other less commonly reported side effects include pharyngitis, abdominal pain, dyspepsia, asthenia, epistaxis, rhinitis, sinusitis, nausea and insomnia. CONTRA-INDICATIONS: Patients with a known hypersensitivity to ebastine or any of its ingredients. The safety of ebastine during pregnancy and lactation has not been established. The safety and efficacy of ebastine tablets in children less than 12 years has not been established. WARNINGS: It is advisable to exercise caution when using Kestine in patients known to have the following conditions: long QT syndrome, hypokalaemia, treatment with any medicine known to produce an increase in QT interval or inhibit CYP3A4 enzyme systems such as azole antifungals and macrolide antibiotics (refer to section on "Interactions").

COMPOSITION
DESCRIPTION
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Levosulpiride-25mg
DESCRIPTION
Levosulpiride the active isomer of sulpiride is a substituted benzamide with antidopaminergic properties. Its chemical name is N-[(1- ethpyrrolidin-2-yl]-2- methoxy-5-methoxy-5-sulfamoyl-benzamide and the molecular formula is C15H23N304S.Its chemical formula is
MODE OF ACTION
MECHANISM OF ACTION Levosulpiride: Mechanism of action: Peripheral It is a D2 receptor antagonist and thereby causes constriction of LES and also increases the peristaltic activity thus decreasing chances of reflux and heart burn and causes early gastric emptying and increases satiety. In addition, it has a 5HT4 agonist activity which also contributes to the same effect. Central It acts on the chemoreceptor trigger zone (CTZ), which lies outside the blood barrier it blocks the D2 receptors, thereby controlling nausea and vomiting either induced by signals coming from GI afferents or due to chemotherapy. Thus to summarize levosulpiride has a significant peripheral action as a D2 antagonist and a 5HT4 agonist. In addition, In spite of having a central mechanism of action, it is a sale drug because, no extra pyramidal symptoms or sedation is encountered since it acts on the chemoreceptor trigger zone (CTZ), which lies outside the blood brain barrier.
INDICATION
GERD (GASTROESOPHAGEAL REFLUX DISEASE),NAUSEA,VOMITING, Reflux Oseophagitis, dyspeptic patients with diabetic gastroparesis
DOSAGE & ADMINISTRATION
levosulpiride 25mg, 3 times daily.
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Liva is a synthetic broad-spectrum antibacterial agent for oral and intravenous administration. Chemically, levofloxacin, a chiral fluorinated carboxyquinolone, is the pure (-)-(S)-enantiomer of the racemic drug substance ofloxacin. The chemical name is (-)-(S)-9-fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido[1,2,3-de]-1,4-benzoxazine-6-carboxylic acid hemihydrate. The empirical formula is C18H20FN3O4 • ½ H2O and the molecular weight is 370.38. Levofloxacin is a light yellowish-white to yellow-white crystal or crystalline powder. The molecule exists as a zwitterion at the pH conditions in the small intestine. The data demonstrate that from pH 0.6 to 5.8, the solubility of levofloxacin is essentially constant (approximately 100 mg/mL). Levofloxacin is considered soluble to freely soluble in this pH range, as defined by USP nomenclature. Above pH 5.8, the solubility increases rapidly to its maximum at pH 6.7 (272 mg/mL) and is considered freely soluble in this range. Above pH 6.7, the solubility decreases and reaches a minimum value (about 50 mg/mL) at a pH of approximately 6.9. Levofloxacin has the potential to form stable coordination compounds with many metalions. This in vitro chelation potential has the following formation order: Al+3 > Cu+2 > Zn+2 > Mg+2 > Ca+2.
DESCRIPTION
Levofloxacin is a 3rd generation fluoroquinolone antibiotic, .Chemically, levofloxacin is the S-enantiomer (L-isomer) of ofloxacin, and has approximately twice the potency of ofloxacin, because the R+enantiomer (D-isomer) of ofloxacin is essentially inactive. In addition, the S-enantiomer (L-isomer) of ofloxacin, has substantially less toxicity. Like other fluoroquinolines, it works by inhibiting DNA gyrase, an enzyme that negatively supercoils DNA. Levofloxacin is effective against a number of gram-positive and gram-negative bacteria. Because of its broad spectrum of action, levofloxacin is frequently prescribed empirically for a wide range of infections (e.g. pneumonia, urinary tract infection) before the specific causal organism is known. If the causal organism is identified, levofloxacin may be discontinued and the patient may be switched to an antibiotic with a narrower spectrum of activity. Levofloxacin is currently the only respiratory fluoroquinolone approved by the U.S. FDA for the treatment of nosocomial pneumonia.
MODE OF ACTION
LIVA-500 Tablets are available as film-coated tablets and contain 500 MG OF LEVOFLOXACIN
INDICATION
Susceptible organisms Gram-positive bacteria · Enterococcus faecalis (many strains are only moderately susceptible) · Staphylococcus aureus (methicillin-susceptible strains) · Staphylococcus epidermidis (methicillin-susceptible strains) · Staphylococcus saprophyticus · Streptococcus pneumoniae (including Multidrug-resistant strains, MDRSP) · Streptococcus pyogenes Gram-negative bacteria · Enterobacter cloacae · Klebsiella pneumoniae · Pseudomonas aeruginosa · Escherichia coli · Legionella pneumophila · Serratia marcescens · Haemophilus influenzae · Moraxella catarrhalis · Haemophilus parainfluenzae · Proteus mirabilis · Campylobacter
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS
Serious and Otherwise Important Adverse Reactions The following serious and otherwise important adverse drug reactions are discussed in greater detail in other sections of labeling: · Hypersensitivity Reactions · Other Serious and Sometimes Fatal Reactions · Tendon Effects · Central Nervous System Effects · Clostridium difficile-Associated Diarrhea · Peripheral Neuropathy · Prolongation of the QT Interval · Musculoskeletal Disorders in Pediatric Patients · Blood Glucose Disturbances · Phototoxicity · Development of Drug Resistant Bacteria

COMPOSITION
Methylprednisolone is a synthetic (man-made) corticosteroid. Corticosteroids are naturally-occurring chemicals produced by the adrenal glands located adjacent to the kidneys. Corticosteroids affect metabolism in various ways and modify the immune system. Corticosteroids also block inflammation and are used in a wide variety of inflammatory diseases affecting many organs.
