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Furosemide is a diuretic which is an anthranilic acid derivative. Furosemide Tablets for oral administration contain furosemide as the active ingredient and the following inactive ingredients: corn starch NF, lactose monohydrate NF, magnesium stearate NF, pregelatinized starch NF, and talc USP. Chemically, it is 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid. Furosemide is available as white-off white tablets for oral administration in dosage strengths of 20, 40 and 80 mg. Furosemide is a white to off-white odorless crystalline powder. It is practically insoluble in water, sparingly soluble in alcohol, freely soluble in dilute alkali solutions and insoluble in dilute acids. The CAS Registry Number is 54-31-9. The structural formula is as follows: Tested by USP Dissolution Test 1. This is an image of the structural formula for furosemide.

CLINICAL PHARMACOLOGY 12.1 Mechanism of Action Nonclinical studies have shown that paroxetine is an SSRI. Paroxetine is not an estrogen, and its mechanism of action for the treatment of VMS is unknown. 12.2 Pharmacodynamics Studies at clinically relevant doses in humans have demonstrated that paroxetine blocks the uptake of serotonin into human platelets. In vitro studies in animals also suggest that paroxetine is a selective inhibitor of neuronal serotonin reuptake and has weak effects on norepinephrine and dopamine neuronal reuptake. In vitro radioligand binding studies indicate that paroxetine has little affinity for muscarinic alpha 1 -, alpha 2 -, beta-adrenergic-, dopamine (D 2 )-, 5-HT 1 -, 5-HT 2 -, and histamine (H 1 )-receptors. 12.3 Pharmacokinetics Absorption, Distribution, Metabolism and Excretion Absorption Paroxetine is completely absorbed after oral dosing of the mesylate salt. In a study in which healthy postmenopausal women (n=24) received Paroxetine Capsules 7.5 mg capsules as a daily dose for 14 days, steady-state paroxetine concentrations were achieved by approximately 12 days of dosing for most subjects, although it may take substantially longer in an occasional patient. Peak concentrations were reached at a median of 6 hours (3 to 8 hours range). Steady-state mean values of C max , C min , and AUC 0-last were 13.10 ng/mL (CV 91%), 7.17 ng/mL (CV 99%), and 237 hr * ng/mL (CV 94%), respectively. Steady-state AUC 0-24 values were about 3 times those of AUC 0-inf following a single dose, indicating non-linear pharmacokinetics. Steady-state C max values were approximately 5 times greater than those attained after a single dose and steady-state exposure based on AUC 0-24 was about 10 times greater than AUC 0-24 after a single dose. The nonlinear kinetics and excess accumulation are due to the fact that CYP2D6, an enzyme that is in part responsible for paroxetine metabolism, is readily saturable. The effects of food on the bioavailability of paroxetine were studied with paroxetine tablets at higher strength. AUC was only slightly increased (6%) when drug was administered with food but the C max was 29% greater, while the time to reach peak plasma concentration decreased from 6.4 hours post-dosing to 4.9 hours. Paroxetine Capsules can be taken with or without food. Distribution Paroxetine distributes throughout the body, including the central nervous system, with only 1% remaining in the plasma. Approximately 95% and 93% of paroxetine is bound to plasma protein at 100 ng/mL and 400 ng/mL, respectively. Under clinical conditions, paroxetine concentrations would normally be less than 100 ng/mL. Paroxetine does not alter the in vitro protein binding of phenytoin or warfarin. Metabolism Paroxetine is extensively metabolized after oral administration. The principal metabolites are polar and conjugated products of oxidation and methylation, which are readily cleared. Conjugates with glucuronic acid and sulfate predominate, and major metabolites have been isolated