Lisinopril

INDICATIONS AND USAGE Hypertension Lisinopril tablets USP are indicated for the treatment of hypertension to lower blood pressure. Lowering blood pressure lowers the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including lisinopril. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more than 1 drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program's Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal. Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g, on angina, heart failure, or diabetic kidney disease). These considerations may guide selection of therapy. Lisinopril tablets USP may be administered alone or with other antihypertensive agents. Heart Failure Lisinopril tablets USP are indicated as adjunctive therapy in the management of heart failure in patients who are not responding adequately to diuretics and digitalis. Acute Myocardial Infarction Lisinopril tablets USP are indicated for the treatment of hemodynamically stable patients within 24 hours of acute myocardial infarction, to improve survival. Patients should receive, as appropriate, the standard recommended treatments such as thrombolytics, aspirin and beta-blockers. In using lisinopril tablets, consideration should be given to the fact that another angiotensin-converting enzyme inhibitor, captopril, has caused agranulocytosis, particularly in patients with renal impairment or collagen vascular disease, and that available data are insufficient to show that lisinopril tablets USP does not have a similar risk. (See WARNINGS ). In considering the use of lisinopril tablets USP, it should be noted that in controlled clinical trials ACE inhibitors have an effect on blood pressure that is less in Black patients than in non-Blacks. In addition, ACE inhibitors have been associated with a higher rate of angioedema in Black than in non-Black patients (see WARNINGS, Anaphylactoid and Possibly Related Reactions ).

DOSAGE AND ADMINISTRATION Hypertension Initial Therapy: In patients with uncomplicated essential hypertension not on diuretic therapy, the recommended initial dose is 10 mg once a day. Dosage should be adjusted according to blood pressure response. The usual dosage range is 20 to 40 mg per day administered in a single daily dose. The antihypertensive effect may diminish toward the end of the dosing interval regardless of the administered dose, but most commonly with a dose of 10 mg daily. This can be evaluated by measuring blood pressure just prior to dosing to determine whether satisfactory control is being maintained for 24 hours. If it is not, an increase in dose should be considered. Doses up to 80 mg have been used but do not appear to give greater effect. If blood pressure is not controlled with lisinopril alone, a low dose of a diuretic may be added. Hydrochlorothiazide, 12.5 mg has been shown to provide an additive effect. After the addition of a diuretic, it may be possible to reduce the dose of lisinopril. Diuretic Treated Patients: In hypertensive patients who are currently being treated with a diuretic, symptomatic hypotension may occur occasionally following the initial dose of lisinopril. The diuretic should be discontinued, if possible, for two to three days before beginning therapy with lisinopril to reduce the likelihood of hypotension (See WARNINGS ). The dosage of lisinopril should be adjusted according to blood pressure response. If the patient's blood pressure is not controlled with lisinopril alone, diuretic therapy may be resumed as described above. If the diuretic cannot be discontinued, an initial dose of 5 mg should be used under medical supervision for at least two hours and until blood pressure has stabilized for at least an additional hour (See WARNINGS and PRECAUTIONS , Drug Interactions ). Concomitant administration of lisinopril with potassium supplements, potassium salt substitutes, or potassium-sparing diuretics may lead to increases of serum potassium (See PRECAUTIONS ). Dosage Adjustment in Renal Impairment: The usual dose of lisinopril tablet (10 mg) is recommended for patients with creatinine clearance > 30 mL/min (serum creatinine of up to approximately 3 mg/dL). For patients with creatinine clearance ≥ 10 mL/min ≤ 30 mL/min (serum creatinine ≥3 mg/dL), the first dose is 5 mg once daily. For patients with creatinine clearance 30 10 Moderate to Severe Impairment ≥10 ≤30 5 Dialysis Patients See WARNINGS, Anaphylactoid Reactions During Membrane Exposure . 3 mg/dL), therapy with lisinopril should be initiated at a dose of 2.5 mg once a day under close medical supervision (See WARNINGS and PRECAUTIONS , Drug Interactions ). Acute Myocardial Infarction In hemodynamically stable patients within 24 hours of the onset of symptoms of acute myocardial infarction, the first dose of lisinopril is 5 mg given orally, followed by 5 mg after 24 hours, 10 mg after 48 hours and then 10 mg of lisinopril once daily. Dosing should continue for six weeks. Patients should receive, as appropriate, the standard recommended treatments such as thrombolytics, aspirin, and beta-blockers. Patients with a low systolic blood pressure (≤ 120 mmHg) when treatment is started or during the first 3 days after the infarct should be given a lower 2.5 mg oral dose of lisinopril (See WARNINGS ). If hypotension occurs (systolic blood pressure ≤ 100 mmHg) a daily maintenance dose of 5 mg may be given with temporary reductions to 2.5 mg if needed. If prolonged hypotension occurs (systolic blood pressure < 90 mmHg for more than 1 hour) lisinopril should be withdrawn. For patients who develop symptoms of heart failure, see DOSAGE AND ADMINISTRATION , Heart Failure . Dosage Adjustment in Patients With Myocardial Infarction with Renal Impairment: In acute myocardial infarction, treatment with lisinopril should be initiated with caution in patients with evidence of renal dysfunction, defined as serum creatinine concentration exceeding 2 …