DESCRIPTION
Mepred Tablets contain methylprednisolone which is a glucocorticoid. Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. Methylprednisolone occurs as a white to practically white, odorless, crystalline powder. It is sparingly soluble in alcohol, in dioxane, and in methanol, slightly soluble in acetone, and in chloroform, and very slightly soluble in ether. It is practically insoluble in water. The chemical name for methylprednisolone is pregna - 1,4 - diene - 3,20-dione, 11, 17, 21-trihydroxy-6-methyl-, (6α, 11β)-and the molecular weight is 374.48
MODE OF ACTION
MethylprednisoloneTablets: 4mg, 8mg, 16 mg
INDICATION
Methylprednisolone is used to achieve prompt suppression of inflammation. Examples of inflammatory conditions for which methylprednisolone is used include rheumatoid arthritis, systemic lupus erythematosus, acute gouty arthritis, psoriatic arthritis, ulcerative colitis, and Crohn's disease. Severe allergic conditions that fail conventional treatment also may respond to methylprednisolone. Examples include bronchial asthma, allergic rhinitis, drug-induced dermatitis, and contact and atopic dermatitis. Chronic skin conditions treated with methylprednisolone include dermatitis herpetiformis, pemphigus, severe psoriasis and severe seborrheic dermatitis. Chronic allergic and inflammatory conditions of the uvea, iris, conjunctiva and optic nerves of the eyes also are treated with methylprednisolone.
DOSAGE & ADMINISTRATION
Dosage requirements of corticosteroids vary among individuals and the diseases being treated. In general, the lowest effective dose is used. The initial oral dose is 4-48 mg daily depending on the disease. The initial dose should be adjusted based on response. Corticosteroids given in multiple doses throughout the day are more effective but also more toxic than the same total daily dose given once daily, or every other day. Methylprednisolone should be taken with food.
INTERACTION
Troleandomycin (TAO), an infrequently used macrolide antibiotic, reduces the liver's ability to metabolize methylprednisolone (and possibly other corticosteroids). This interaction can result in higher blood levels of methylprednisolone and a higher probability of side effects. Erythromycin and clarithromycin (Biaxin) are likely to share this interaction, and ketoconazole (Nizoral) also inhibits the metabolism of methylprednisolone. Estrogens, including birth control pills, can increase the effect of corticosteroids by 50% by mechanisms that are not completely understood. For all of the above interactions, the dose of methylprednisolone may need to be lowered. Cyclosporin reduces the metabolism of methylprednisolone while methylprednisolone reduces the metabolism of cyclosporin. When given together, the dose of both drugs may need to be reduced to avoid increased side effects. Methylprednisolone may increase or decrease the effect of blood thinners [for example, warfarin (Coumadin)]. Blood clotting should be monitored and therapy adjusted in order to achieve the desired level of blood thinning (anti-coagulation). Phenobarbital, phenytoin (Dilantin), and rifampin (Rifadin, Rimactane) may increase the metabolism of methylprednisolone and other corticosteroids, resulting in lower blood levels and reduced effects. Therefore, the dose of methylprednisolone may need to be increased if treatment with phenobarbital is begun.
PREGNANCY INSTRUCTIONS
Methylprednisolone has not been adequately evaluated in pregnant women.
NURSING MOTHERS
Methylprednisolone has not been adequately evaluated in nursing mothers.
SIDE EFFECTS
Adverse effects of methylprednisolone depend on dose, duration and frequency of administration. Short courses of methylprednisolone are usually well-tolerated with few, mild side effects. Long term, high doses of methylprednisolone may produce predictable and potentially serious side effects. Whenever possible, the lowest effective doses of methylprednisolone should be used for the shortest length of time to minimize side effects. Alternate day dosing also can help reduce side effects. Side effects of methylprednisolone and other corticosteroids range from mild annoyances to serious irreversible bodily damage. Side effects include fluid retention, weight gain, high blood pressure, potassium loss, headache, muscle weakness, puffiness of the face, hair growth on the face, thinning and easy bruising of the skin, glaucoma, cataracts, peptic ulceration, worsening of diabetes, irregular menses, growth retardation in children, convulsions, and psychic disturbances. Psychic disturbances may include depression, euphoria, insomnia, mood swings, personality changes, and even psychotic behavior. Prolonged use of methylprednisolone can depress the ability of the body's adrenal glands to produce corticosteroids. Abruptly stopping methylprednisolone in these individuals can cause symptoms of corticosteroid insufficiency, with accompanying nausea, vomiting, and even shock. Therefore, withdrawal of methylprednisolone usually is accomplished by gradually lowering the dose. Gradually tapering methylprednisolone not only minimizes the symptoms of corticosteroid insufficiency, it also reduces the risk of an abrupt flare of the disease being treated. Methylprednisolone and other corticosteroids can mask signs of infection and impair the body's natural immune response to infection. Patients on corticosteroids are more susceptible to infections and can develop more serious infections than individuals not on corticosteroids. For example, chickenpox and measles viruses can produce serious and even fatal illnesses in patients on high doses of methylprednisolone. Live virus vaccines, such as smallpox vaccine, should be avoided in patients taking high doses of methylprednisolone since even vaccine viruses may cause disease in these patients. Some infectious organisms, such as tuberculosis (TB) and malaria, can remain dormant in patients for years. Methylprednisolone and other corticosteroids can allow these infections to reactivate and cause serious illness. Patients with dormant TB may require anti-TB medications while undergoing prolonged corticosteroid treatment. By interfering with the patient's immune response, methylprednisolone can prevent vaccines from being effective. Methylprednisolone also can interfere with the TB skin test and cause falsely negative results in patients with dormant TB infections. Methylprednisolone impairs calcium absorption and new bone formation. Patients on prolonged treatment with methylprednisolone and other corticosteroids can develop osteoporosis and an increased risk of bone fractures. Supplemental calcium and vitamin D are encouraged to slow this process of bone thinning. In rare individuals, destruction of large joints can occur while undergoing treatment with methylprednisolone or other corticosteroids (aseptic necrosis). These patients experience severe pain in the joints involved, and can require joint replacement. The reason behind such destruction is not clear. Methylprednisolone can be used in pregnancy, but is generally avoided.

COMPOSITION
DESCRIPTION
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Each tablet contains: Montelukast Sodium 10 mg, Levocetrizine Dihydrochloride IP 5 mg,
DESCRIPTION
Montelukast is used to prevent difficulty breathing, chest tightness, wheezing and coughing caused by asthma. Montelukast is also used to prevent bronchospasm (breathing difficulties) during exercise. Montelukast is also used to treat the symptoms of seasonal (occurs only at certain times of the year), and perennial (occurs all year round) allergic rhinitis (a condition associated with sneezing and stuffy, runny or itchy nose). Montelukast is in a class of medications called leukotriene receptor antagonists (LTRAs). It works by blocking the action of substances in the body that cause the symptoms of asthma and allergic rhinitis
MODE OF ACTION
The cysteinyl leukotrienes (LTC4, LTD4, LTE4) are products of arachidonic acid metabolism and are released from various cells, including mast cells and eosinophils. These eicosanoids bind to cysteinyl leukotriene (CysLT) receptors. The CysLT type-1 (CysLT1) receptor is found in the human airway (including airway smooth muscle cells and airway macrophages) and on other proinflammatory cells (including eosinophils and certain myeloid stem cells). CysLTs have been correlated with the pathophysiology of asthma and allergic rhinitis. In asthma, leukotriene-mediated effects include airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process. In allergic rhinitis, CysLTs are released from the nasal mucosa after allergen exposure during both early- and late-phase reactions and are associated with symptoms of allergic rhinitis. Intranasal challenge with CysLTs has been shown to increase nasal airway resistance and symptoms of nasal obstruction. MOTELUKAST has not been assessed in intranasal challenge studies. The clinical relevance of intranasal challenge studies is unknown. Montelukast is an orally active compound that binds with high affinity and selectivity to the CysLT1 receptor (in preference to other pharmacologically important airway receptors, such as the prostanoid, cholinergic, or β-adrenergic receptor). Montelukast inhibits physiologic actions of LTD4 at the CysLT1 receptor without any agonist activity.