and identified. Data indicate that the metabolites have no more than 1/50 the potency of the parent compound at inhibiting serotonin uptake. The metabolism of paroxetine is accomplished in part by cytochrome CYP2D6. Saturation of this enzyme at clinical doses appears to account for the nonlinearity of paroxetine kinetics with increasing dose and increasing duration of treatment. The role of this enzyme in paroxetine metabolism also suggests potential drug-drug interactions [see Drug Interactions ( 7 )] . At steady state, when the CYP2D6 pathway is essentially saturated, paroxetine clearance is governed by alternative P450 isozymes, which, unlike CYP2D6, show no evidence of saturation. Excretion Approximately 64% of a 30 mg oral solution of paroxetine was excreted in the urine with 2% as the parent compound and 62% as metabolites over a 10-day post-dosing period. About 36% of the dose was excreted in the feces (probably via the bile), mostly as metabolites and less than 1% as the parent compound over the 10-day post-dosing period. Specific Populations Renal and Liver Impairment Increased plasma concentrations of paroxetine occur in subjects with renal and hepatic impairment. The mean plasma concentration in patients with creatinine clearance below 30 mL/min was approximately 4 times greater than seen in normal volunteers. Patients with creatinine clearance of 30 to 60 mL/min and patients with hepatic impairment had about a 2-fold increase in plasma concentrations (AUC, C max ). No Paroxetine Capsules dose adjustment is considered necessary in patients with renal or hepatic impairment. Elderly Patients In a multiple-dose study in the elderly at daily paroxetine doses of 20, 30, and 40 mg, C min concentrations were about 70% to 80% greater than the respective C min concentrations in nonelderly subjects. No Paroxetine Capsules dose adjustment is considered necessary in elderly patients. Drug Interaction Studies Potential Effect of Paroxetine Capsules on Other Drugs Drugs Metabolized by CYP3A4 An in vivo drug interaction study involving the co-administration under steady-state conditions of paroxetine and terfenadine, a substrate for cytochrome CYP3A4, revealed no effect of paroxetine on terfenadine pharmacokinetics. In vitro studies have shown ketoconazole, a potent inhibitor of CYP3A4 activity, to be at least 100 times more potent than paroxetine as an inhibitor of the metabolism of several substrates for CYP3A4, including astemizole, triazolam, and cyclosporine. Based on the assumption that the relationship between paroxetine’s in vitro Ki and its lack of effect on terfenadine’s in vivo clearance predicts its effect on other CYP3A4 substrates, paroxetine’s extent of inhibition of CYP3A4 activity is not likely to be of clinical significance. Drugs Metabolized by CYP2D6 Many drugs are metabolized by the cytochrome P450 isozyme CYP2D6. Like other agents that are metabolized by CYP2D6, paroxetine may significantly inhibit the activity of this isozyme. In most patients (> 90%), this CYP2D6 isozyme is saturated early during paroxetine dosing. Specific studies investigating the effect of paroxetine on drugs metabolized by CYP2D6 are listed below: Pimozide: Higher doses of paroxetine have been shown to elevate plasma levels of pimozide. In a controlled study of healthy volunteers, after paroxetine was titrated to 60 mg daily, co-administration of a single dose of 2 mg pimozide was associated with mean increases in pimozide AUC of 151% and C max of 62%, compared to pimozide administered alone [see Drug Interactions ( 7.1 )] . Tamoxifen: It is uncertain whether the co-administration of paroxetine and tamoxifen has a significant adverse effect on the efficacy of tamoxifen. Some studies have shown that the efficacy of tamoxifen, as measured by the risk of breast cancer relapse/mortality, may be reduced when co-prescribed with paroxetine as a result of paroxetine’s irreversible