3 DOSAGE FORMS AND STRENGTHS 2.5 mg Tablets: White to off-white, round, unscored, biconvex tablets, debossed “WATSON” on one side and “405” on the other side. 5 mg Tablets: White to off-white, capsule-shaped, biconvex tablets, scored on one side, debossed “WAT” on the left and “SON” on the right of the score and “406” on the other side. 10 mg Tablets: Light blue, round, unscored, flat-faced, beveled-edge tablets, debossed “WATSON” and “407” on the periphery of one side and plain on the other side. 20 mg Tablets: Yellow, round, unscored, flat-faced, beveled-edge tablets, debossed “WATSON” and “408” on the periphery of one side and plain on the other side. 30 mg Tablets: Yellow, round, unscored, flat-faced, beveled-edge tablets, debossed “WATSON” and “885” on the periphery of one side and plain on the other side. 40 mg Tablets: Yellow, round, unscored, flat-faced, beveled-edge tablets, debossed “WATSON” and “409” on the periphery of one side and plain on the other side. Tablets: 2.5 mg, 5 mg, 10 mg, 20 mg, 30 mg, 40 mg ( 3 )

4 CONTRAINDICATIONS Lisinopril tablets are contraindicated in patients with: • a history of angioedema or hypersensitivity related to previous treatment with an angiotensin converting enzyme inhibitor • hereditary or idiopathic angioedema. Do not coadminister aliskiren with lisinopril tablets in patients with diabetes [see Drug Interactions (7.4)]. Lisinopril tablets are contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). Do not administer lisinopril tablets within 36 hours of switching to or from sacubitril/valsartan, a product containing a neprilysin inhibitor [see Warnings and Precautions (5.2) and Drug Interactions (7.8)]. • Angioedema or a history of hereditary or idiopathic angioedema (4) • Hypersensitivity (4) • Co-administration of aliskiren with lisinopril tablets in patients with diabetes ( 4, 7.4) • Lisinopril tablets are contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). Do not administer lisinopril tablets within 36 hours of switching to or from sacubitril/valsartan, a product containing a neprilysin inhibitor (4)