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS
Side effects include gastrointestinal disturbances, hypersensitivity reactions, sleep disorders and increased bleeding tendency, aside from many other generic adverse reactions. Its use is associated with a higher incidence of Churg-Strauss syndrome (whether or not this drug is 'unmasking' subclinical Churg-Strauss is as yet uncertain)

COMPOSITION
Each 5 ml contains : Dextromethorphan Hydrobromide I.P---10 mg. Chlorpheniramine Maleate I.P--- 2 mg. Phenylpropanolamine Hydrochloride B.P--- 12.5 mg. menthol I.P--- 1 mg.
DESCRIPTION
FIRST TIME IN INDIA SUGAR FREE + SODIUM FREE BASE
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Each 5 ml. contains: Levocetirizine Hydrochloride I.P---2.5 mg. Ambroxol Hydrochloride I.P---30 mg.
DESCRIPTION
FIRST TIME IN INDIA SUGAR FREE + SODIUM FREE BASE
MODE OF ACTION
It is a potent Mucolytic and Mucokinetic agent capable of enhancing thin copious bronchial secretion. It breaks down the mucopolysaccharide fibers in the thick sticky sputum by depolymerising them
INDICATION
Cough associated with thick, tenacious sputum and bronchospasm.
DOSAGE & ADMINISTRATION
Adult – 10ml , 3 to 4 times daily. Children above 3years -2.5 -5ml, 3 to 4 times daily
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Each 5 ml contains : Ambroxol Hydrochloride I.P--- 15 mg. Terbutaline Hydrochloride I.P---1.50 mg. Guaiphenesin I.P---50 mg. menthol I.P--- 1.0 mg.
DESCRIPTION
FIRST TIME IN INDIA SUGAR FREE + SODIUM FREE BASE
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Each 5 ml contains: Magaldrate I.P---480 mg. Simethicone I.P----20mg.
DESCRIPTION
FIRST TIME IN INDIA SUGAR FREE BASE
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
– By raising gastric PH & by forming complex the non absorbable antacid decrease absorption of many drugs eg tetracycline , iron salts, fluroquinolones , ketakenazole ,H2 blockers , diazepam, phenathiazine , indomethacin ,phenytoin, INH ,ethambutol & nitrofurotoin.
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Hydroquinone U.S.P-----2.0%w/w Tretinion U.S.P-----------0.025%w/w Mometasone Furoate U.S.P---0.1%w/w
DESCRIPTION
FOR MELASAMA & HYPER PIGMENTATION
MODE OF ACTION
Topical Application of hydroquinone produces a reversible depigmentation of the skin by inhibition of the enzymatic oxidation of tyrosine to 3, 4 dihydroxphenlalanine and suppression of other melanocyle metabolic processes. Trerinoin is classified as keratolytic agent. Tretinoin is a retinoid metabolite of vitamine a that bind to intracellular receptor in the cytosol and nucleus but cutaneous levels of tretinoin in excess of physiologic concentration occur following application of a tretinoin-containing topical drug product. Mometasone furoate is a synthetic corticosteroid with anti inflammatory activity. Pigmet cream act by inhibiting one or more steps in the tyrosin-tyrosinase pathway of melanin synthsis. It also affects the formation of melanosomes and degradation of melanosome and eventually causes necrosis of the whole melanocytes. The hyperpigmented areas fade rapidly than surrounding normal skin, 80% of the patients with melasma may note some improvement within 8 week period.
INDICATION
The cream is indicated for the gradual bleaching of hyperpigmented dematological condition such as chloasma, melasma, freckeless and senile lentiginess with measures for sun avoidance, including the use of sunscreens.
DOSAGE & ADMINISTRATION
It should be applied once daily at night. It should be applied at least 30 minutes before bedtime. Gently wash the face and neck with a mild cleanser, Rinse the skin and make it dry. Apply a thin film of the cream to the hyperpigmented areas. Apply uniformly on the skin. Do not use occlusive dressing. Duration of application would be decided by the physician. During the day, use a broad spectrum sunscreen and wear protective clothing. Avoid sunlight exposure.
INTERACTION
Patient should avoid soaps and cosmetics with drying effects, products with high concentration of alcohol and assitringent and other irritants or keratolytic drugs while on this treatment. Patients are cautioned on concomitant use of medications that are known to be photosensitizing.
PREGNANCY INSTRUCTIONS
The safely of Pigmet cream during pregnancy and children (below 12 yrs) has not been established. Caurion should be exercised when Pigmet cream is administered to nursing mothers. Pigmet cream is strictly for external use only. Avoid contact with eyes & mucous membranes. Exposure to sunlight or ultra-violet light will cause repigmentation of bleached areas.
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Pantoprazole 40 mg tablets
DESCRIPTION
The active ingredient in pantoprazole sodium Tablets is a substituted benzimidazole, sodium 5-(difluoromethoxy)-2-[[(3,4-dimethoxy-2-pyridinyl)methyl] sulfinyl]-1H-benzimidazole sesquihydrate, a compound that inhibits gastric acid secretion. Its empirical formula is C16H14F2N3NaO4S x 1.5 H2O, with a molecular weight of 432.4. Pantoprazole sodium sesquihydrate is a white to off-white crystalline powder and is racemic. Pantoprazole has weakly basic and acidic properties. Pantoprazole sodium sesquihydrate is freely soluble in water, very slightly soluble in phosphate buffer at pH 7.4, and practically insoluble in n-hexane. The stability of the compound in aqueous solution is pH-dependent. The rate of degradation increases with decreasing pH. At ambient temperature, the degradation half-life is approximately 2.8 hours at pH 5.0 and approximately 220 hours at pH 7.8.
MODE OF ACTION
INDICATION
Short-Term Treatment of Erosive Esophagitis Associated With Gastroesophageal Reflux Disease (GERD) Pantoprazole is indicated for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For those patients who have not healed after 8 weeks of treatment, an additional 8-week course of Pantoprazole may be considered. Maintenance of Healing of Erosive Esophagitis Pantoprazole is indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in patients with gastroesophageal reflux disease (GERD). Controlled studies did not extend beyond 12 months. Pathological Hypersecretory Conditions Including Zollinger-Ellison Syndrome Pantoprazole is indicated for the long-term treatment of pathological hypersecretory conditions, including Zollinger-Ellison syndrome.