inhibition of CYP2D6. However, other studies have failed to demonstrate such a risk [see Warnings and Precautions ( 5.3 ) and Drug Interactions ( 7.1 )] . Desipramine: In one study, daily dosing of paroxetine (20 mg once daily) under steady-state conditions increased single dose desipramine (100 mg) C max , AUC, and T 1/2 by an average of approximately 2-, 5-, and 3-fold, respectively [see Drug Interactions ( 7.1 )] . Risperidone: Daily dosing of paroxetine 20 mg in patients stabilized on risperidone (4 to 8 mg/day), a CYP2D6 substrate, increased mean plasma concentrations of risperidone approximately 4-fold, decreased 9-hydroxyrisperidone concentrations approximately 10%, and increased concentrations of the active moiety (the sum of risperidone plus 9-hydroxyrisperidone) approximately 1.4-fold [see Drug Interactions ( 7.1 )] . Atomoxetine: The effect of paroxetine on the pharmacokinetics of atomoxetine has been evaluated when both drugs were at steady state. In healthy volunteers who were extensive metabolizers of CYP2D6, paroxetine 20 mg daily was given in combination with 20 mg atomoxetine every 12 hours. This resulted in increases in steady-state atomoxetine AUC values that were 6-to 8-fold greater and in atomoxetine C max values that were 3-to 4-fold greater than when atomoxetine was given alone [see Drug Interactions ( 7.1 )] . Digoxin: Mean digoxin AUC at steady state decreased by 15% in the presence of paroxetine [see Drug Interactions ( 7.1 )] . Beta Blockers: In a study in which propranolol (80 mg twice daily) was dosed orally for 18 days, the steady-state plasma concentrations of propranolol were unaltered during co-administration with paroxetine (30 mg once daily) for the final 10 days. The effects of propranolol on paroxetine have not been evaluated. Potential Effect of Other Drugs on Paroxetine Capsules Concomitant use of paroxetine with other drugs that alter CYP enzymes activities including CYP2D6 may affect the plasma concentrations of paroxetine. Specific studies investigating the effect of other drugs on paroxetine are listed below: Cimetidine: Cimetidine inhibits many cytochrome P450 enzymes. In a study in which paroxetine (30 mg once daily) was dosed orally for 4 weeks, steady-state plasma concentrations of paroxetine were increased by approximately 50% during co-administration with oral cimetidine (300 mg three times daily) for the final week [see Drug Interactions ( 7.2 )] . Phenobarbital: Phenobarbital induces many cytochrome P450 enzymes. When a single oral 30 mg dose of paroxetine was administered at phenobarbital steady state (100 mg once daily for 14 days), paroxetine AUC and T 1/2 were reduced (by an average of 25% and 38%, respectively) compared to paroxetine administered alone. The effect of paroxetine on phenobarbital pharmacokinetics was not studied. Because paroxetine exhibits nonlinear pharmacokinetics, the results of this study may not address the case where the 2 drugs are both being chronically dosed [see Drug Interactions ( 7.2 )] . Phenytoin: When a single oral 30 mg dose of paroxetine was administered at phenytoin steady state (300 mg once daily for 14 days), paroxetine AUC and T 1/2 were reduced (by an average of 50% and 35%, respectively) compared to paroxetine administered alone. In a separate study, when a single oral 300 mg dose of phenytoin was administered at paroxetine steady state (30 mg once daily for 14 days), phenytoin AUC was slightly reduced (12% on average) compared to phenytoin administered alone. Because both drugs exhibit nonlinear pharmacokinetics, the above studies may not address the case where the 2 drugs are both being chronically dosed [see Drug Interactions ( 7.2 )] . Digoxin: A clinical drug interaction study showed that concurrent use of digoxin did not affect paroxetine exposure. Diazepam: A clinical drug interaction study showed that concurrent use of diazepam did not affect paroxetine exposure.