DOSAGE & ADMINISTRATION
Treatment of Erosive Esophagitis The recommended adult oral dose is 40 mg given once daily for up to 8 weeks. For those patients who have not healed after 8 weeks of treatment, an additional 8-week course of Pantoprazole may be considered Maintenance of Healing of Erosive Esophagitis The recommended adult oral dose is Pantoprazole 40 mg, taken daily Pathological Hypersecretory Conditions Including Zollinger-Ellison Syndrome The dosage of Pantoprazole in patients with pathological hypersecretory conditions varies with the individual patient. The recommended adult starting dose is 40 mg twice daily. Dosage regimens should be adjusted to individual patient needs and should continue for as long as clinically indicated. Doses up to 240 mg daily have been administered. Some patients have been treated continuously with Pantoprazole for more than 2 years. No dosage adjustment is necessary in patients with renal impairment, hepatic impairment, or for elderly patients. Doses higher than 40 mg/day have not been studied in hepatically-impaired patients. No dosage adjustment is necessary in patients undergoing hemodialysis. Pantoprazole Tablets should be swallowed whole, with or without food in the stomach.. Concomitant administration of antacids does not affect the absorption of Pantoprazole Tablets.
INTERACTION
Pantoprazole is metabolized through the cytochrome P450 system, primarily the CYP2C19 and to a minor extent the CYP3A4 isozymes, and subsequently undergoes Phase II conjugation .Based on studies evaluating possible interactions of pantoprazole with other drugs, no dosage adjustment is needed with concomitant use of the following: theophylline, cisapride, antipyrine, caffeine, carbamazepine, diazepam (and its active metabolite, desmethyldiazepam), diclofenac, naproxen, piroxicam, digoxin, ethanol, glyburide, an oral contraceptive (levonorgestrel/ethinyl estradiol), metoprolol, nifedipine, phenytoin, warfarin (see below), midazolam, clarithromycin, metronidazole, or amoxicillin. Clinically relevant interactions of pantoprazole with other drugs with the same metabolic pathways are not expected. Therefore, when coadministered with pantoprazole, adjustment of the dosage of pantoprazole or of such drugs may not be necessary. There was also no interaction with concomitantly administered antacids. There have been postmarketing reports of increased INR and prothrombin time in patients receiving proton pump inhibitors, including pantoprazole, and warfarin concomitantly. Increases in INR and prothrombin time may lead to abnormal bleeding and even death. Patients treated with proton pump inhibitors and warfarin concomitantly should be monitored for increases in INR and prothrombin time. Concomitant use of atazanavir and proton pump inhibitors is not recommended. Coadministration of atazanavir with proton pump inhibitors is expected to substantially decrease atazanavir plasma concentrations and thereby reduce its therapeutic effect. Because of profound and long lasting inhibition of gastric acid secretion, pantoprazole may interfere with absorption of drugs where gastric pH is an important determinant of their bioavailability (eg, ketoconazole, ampicillin esters, and iron salts).
PREGNANCY INSTRUCTIONS
Pregnancy Category B Teratology studies have been performed in rats at oral doses up to 450 mg/kg/day (88 times the recommended human dose based on body surface area) and rabbits at oral doses up to 40 mg/kg/day (16 times the recommended human dose based on body surface area) and have revealed no evidence of impaired fertility or harm to the fetus due to pantoprazole. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.
NURSING MOTHERS
Pantoprazole and its metabolites are excreted in the milk of rats. Pantoprazole excretion in human milk has been detected in a study of a single nursing mother after a single 40 mg oral dose. The clinical relevance of this finding is not known. Many drugs which are excreted in human milk have a potential for serious adverse reactions in nursing infants. Based on the potential for tumorigenicity shown for pantoprazole in rodent carcinogenicity studies, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the benefit of the drug to the mother.
SIDE EFFECTS
SIDE EFFECTS Worldwide, more than 11,100 patients have been treated with pantoprazole in clinical trials involving various dosages and duration of treatment. In general, pantoprazole has been well tolerated in both short-term and long-term trials.

COMPOSITION
Each capsule contains: Pantoprazol Sodium Sesquithydrate equilant to Pantoprazole--------40mg (as enteric coated pellets) Domperidone BP-------10mg
DESCRIPTION
MODE OF ACTION
Gastric ulcer, Peptic ulcer, Doudenal ulcer, GERD
INDICATION
Short-Term Treatment of Erosive Esophagitis Associated With Gastroesophageal Reflux Disease (GERD) Pantoprazole is indicated for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For those patients who have not healed after 8 weeks of treatment, an additional 8-week course of Pantoprazole may be considered. Maintenance of Healing of Erosive Esophagitis Pantoprazole is indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in patients with gastroesophageal reflux disease (GERD). Controlled studies did not extend beyond 12 months. Pathological Hypersecretory Conditions Including Zollinger-Ellison Syndrome Pantoprazole is indicated for the long-term treatment of pathological hypersecretory conditions, including Zollinger-Ellison syndrome.
DOSAGE & ADMINISTRATION
Treatment of Erosive Esophagitis The recommended adult oral dose is 40 mg given once daily for up to 8 weeks. For those patients who have not healed after 8 weeks of treatment, an additional 8-week course of Pantoprazole may be considered Maintenance of Healing of Erosive Esophagitis The recommended adult oral dose is Pantoprazole 40 mg, taken daily Pathological Hypersecretory Conditions Including Zollinger-Ellison Syndrome The dosage of Pantoprazole in patients with pathological hypersecretory conditions varies with the individual patient. The recommended adult starting dose is 40 mg twice daily. Dosage regimens should be adjusted to individual patient needs and should continue for as long as clinically indicated. Doses up to 240 mg daily have been administered. Some patients have been treated continuously with Pantoprazole for more than 2 years. No dosage adjustment is necessary in patients with renal impairment, hepatic impairment, or for elderly patients. Doses higher than 40 mg/day have not been studied in hepatically-impaired patients. No dosage adjustment is necessary in patients undergoing hemodialysis. Pantoprazole Tablets should be swallowed whole, with or without food in the stomach.. Concomitant administration of antacids does not affect the absorption of Pantoprazole Tablets.
INTERACTION
Pantoprazole is metabolized through the cytochrome P450 system, primarily the CYP2C19 and to a minor extent the CYP3A4 isozymes, and subsequently undergoes Phase II conjugation .Based on studies evaluating possible interactions of pantoprazole with other drugs, no dosage adjustment is needed with concomitant use of the following: theophylline, cisapride, antipyrine, caffeine, carbamazepine, diazepam (and its active metabolite, desmethyldiazepam), diclofenac, naproxen, piroxicam, digoxin, ethanol, glyburide, an oral contraceptive (levonorgestrel/ethinyl estradiol), metoprolol, nifedipine, phenytoin, warfarin (see below), midazolam, clarithromycin, metronidazole, or amoxicillin. Clinically relevant interactions of pantoprazole with other drugs with the same metabolic pathways are not expected. Therefore, when coadministered with pantoprazole, adjustment of the dosage of pantoprazole or of such drugs may not be necessary. There was also no interaction with concomitantly administered antacids. There have been postmarketing reports of increased INR and prothrombin time in patients receiving proton pump inhibitors, including pantoprazole, and warfarin concomitantly. Increases in INR and prothrombin time may lead to abnormal bleeding and even death. Patients treated with proton pump inhibitors and warfarin concomitantly should be monitored for increases in INR and prothrombin time. Concomitant use of atazanavir and proton pump inhibitors is not recommended. Coadministration of atazanavir with proton pump inhibitors is expected to substantially decrease atazanavir plasma concentrations and thereby reduce its therapeutic effect. Because of profound and long lasting inhibition of gastric acid secretion, pantoprazole may interfere with absorption of drugs where gastric pH is an important determinant of their bioavailability (eg, ketoconazole, ampicillin esters, and iron salts).
PREGNANCY INSTRUCTIONS
Pregnancy Category B Teratology studies have been performed in rats at oral doses up to 450 mg/kg/day (88 times the recommended human dose based on body surface area) and rabbits at oral doses up to 40 mg/kg/day (16 times the recommended human dose based on body surface area) and have revealed no evidence of impaired fertility or harm to the fetus due to pantoprazole. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.
NURSING MOTHERS
Pantoprazole and its metabolites are excreted in the milk of rats. Pantoprazole excretion in human milk has been detected in a study of a single nursing mother after a single 40 mg oral dose. The clinical relevance of this finding is not known. Many drugs which are excreted in human milk have a potential for serious adverse reactions in nursing infants. Based on the potential for tumorigenicity shown for pantoprazole in rodent carcinogenicity studies, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the benefit of the drug to the mother.
SIDE EFFECTS
SIDE EFFECTS Worldwide, more than 11,100 patients have been treated with pantoprazole in clinical trials involving various dosages and duration of treatment. In general, pantoprazole has been well tolerated in both short-term and long-term trials.

COMPOSITION
Salfer-L is a soft gelatine capsule that contains:- Lycopene - 5000 mcg Vitamin A - 2500 IU Vitamin C - 50 mg Vitamin E - 25 IU Zinc Sulphate Monohydrate - 27.45 mg Selenium - 70 mcg
DESCRIPTION
Lycopene is a bright red carotenoid pigment, a phytochemical found in tomatoes and other red fruits. Lycopene is the most common carotenoid in the human body and is one of the most potent carotenoid antioxidants. Its name is derived from the tomato's species classification, Solanum lycopersicum (formerly Lycopersicon esculentum
MODE OF ACTION
Lycopene is a terpene assembled from 8 isoprene units. The color of lycopene is due to its many conjugated carbon double bonds. Each double bond reduces the energy required for electrons to transition to higher energy states, allowing the molecule to absorb visible light of progressively longer wavelengths. Lycopene absorbs most of the visible spectrum, so it appears red. If lycopene is oxidized (for example, by reacting with bleaches or acids), the double bonds between carbon atoms will be broken, cleaving the molecule into smaller molecules each double-bonded to an oxygen atom. Although C=O bonds are also chromophoric, the much shorter molecules are unable to absorb enough light to appear colorful. A similar effect occurs if lycopene is reduced; reduction may saturate (convert the double bonds to single bonds) the lycopene molecule, diminishing its ability to absorb light. Dietary sources Fruits and vegetables that are high in lycopene include tomatoes, watermelon, pink grapefruit, pink guava, papaya, red bell pepper, gac, and rosehip. Unlike other fruits and vegetables, where nutritional content such as vitamin C is diminished upon cooking, processing of tomatoes increases the concentration of bioavailable lycopene. Lycopene in tomato paste is four times more bioavailable than in fresh tomatoes. This is because lycopene is insoluble in water and is tightly bound to vegetable fiber. Thus processed tomato products such as pasteurized tomato juice, soup, sauce, and ketchup contain the highest concentrations of bioavailable lycopene. Cooking and crushing tomatoes (as in the canning process) and serving in oil-rich dishes (such as spaghetti sauce or pizza) greatly increases assimilation from the digestive tract into the bloodstream. Lycopene is fat-soluble, so the oil is said to help absorption. Production Lycopene may be obtained from vegetables and fruits such as the tomato, but another source of lycopene is the fungus Blakeslea trispora. Nutritional benefits Lycopene is the most powerful carotenoid quencher of singlet oxygen[1], being 100 times more efficient in the singlet-oxygen quenching action than Vitamin E, which in turn has 125 times the quenching action of glutathione (water soluble). Singlet oxygen produced during exposure to ultraviolet light is a primary cause of skin aging.[2] Given its antioxidant properties, some scientific research has investigated the correlation between lycopene consumption and general health. Early research suggested some amelioration of cardiovascular disease, cancer, diabetes, osteoporosis, and even male infertility.[3] [4][5][6]. The most recent study, however, has cast significant doubt on these benefits, showing no link between lycopene and cancer prevention. In fact, a related antioxidant, beta-carotene, was shown to increase the number of prostate cancer cases[7]. Food coloring Lycopene, here dissolved in dichloromethane, is an intense bright red pigment. Due to its ubiquity, lycopene has been licensed for use as a food coloring. Lycopene is not water-soluble and instantly stains any sufficiently porous material, including most plastics. While a tomato stain can be fairly easily removed from fabric (provided the stain is fresh), lycopene diffuses into plastic, making it impossible to remove with hot water, soap, or detergent. (Bleach will destroy lycopene, however.) Plastics are especially susceptible to staining if heated, scratched, oiled, or pitted, for example by acids.
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS

COMPOSITION
Each Tablet contains: Ferrous ascorbate equivalent to elemental iron ………..100 mg Folic acid…………..1.5 mg
DESCRIPTION
Both ferrous ascorbate and folic acid play a crucial role during pregnancy and lactation ferrous ascorbate takes care of iron deficiency anemia occurring during pregnancy and lactation while folic acid takes care of the neural tube defects. As the requirement of both the nutrients that is iron and folic acid is increased in the two phases of motherhood pregnancy and lactation; therefore the combination is indicated as a nutritional requirement in both pregnancy and lactation. Thus, Salfer XT is a logical choice to be prescribed.