Bumetanide is a loop diuretic available as 0.5 mg, 1 mg and 2 mg tablets for oral administration; each tablet also contains lactose anhydrous, magnesium stearate, microcrystalline cellulose, pregelatinized starch. Chemically, 3-Butylamino-4-phenoxy-5-sulphamoylbenzoic Acid. It is a practically white crystalline powder having a calculated molecular weight of 364.42, and the following structural formula: C 17 H 20 N 2 O 5 S The product meets USP Dissolution Test 2. structure

Candesartan cilexetil and hydrochlorothiazide tablets combine an angiotensin II receptor (type AT 1 ) antagonist and a diuretic, hydrochlorothiazide. Candesartan cilexetil, a nonpeptide, is chemically described as (±)-1-Hydroxyethyl 2-ethoxy-1-[ p -( o -1 H -tetrazol-5-ylphenyl)benzyl]-7-benzimidazolecarboxylate, cyclohexyl carbonate (ester). Its empirical formula is C 33 H 34 N 6 O 6 and its structural formula is: Candesartan cilexetil is a white to off-white powder with a molecular weight of 610.67. It is practically insoluble in water and sparingly soluble in methanol. Candesartan cilexetil is a racemic mixture containing one chiral center at the cyclohexyloxycarbonyloxy ethyl ester group. Following oral administration, candesartan cilexetil undergoes hydrolysis at the ester link to form the active drug, candesartan, which is achiral. Hydrochlorothiazide is 6-chloro-3,4-dihydro-2 H -1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is C 7 H 8 ClN 3 O 4 S 2 and its structural formula is: Hydrochlorothiazide is a white, or practically white, crystalline powder with a molecular weight of 297.72, which is slightly soluble in water, but freely soluble in sodium hydroxide solution. Candesartan cilexetil and hydrochlorothiazide tablets, USP, are available for oral administration in three tablet strengths of candesartan cilexetil, USP, and hydrochlorothiazide, USP. Candesartan cilexetil and hydrochlorothiazide tablets 16 mg/12.5 mg contain 16 mg of candesartan cilexetil and 12.5 mg of hydrochlorothiazide. Candesartan cilexetil and hydrochlorothiazide tablets 32 mg/12.5 mg contain 32 mg of candesartan cilexetil and 12.5 mg of hydrochlorothiazide. Candesartan cilexetil and hydrochlorothiazide tables 32 mg/25 mg contain 32 mg of candesartan cilexetil and 25 mg of hydrochlorothiazide. The inactive ingredients of the tablets are carboxymethylcellulose calcium, hydroxypropyl cellulose, lactose monohydrate, magnesium stearate, corn starch, polyethylene glycol 6000, and microcrystalline cellulose. Ferric oxide (yellow) is also added to the 32 mg/12.5 mg tablets as colorant. Structural Formula 1 Structural Formula 2

Clonazepam Tablets USP, a benzodiazepine, is available as scored tablets containing 0.5 mg of clonazepam USP, and unscored tablets containing 1 mg or 2 mg of clonazepam USP. Each tablet also contains colloidal silicon dioxide, croscarmellose sodium, lactose monohydrate, magnesium stearate and microcrystalline cellulose, with the following colorants: 0.5 mg – D&C Yellow #10 aluminum lake; 1 mg – FD&C Blue #1 aluminum lake. Chemically, clonazepam is 5-(2-chlorophenyl)-1,3-dihydro-7-nitro-2 H -1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has a molecular weight of 315.72 and the following structural formula: STRUCTUEAL FORMULA

Clonidine hydrochloride extended-release tablets is a centrally acting alpha 2 -adrenergic agonist available as 0.1 mg extended-release tablets for oral administration. Each 0.1 mg tablet is equivalent to 0.087 mg of the free base. The inactive ingredients are sodium lauryl sulfate, lactose monohydrate, hypromellose type 2208, partially pregelatinized starch, colloidal silicon dioxide, and magnesium stearate. The formulation is designed to delay the absorption of active drug in order to decrease peak to trough plasma concentration differences. Clonidine hydrochloride is an imidazoline derivative and exists as a mesomeric compound. The chemical name is 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride. The following is the structural formula: C 9 H 9 Cl 2 N 3 ·HCl Mol. Wt. 266.56 Clonidine hydrochloride is an odorless, bitter, white, crystalline substance soluble in water and alcohol. Structural Formula