MODE OF ACTION
Supplementation of iron in the form of other conventional ferrous salts is subject to oxidation by food constituents, oxidation by alkaline environment and thereby reduced absorption and increased GI side effects. However, administration of iron in the form of ferrous ascorbate delivers maximum amount of ferrous iron to the duodenal brush border and at the same time produces minimum GI adverse effects and henceforth a significant Hb rise. After a week’s therapy, significant hemoglobin rise can be seen which is better than the conventional ferrous forms of iron as well as carbonyl and IPC forms of iron. Role of Ascorbic Acid in iron absorption: •Ascorbic Acid has been shown to inhibit the effect of phytates, phosphates and oxalates on iron absorption by the formation of soluble iron ascorbate complexes and by inhibiting the formation of insoluble iron complexes. •Ascorbic acid also inhibits the conversion of ferrous to ferric iron, this leads to increased absorption of iron. •Ascorbic acid also facilities the iron absorption by the formation of soluble iron ascorbate complex and inhibiting the formation of insoluble iron complexes. •Inhibition of conversion of ferrous to ferric iron reduces the amount of free radicals generated, thereby minimizing GI adverse effects. •Moreover, ascorbic acid mobilizes iron from the core of ferritin to the sites of erythropoesis and at the same time inhibits conversion of ferritin to hemosiderin which cannot be utilized. Thus, ascorbic acid improved iron utilization and prevents iron overload. B) Anti-oxidant property: Ferrous asccorbate has an intrinsic free radical scavenging property thus it is known to have antioxidant property. Free radicals are generally toxic molecules as a missing pair of electron is present and thus making the molecule unstable and further causing damage to cells by oxidation process. Here ferrous ascorbate acts as an antioxidant as its acts by neutralizing free radical and thus donates its ferrous atom to form a ferrous ascorbate introsyl complex in vivo with nitric acid (Fe-AA-NO). this complex formed thus inhibits cytochrome oxidase which helps in free radical production (a toxic molecule).
INDICATION
To take care of nutritional requirements in: a) Pregnancy b) Lactation USPs of Salfer XT •Complete supplement of iron in pregnancy and lactation. •Salfer Xt has iron in the form ferrous ascorbate which has an edge over the other conventional iron salts like adequate element iron confirming to WHO standards, superior absorption and hence better bioavailability, additional anti-oxidant properties, maximum iron utilization, with no food interaction and better tolerability in G.I.T. •Ease of dose-OD dosage •Reducing the cost of therapy
DOSAGE & ADMINISTRATION
Once a day before or after meals (no interaction with food)
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
oral iron preparations may aggravate existing peptic ulcer, regional enteritis and ulcerative colitis. Iron compounds taken orally can impair the absorption of tetracycline antibiotics. Antacids given concomitantly with iron compounds decrease iron absorption.
SIDE EFFECTS
Upper abdominal discomfort, nausea, diarrhea, constipation- often appear at daily doses>60 mg •Black Stools •Constipation may lead to fecal impaction, especially in elderly individuals.

COMPOSITION
Mechanism of Action: Micropuncture studies in animals have shown that torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the Na+/K+/2CI--carrier system. Clinical pharmacology studies have confirmed this site of action in humans, and effects in other segments of the nephron have not been demonstrated. Diuretic activity thus correlates better with the rate of drug excretion in the urine than with the concentration in the blood. Torsemide increases the urinary excretion of sodium, chloride, and water, but it does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance. Pharmacokinetics and Metabolism: The bioavailability of Torsemide tablets is approximately 80%, with little intersubject variation; the 90% confidence interval is 75% to 89%. The drug is absorbed with little first-pass metabolism, and the serum concentration reaches its peak (Cmax) within 1 hour after oral administration. Cmax and area under the serum concentration-time curve (AUC) after oral administration are proportional to dose over the range of 2.5 mg to 200 mg. Simultaneous food intake delays the time to Cmax by about 30 minutes, but overall bioavailability (AUC) and diuretic activity are unchanged. Absorption is essentially unaffected by renal or hepatic dysfunction. The volume of distribution of torsemide is 12 liters to 15 liters in normal adults or in patients with mild to moderate renal failure or congestive heart failure. In patients with hepatic cirrhosis, the volume of distribution is approximately doubled. In normal subjects the elimination half-life of torsemide is approximately 3.5 hours. Torsemide is cleared from the circulation by both hepatic metabolism (approximately 80% of total clearance) and excretion into the urine (approximately 20% of total clearance in patients with normal renal function). The major metabolite in humans is the carboxylic acid derivative, which is biologically inactive. Two of the lesser metabolites possess some diuretic activity, but for practical purposes metabolism terminates the action of the drug. Because torsemide is extensively bound to plasma protein (>99%), very little enters tubular urine via glomerular filtration. Most renal clearance of torsemide occurs via active secretion of the drug by the proximal tubules into tubular urine. In patients with decompensated congestive heart failure, hepatic and renal clearance are both reduced, probably because of hepatic congestion and decreased renal plasma flow, respectively. The total clearance of torsemide is approximately 50% of that n in healthy volunteers, and the plasma half-life and AUC are correspondingly increased. Because of reduced renal clearance, a smaller fraction of any given dose is delivered to the intraluminal site of action, so at any given dose there is less natriuresis in patients with congestive heart failure than in normal subjects. In patients with renal failure, renal clearance of torsemide is markedly decreased but total plasma clearance is not significantly altered. A smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action of any given dose of diuretic is reduced. A diuretic response in renal failure may still be achieved if patients are given higher doses. The total plasma clearance and elimination half-life of torsemide remain normal under the conditions of impaired renal function because metabolic elimination by the liver remains intact.
DESCRIPTION
Torsemide is a diuretic of the pyridine-sulfonylurea class. Its chemical name is 1-isopropyl-3-[(4-m-toluidino-3-pyridyl) sulfonyl]urea. Its empirical formula is C16H20N4O3S, its pKa is 7.1, and its molecular weight is 348.43.Torsemide is a white to off-white crystalline powder. The tablets for oral administration also contain lactose NF, crospovidone NF, povidone USP, microcrystalline cellulose NF, and magnesium stearate NF. Torsemide ampuls for intravenous injection contain a sterile solution of torsemide (10 mg/mL), polyethylene glycol-400 NF, tromethamine USP, and sodium hydroxide NF (as needed to adjust pH) in water for injection USP. Torsemide is a diuretic of the pyridine-sulfonylurea class. Its chemical name is 1-isopropyl-3-[(4-m-toluidino-3-pyridyl) sulfonyl]urea. Its empirical formula is C16H20N4O3S, its pKa is 7.1, and its molecular weight is 348.43.Torsemide is a white to off-white crystalline powder. The tablets for oral administration also contain lactose NF, crospovidone NF, povidone USP, microcrystalline cellulose NF, and magnesium stearate NF. Torsemide ampuls for intravenous injection contain a sterile solution of torsemide (10 mg/mL), polyethylene glycol-400 NF, tromethamine USP, and sodium hydroxide NF (as needed to adjust pH) in water for injection USP.
MODE OF ACTION
Uritor for oral administration is available as white, scored tablets containing, 10 mg & 20 mg, of torsemide.
INDICATION
Torsemide is indicated for the treatment of edema associated with congestive heart failure, renal disease, or hepatic disease. Use of torsemide has been found to be effective for the treatment of edema associated with chronic renal failure. Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials. Torsemide is indicated for the treatment of hypertension alone or in combination with other antihypertensive agents.
DOSAGE & ADMINISTRATION
General: Torsemide tablets may be given at any time in relation to a meal, as convenient. Special dosage adjustment in the elderly is not necessary. Because of the high bioavailability of Torsemide, oral and intravenous doses are therapeutically equivalent, so patients may be switched to and from the intravenous form with no change in dose. Congestive Heart Failure: The usual initial dose is 10 mg or 20 mg of once-daily oral or intravenous Torsemide. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied. Chronic Renal Failure: The usual initial dose of Torsemide is 20 mg of once-daily oral or intravenous Torsemide. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied. Hepatic Cirrhosis: The usual initial dose is 5 mg or 10 mg of once-daily oral or intravenous Torsemide, administered together with an aldosterone antagonist or a potassium-sparing diuretic. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 40 mg have not been adequately studied. Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials. Hypertension: The usual initial dose is 5 mg once daily. If the 5 mg dose does not provide adequate reduction in blood pressure within 4 to 6 weeks, the dose may be increased to 10 mg once daily. If the response to 10 mg is insufficient, an additional antihypertensive agent should be added to the treatment regimen.
INTERACTION
In patients with essential hypertension, Torsemide has been administered together with beta-blockers, ACE inhibitors, and calcium-channel blockers. In patients with congestive heart failure, Torsemide has been administered together with digitalis glycosides, ACE inhibitors, and organic nitrates. None of these combined uses was associated with new or unexpected adverse events. Torsemide does not affect the protein binding of glyburide or of warfarin, the anticoagulant effect of phenprocoumon (a related coumarin derivative), or the pharmacokinetics of digoxin or carvedilol (a vasodilator/beta-blocker). In healthy subjects, coadministration of Torsemide was associated with significant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. However, clinical experience indicates that dosage adjustment of either agent is not required. Because Torsemide and salicylates compete for secretion by renal tubules, patients receiving high doses of salicylates may experience salicylate toxicity when Torsemide is concomitantly administered. Also, although possible interactions between torsemide and nonsteroidal anti-inflammatory agents (including aspirin) have not been studied, coadministration of these agents with another loop diuretic (furosemide) has occasionally been associated with renal dysfunction. The natriuretic effect of Torsemide (like that of many other diuretics) is partially inhibited by the concomitant administration of indomethacin. This effect has been demonstrated for Torsemide under conditions of dietary sodium restriction (50 mEq/day) but not in the presence of normal sodium intake (150 mEq/day). The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine or spironolactone. Coadministration of digoxin is reported to increase the area under the curve for torsemide by 50%, but dose adjustment of Torsemide is not necessary. Concomitant use of torsemide and cholestyramine has not been studied in humans but, in a study in animals, coadministration of cholestyramine decreased the absorption of orally administered torsemide. If Torsemide and cholestyramine are used concomitantly, simultaneous administration is not recommended. Coadministration of probenecid reduces secretion of Torsemide into the proximal tubule and thereby decreases the diuretic activity of Torsemide. Other diuretics are known to reduce the renal clearance of lithium, inducing a high risk of lithium toxicity, so coadministration of lithium and diuretics should be undertaken with great caution, if at all. Coadministration of lithium and Torsemide has not been studied. Other diuretics have been reported to increase the ototoxic potential of aminoglycoside antibiotics and of ethacrynic acid, especially in the presence of impaired renal function. These potential interactions with Torsemide have not been studied.
PREGNANCY INSTRUCTIONS
Pregnancy Category B. There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/kg basis, this is 15 times a human dose of 20 mg/day; on a mg/m2 basis, the animal dose is 10 times the human dose), or in rabbits, treated with 1.6 mg/kg/day (on a mg/kg basis, 5 times the human dose of 20 mg/kg/day; on a mg/m2 basis, 1.7 times this dose). Fetal and maternal toxicity (decrease in average body weight, increase in fetal resorption and delayed fetal ossification) occurred in rabbits and rats given doses 4 (rabbits) and 5 (rats) times larger. Adequate and well-controlled studies have not been carried out in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed. Labor and Delivery: The effect of Torsemide on labor and delivery is unknown.
NURSING MOTHERS
It is not known whether Torsemide is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when DEMADEX is administered to a nursing woman
SIDE EFFECTS
At the time of approval, Torsemide (Demadex) had been evaluated for safety in approximately 4000 subjects: over 800 of these subjects received Torsemide for at least 6 months, and over 380 were treated for more than 1 year. Among these subjects were 564 who received Torsemide during United States-based trials in which 274 other subjects received placebo. The reported side effects of Torsemide were generally transient, and there was no relationship between side effects and age, sex, race, or duration of therapy. Discontinuation of therapy due to side effects occurred in 3.5% of United States patients treated with Torsemide and in 4.4% of patients treated with placebo. In studies conducted in the United States and Europe, discontinuation rates due to side effects were 3.0% (38/1250) with Torsemide and 3.4% (13/380) with furosemide in patients with congestive heart failure, 2.0% (8/409) with Torsemide and 4.8% (11/230) with furosemide in patients with renal insufficiency, and 7.6% (13/170) with Torsemide and 0% (0/33) with furosemide in patients with cirrhosis. The most common reasons for discontinuation of therapy with Torsemide were (in descending order of frequency) dizziness, headache, nausea, weakness, vomiting, hyperglycemia, excessive urination, hyperuricemia, hypokalemia, excessive thirst, hypovolemia, impotence, esophageal hemorrhage, and dyspepsia. Dropout rates for these adverse events ranged from 0.1% to 0.5%. The side effects considered possibly or probably related to study drug that occurred in United States placebo-controlled trials in more than 1% of patients treated with Torsemide. The daily doses of Torsemide used in these trials ranged from 1.25 mg to 20 mg, with most patients receiving 5 mg to 10 mg; the duration of treatment ranged from 1 to 52 days, with a median of 41 days. Of the side effects listed in the table, only excessive urination occurred significantly more frequently in patients treated with Torsemide than in patients treated with placebo. In the placebo-controlled hypertension studies whose design allowed side-effect rates to be attributed to dose, excessive urination was reported by 1% of patients receiving placebo, 4% of those treated with 5 mg of daily Torsemide, and 15% of those treated with 10 mg. The complaint of excessive urination was generally not reported as an adverse event among patients who received Torsemide for cardiac, renal, or hepatic failure. Serious adverse events reported in the clinical studies for which a drug relationship could not be excluded were atrial fibrillation, chest pain, diarrhea, digitalis intoxication, gastrointestinal hemorrhage, hyperglycemia, hyperuricemia, hypokalemia, hypotension, hypovolemia, shunt thrombosis, rash, rectal bleeding, syncope, and ventricular tachycardia. Angioedema has been reported in a patient exposed to Torsemide who was later found to be allergic to sulfa drugs. Of the adverse reactions during placebo-controlled trials listed without taking into account assessment of relatedness to drug therapy, arthritis and various other nonspecific musculoskeletal problems were more frequently reported in association with Torsemide than with placebo, even though gout was somewhat more frequently associated with placebo. These reactions did not increase in frequency or severity with the