Clonidine hydrochloride, USP is a centrally acting alpha-agonist hypotensive agent available as tablets for oral administration in three dosage strengths: 0.1 mg, 0.2 mg and 0.3 mg. The 0.1 mg tablet is equivalent to 0.087 mg of the free base. The inactive ingredients are dibasic calcium phosphate, lactose monohydrate, magnesium stearate, microcrystalline cellulose, sodium lauryl sulfate, sodium starch glycolate. The clonidine hydrochloride tablets 0.2 mg and 0.3 mg also contains FD&C Yellow #6 aluminum lake. Clonidine hydrochloride is an imidazoline derivative and exists as a mesomeric compound. The chemical name is 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride. The following is the structural formula: Clonidine hydrochloride is an odorless, bitter, white, crystalline substance soluble in water and alcohol. This is an image of the structural formula for clonidine hydrochloride. Clonidine hydrochloride is an imidazoline derivative and exists as a mesomeric compound. The chemical name is 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride. The following is the structural formula: Clonidine hydrochloride is an odorless, bitter, white, crystalline substance soluble in water and alcohol. This is an image of the structural formula for clonidine hydrochloride.

Entecavir is a guanosine nucleoside analogue with selective activity against HBV. The chemical name for entecavir is 2-amino-1,9-dihydro-9-[( 1S,3R,4S )-4-hydroxy-3-(hydroxymethyl)-2-methylenecyclopentyl]-6 H -purin-6-one, monohydrate. Its molecular formula is C 12 H 15 N 5 O 3 •H 2 O, which corresponds to a molecular weight of 295.3. Entecavir has the following structural formula: Entecavir is a white to off-white powder. It is slightly soluble in water (2.4 mg/mL), and the pH of the saturated solution in water is 7.9 at 25 o C ± 0.5 o C. Entecavir film-coated tablets, USP, are available for oral administration in strengths of 0.5 mg and 1 mg of entecavir. Entecavir 0.5 mg and 1 mg film-coated tablets contain the following inactive ingredients: lactose monohydrate, microcrystalline cellulose, crospovidone, povidone, and magnesium stearate. The tablet coating contains titanium dioxide, talc, polyethylene glycol 3350, lecithin (soya), polyvinyl alcohol-part hydrolyzed, and iron oxide red (1 mg tablet only). USP dissolution test pending. C:\Users\RA\Desktop\Untitled.jpg

Fosinopril sodium is the sodium salt of fosinopril, the ester prodrug of an angiotensin-converting enzyme (ACE) inhibitor, fosinoprilat. It contains a phosphinate group capable of specific binding to the active site of angiotensin-converting enzyme. Fosinopril sodium is designated chemically as: L-proline, 4-cyclohexyl-1-[[[2-methyl-1-(1-oxopropoxy) propoxy] (4-phenylbutyl) phosphinyl] acetyl]-, sodium salt, trans- . Fosinopril sodium is a white to off-white crystalline powder. It is soluble in water (100 mg/mL), methanol, and ethanol and slightly soluble in hexane. Its structural formula is: C 30 H 45 NNaO 7 P M.W. 585.65 Fosinopril sodium, USP, is available for oral administration as 10 mg, 20 mg, and 40 mg tablets. Inactive ingredients include: crospovidone, lactose monohydrate, microcrystalline cellulose, povidone, and sodium stearyl fumarate. D:\FOSINOPRIL SODIUM\FOSINOPRILSODIUM-TEVA,2009\SPL-FOSINOPRILSODIUM07232012-TEVA,2009\6213b69f-39e1-4f48-a110-a83bd5459c4a-01.jpg