dose of Torsemide. One patient in the group treated with Torsemide withdrew due to myalgia, and one in the placebo group withdrew due to gout. Warnings Hepatic Disease With Cirrhosis and Ascites: Torsemide should be used with caution in patients with hepatic disease with cirrhosis and ascites, since sudden alterations of fluid and electrolyte balance may precipitate hepatic coma. In these patients, diuresis with Torsemide (or any other diuretic) is best initiated in the hospital. To prevent hypokalemia and metabolic alkalosis, an aldosterone antagonist or potassium-sparing drug should be used concomitantly with Torsemide. Ototoxicity: Tinnitus and hearing loss (usually reversible) have been observed after rapid intravenous injection of other loop diuretics and have also been observed after oral Torsemide. It is not certain that these events were attributable to Torsemide. Ototoxicity has also been seen in animal studies when very high plasma levels of torsemide were induced. Administered intravenously, Torsemide should be injected slowly over 2 minutes, and single doses should not exceed 200 mg. Volume and Electrolyte Depletion: Patients receiving diuretics should be observed for clinical evidence of electrolyte imbalance, hypovolemia, or prerenal azotemia. Symptoms of these disturbances may include one or more of the following: dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, nausea, and vomiting. Excessive diuresis may cause dehydration, blood-volume reduction, and possibly thrombosis and embolism, especially in elderly patients. In patients who develop fluid and electrolyte imbalances, hypovolemia, or prerenal azotemia, the observed laboratory changes may include hyper- or hyponatremia, hyper- or hypochloremia, hyper- or hypokalemia, acid-base abnormalities, and increased blood urea nitrogen (BUN). If any of these occur, Torsemide should be discontinued until the situation is corrected; Torsemide may be restarted at a lower dose. In controlled studies in the United States, Torsemide was administered to hypertensive patients at doses of 5 mg or 10 mg daily. After 6 weeks at these doses, the mean decrease in serum potassium was approximately 0.1 mEq/L. The percentage of patients who had a serum potassium level below 3.5 mEq/L at any time during the studies was essentially the same in patients who received Torsemide (1.5%) as in those who received placebo (3%). In patients followed for 1 year, there was no further change in mean serum potassium levels. In patients with congestive heart failure, hepatic cirrhosis, or renal disease treated with Torsemide at doses higher than those studied in United States antihypertensive trials, hypokalemia was observed with greater frequency, in a dose-related manner. In patients with cardiovascular disease, especially those receiving digitalis glycosides, diuretic-induced hypokalemia may be a risk factor for the development of arrhythmias. The risk of hypokalemia is greatest in patients with cirrhosis of the liver, in patients experiencing a brisk diuresis, in patients who are receiving inadequate oral intake of electrolytes, and in patients receiving concomitant therapy with corticosteroids or ACTH. Periodic monitoring of serum potassium and other electrolytes is advised in patients treated with Torsemide.

COMPOSITION
Levocetrizine tablets:-5mg
DESCRIPTION
This medicine contains the active ingredient levocetirizine dihydrochloride, which is a type of medicine called a non-sedating antihistamine. It works by preventing the actions of histamine. Histamine is a substance produced by the body as part of its defence mechanisms. It is stored in cells called mast cells, in almost all tissues of the body. When the body reacts to a foreign substance (known as an allergen, eg flower pollen), the mast cells stimulated by the allergen release their stores of histamine. The released histamine then binds to its receptors (H-1 receptors), causing a chain reaction that results in allergic symptoms. It causes an increase in blood flow to the area of the allergy, and the release of other chemicals that add to the allergic response. All this results in the symptoms of an allergic reaction. In hayfever, histamine causes inflammation of the nose, eyes, skin or airways and results in itchy watery eyes, a runny nose, sneezing and nasal congestion. Levocetirizine works by blocking histamine receptors. It does not prevent the actual release of histamine from mast cells, but prevents it binding to its receptors. This in turn prevents the release of other allergy chemicals and increased blood supply to the area, and provides relief from the typical symptoms of hayfever. Levocetirizine can also be used to relieve the symptoms of a condition called chronic idiopathic urticaria. This is a chronic itchy rash, similar to nettle rash, but with no apparant cause. Blocking the actions of histamine relieves the itching and reduces the rash associated with this condition. Levocetirizine is called a non-sedating antihistamine as it does not enter the brain, and is therefore unlikely to cause drowsiness. However, some people may experience some slight sleepiness or fatigue.
MODE OF ACTION
INDICATION
Allergic diseases • Hayfever • Hayfever that occurs throughout the year due to allergies, eg pets, dust mites • Ongoing itchy rash with no known cause
DOSAGE & ADMINISTRATION
INTERACTION
Warning! • Avoid drinking large amounts of alcohol when taking this medicine. • This medicine may reduce your ability to drive or operate machinery safely. Do not drive or operate machinery until you know how this medicine affects you and you are sure it won't affect your performance. • This medicine is not recommended for children under six years of age. Use with caution in • Decreased kidney function Not to be used in • Allergy to medicines that contain piperazine derivatives (your doctor will know more about this - tell them if you are allergic to any medicines) • Hereditary galactose intolerance • Hereditary Lapp lactase deficiency • Inherited inability to absorb the sugars glucose and galactose (glucose-galactose malabsorption) • Severely decreased kidney function This medicine should not be used if you are allergic to one or any of its ingredients. Please inform your doctor or pharmacist if you have previously experienced such an allergy. If you feel you have experienced an allergic reaction, stop using this medicine and inform your doctor or pharmacist immediately.
PREGNANCY INSTRUCTIONS
Certain medicines should not be used during pregnancy or breastfeeding. However, other medicines may be safely used in pregnancy or breastfeeding providing the benefits to the mother outweigh the risks to the unborn baby. Always inform your doctor if you are pregnant or planning a pregnancy, before using any medicine. • The safety of this medicine in pregnancy has not been established. It should therefore be used with caution during pregnancy, and only if the benefits to the mother outweigh any risks to the foetus. Seek medical advice from your doctor. • This medicine passes into breast milk. It should be used with caution by breastfeeding mothers, and only if the expected benefit to the mother is greater than the possible risk to the nursing infant. Seek medical advice from your doctor.
NURSING MOTHERS
SIDE EFFECTS
Medicines and their possible side effects can affect individual people in different ways. The following are some of the side effects that are known to be associated with this medicine. Because a side effect is stated here, it does not mean that all people using this medicine will experience that or any side effect. • Headache • Abdominal pain • Dry mouth • Fatigue • Inflammation of the throat (pharyngitis) • Sleepiness • Weakness or loss of strength (asthenia) • Inflammation of the lining of the nose (rhinitis) causing a blocked or runny nose • Migraine The side effects listed above may not include all of the side effects reported by the drug's manufacturer. For more information about any other possible risks associated with this medicine, please read the information provided with the medicine or consult your doctor or pharmacist.

COMPOSITION
Each film coated Tablet contains : Levocetrizine dihydrochloride--------5mg, Paracetamol I P--------500mg, Phenylpropanolamine hydrchloride--25mg
DESCRIPTION
MODE OF ACTION
INDICATION
DOSAGE & ADMINISTRATION
INTERACTION
PREGNANCY INSTRUCTIONS
NURSING MOTHERS
SIDE EFFECTS