Lisinopril and hydrochlorothiazide tablets combine an angiotensin converting enzyme inhibitor, lisinopril, and a diuretic, hydrochlorothiazide. Lisinopril, a synthetic peptide derivative, is an oral long-acting angiotensin converting enzyme inhibitor. It is chemically described as (S)-1-[N2-(1-carboxy-3-phenylpropyl)-L-lysyl]-L-proline dihydrate. Its empirical formula is C 21 H 31 N 3 O 5 • 2H 2 O and its structural formula is: Lisinopril, USP is a white to off-white, crystalline powder, with a molecular weight of 441.52. It is soluble in water, sparingly soluble in methanol, and practically insoluble in ethanol. Hydrochlorothiazide is 6-chloro-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is C 7 H 8 ClN 3 O 4 S 2 and its structural formula is: Hydrochlorothiazide, USP is a white, or practically white, crystalline powder with a molecular weight of 297.73, which is slightly soluble in water, but freely soluble in sodium hydroxide solution. Lisinopril and hydrochlorothiazide tablets, USP are available for oral use in three tablet combinations of lisinopril with hydrochlorothiazide: lisinopril and hydrochlorothiazide tablets 10 mg/12.5 mg containing 10 mg lisinopril and 12.5 mg hydrochlorothiazide; lisinopril and hydrochlorothiazide tablets 20 mg/12.5 mg containing 20 mg lisinopril and 12.5 mg hydrochlorothiazide; and, lisinopril and hydrochlorothiazide tablets 20 mg/25 mg containing 20 mg lisinopril and 25 mg hydrochlorothiazide. Inactive Ingredients: 10 mg/12.5 mg Tablets - dibasic calcium phosphate dihydrate, magnesium stearate, mannitol, pregelatinized starch. 20 mg/12.5 mg Tablets - dibasic calcium phosphate dihydrate, magnesium stearate, mannitol, pregelatinized starch, yellow ferric oxide. 20 mg/25 mg Tablets - dibasic calcium phosphate dihydrate, magnesium stearate, mannitol, pregelatinized starch, red ferric oxide. picture 1 picture 2

Methocarbamol tablets, USP, a carbamate derivative of guaifenesin, are a central nervous system (CNS) depressant with sedative and musculoskeletal relaxant properties. The chemical name of methocarbamol is 3-(2-meth-oxyphenoxy)-1,2-propanediol 1-carbamate and has the empirical formula C 11 H 15 NO 5 . Its molecular weight is 241.24. The structural formula is shown below. Methocarbamol, USP is a white powder, sparingly soluble in water and chloroform, soluble in alcohol (only with heating) and propylene glycol, and insoluble in benzene and n -hexane. Methocarbamol tablets, USP are available as 500 mg and 750 mg tablets for oral administration. Methocarbamol tablets USP, 500 mg and 750 mg contain the following inactive ingredients: magnesium stearate, povidone, and sodium starch glycolate. Figure 1 structural formula

Pioglitazone tablets are a thiazolidinedione and an agonist for peroxisome proliferator-activated receptor (PPAR) gamma that contains an oral antidiabetic medication: pioglitazone. Pioglitazone [(±)-5-[[4-[2-(5-ethyl-2-pyridinyl) ethoxy] phenyl] methyl]-2,4-] thiazolidinedione monohydrochloride contains one asymmetric carbon, and the compound is synthesized and used as the racemic mixture. The two enantiomers of pioglitazone interconvert in vivo . No differences were found in the pharmacologic activity between the two enantiomers. The structural formula is as shown: Pioglitazone hydrochloride is an odorless white crystalline powder that has a molecular formula of C 19 H 20 N 2 O 3 S•HCl and a molecular weight of 392.90 daltons. It is soluble in N,N -dimethylformamide, slightly soluble in anhydrous ethanol, very slightly soluble in acetone and acetonitrile, practically insoluble in water, and insoluble in ether. Pioglitazone tablets, USP, are available as tablets for oral administration containing 15 mg, 30 mg, or 45 mg of pioglitazone, USP, (as the base) formulated with the following excipients: lactose monohydrate NF, hydroxypropyl cellulose NF, carboxymethylcellulose calcium NF, and magnesium stearate NF. Structural Formula

Potassium chloride extended-release capsules are an oral dosage form of microencapsulated potassium chloride containing 600 mg and 750 mg of potassium chloride USP, equivalent to 8 mEq and 10 mEq of potassium, respectively. The chemical name of the active ingredient is potassium chloride and the structural formula is KCl. It has a molecular mass of 74.55. Potassium chloride USP, occurs as a white granular powder or as colorless crystals. It is odorless and has a saline taste. Its solutions are neutral to litmus. It is freely soluble in water and insoluble in alcohol. Inactive ingredients of pellets in potassium chloride extended-release capsules include ethylcellulose and talc. The 8 mEq strength capsules contain gelatin and titanium dioxide. The 10 mEq strength capsules contain Brilliant Blue FCF-FD&C Blue 1, FD&C Red 3, gelatin and titanium dioxide. The capsules in both strengths are printed with edible ink of black oil Black SW9008, containing black iron oxide, potassium hydroxide, propylene glycol and shellac. USP dissolution method is pending.

The potassium chloride extended-release tablets, USP 20 mEq product is an immediately dispersing extended release oral dosage form of potassium chloride containing 1500 mg of microencapsulated potassium chloride, USP equivalent to 20 mEq of potassium in a tablet. The potassium chloride extended-release tablets, USP 15 mEq product is an immediately dispersing extended release oral dosage form of potassium chloride containing 1125 mg of microencapsulated potassium chloride, USP equivalent to 15 mEq of potassium in a tablet. The potassium chloride extended-release tablets, USP 10 mEq product is an immediately dispersing extended release oral dosage form of potassium chloride containing 750 mg of microencapsulated potassium chloride, USP equivalent to 10 mEq of potassium in a tablet. These formulations are intended to slow the release of potassium so that the likelihood of a high localized concentration of potassium chloride within the gastrointestinal tract is reduced. Potassium chloride is an electrolyte replenisher. The chemical name of the active ingredient is potassium chloride, and the structural formula is KCl. Potassium chloride, USP occurs as a white, granular powder or as colorless crystals. It is odorless and has a saline taste. Its solutions are neutral to litmus. It is freely soluble in water and insoluble in alcohol. Potassium chloride is a tablet formulation (not enteric coated or wax matrix) containing individually microencapsulated potassium chloride crystals which disperse upon tablet disintegration. In simulated gastric fluid at 37°C and in the absence of out-side agitation, potassium chloride tablets begin disintegrating into microencapsulated crystals within seconds and completely disintegrates within 1 minute. The microencapsulated crystals are formulated to provide an extended release of potassium chloride. Inactive Ingredients: croscarmellose sodium, ethylcellulose, microcrystalline cellulose, copovidone and sodium stearyl fumarate. USP sample preparation 2 is used in the assay. FDA approved dissolution test specifications differ from USP.

Telmisartan and hydrochlorothiazide tablets are a combination of telmisartan, an orally active angiotensin II antagonist acting on the AT 1 receptor subtype, and hydrochlorothiazide, a thiazide diuretic. Telmisartan, a non-peptide molecule, is chemically described as 4'-[(1,4'-dimethyl-2'-propyl[2,6'-bi-1H-benzimidazol]-1'-yl)methyl]-[1,1'-biphenyl]-2-carboxylic acid. Its empirical formula is C 33 H 30 N 4 O 2 , its molecular weight is 514.63, and its structural formula is: Telmisartan, USP is a white to slightly yellowish solid. It is practically insoluble in water and in the pH range of 3 to 9, sparingly soluble in strong acid (except insoluble in hydrochloric acid), and soluble in strong base. Hydrochlorothiazide, USP is a white, or practically white, practically odorless, crystalline powder with a molecular weight of 297.74. It is slightly soluble in water, and freely soluble in sodium hydroxide solution. Hydrochlorothiazide is chemically described as 6-chloro-3,4-dihydro-2 H -1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is C 7 H 8 ClN 3 O 4 S 2 , and its structural formula is: Telmisartan and hydrochlorothiazide tablets USP, are formulated for oral administration in three combinations of 40 mg/12.5 mg, 80 mg/12.5 mg, and 80 mg/25 mg telmisartan, USP, and hydrochlorothiazide, USP, respectively. The tablets contain the following inactive ingredients: crospovidone (Type B), hypromellose, lactose monohydrate, magnesium stearate, mannitol, meglumine, microcrystalline cellulose, povidone, sodium hydroxide, sodium starch glycolate, and sodium stearyl fumarate. As coloring agents, the 40 mg/12.5 mg and 80 mg/12.5 mg tablets contain ferric oxide red, and the 80 mg/25 mg tablets contain ferric oxide yellow. Telmisartan and hydrochlorothiazide tablets are hygroscopic and require protection from moisture. Structural Formula 1 Structural Formula 2