ADVERSE REACTIONS Lisinopril has been found to be generally well tolerated in controlled clinical trials involving 1969 patients with hypertension or heart failure. For the most part, adverse experiences were mild and transient. Hypertension In clinical trials in patients with hypertension treated with lisinopril, discontinuation of therapy due to clinical adverse experiences occurred in 5.7% of patients. The overall frequency of adverse experiences could not be related to total daily dosage within the recommended therapeutic dosage range. For adverse experiences occurring in greater than 1% of patients with hypertension treated with lisinopril or lisinopril plus hydrochlorothiazide in controlled clinical trials, and more frequently with lisinopril and/or lisinopril plus hydrochlorothiazide than placebo, comparative incidence data are listed in the table below: PERCENT OF PATIENTS IN CONTROLLED STUDIES Lisinopril (n=1349) Incidence (discontinuation) Lisinopril/ Hydrochlorothiazide (n=629) Incidence (discontinuation) Placebo (n=207) Incidence (discontinuation) Body as a Whole Fatigue 2.5 (0.3) 4.0 (0.5) 1.0 (0.0) Asthenia 1.3 (0.5) 2.1 (0.2) 1.0 (0.0) Orthostatic Effects 1.2 (0.0) 3.5 (0.2) 1.0 (0.0) Cardiovascular Hypotension 1.2 (0.5) 1.6 (0.5) 0.5 (0.5) Digestive Diarrhea 2.7 (0.2) 2.7 (0.3) 2.4 (0.0) Nausea 2.0 (0.4) 2.5 (0.2) 2.4 (0.0) Vomiting 1.1 (0.2) 1.4 (0.1) 0.5 (0.0) Dyspepsia 0.9 (0.0) 1.9 (0.0) 0.0 (0.0) Musculoskeletal Muscle Cramps 0.5 (0.0) 2.9 (0.8) 0.5 (0.0) Nervous/Psychiatric Headache 5.7 (0.2) 4.5 (0.5) 1.9 (0.0) Dizziness 5.4 (0.4) 9.2 (1.0) 1.9 (0.0) Paresthesia 0.8 (0.1) 2.1 (0.2) 0.0 (0.0) Decreased Libido 0.4 (0.1) 1.3 (0.1) 0.0 (0.0) Vertigo 0.2 (0.1) 1.1 (0.2) 0.0 (0.0) Respiratory Cough 3.5 (0.7) 4.6 (0.8) 1.0 (0.0) Upper Respiratory Infection 2.1 (0.1) 2.7 (0.1) 0.0 (0.0) Common Cold 1.1 (0.1) 1.3 (0.1) 0.0 (0.0) Nasal Congestion 0.4 (0.1) 1.3 (0.1) 0.0 (0.0) Influenza 0.3 (0.1) 1.1 (0.1) 0.0 (0.0) Skin Rash 1.3 (0.4) 1.6 (0.2) 0.5 (0.5) Urogenital Impotence 1.0 (0.4) 1.6 (0.5) 0.0 (0.0) Chest pain and back pain were also seen, but were more common on placebo than lisinopril. Heart Failure In patients with heart failure treated with lisinopril for up to four years, discontinuation of therapy due to clinical adverse experiences occurred in 11% of patients. In controlled studies in patients with heart failure, therapy was discontinued in 8.1% of patients treated with lisinopril for 12 weeks, compared to 7.7% of patients treated with placebo for 12 weeks. The following table lists those adverse experiences which occurred in greater than 1% of patients with heart failure treated with lisinopril or placebo for up to 12 weeks in controlled clinical trials, and more frequently on lisinopril than placebo. Controlled Trials Lisinopril (n=407) Incidence (discontinuation) 12 weeks Placebo (n=155) Incidence (discontinuation) 12 weeks Body as a Whole Chest Pain Abdominal Pain 3.4 (0.2) 2.2 (0.7) 1.3 (0.0) 1.9 (0.0) Cardiovascular Hypotension 4.4 (1.7) 0.6 (0.6) Digestive Diarrhea 3.7 (0.5) 1.9 (0.0) Nervous/Psychiatric Dizziness Headache 11.8 (1.2) 4.4 (0.2) 4.5 (1.3) 3.9 (0.0) Respiratory Upper Respiratory Infection 1.5 (0.0) 1.3 (0.0) Skin Rash 1.7 (0.5) 0.6 (0.6) Also observed at > 1% with lisinopril but more frequent or as frequent on placebo than lisinopril in controlled trials were asthenia, angina pectoris, nausea, dyspnea, cough, and pruritus. Worsening of heart failure, anorexia, increased salivation, muscle cramps, back pain, myalgia, depression, chest sound abnormalities, and pulmonary edema were also seen in controlled clinical trials, but were more common on placebo than lisinopril. In the two-dose ATLAS trial in heart failure patients, withdrawals due to adverse events were not different between the low and high groups, either in total number of discontinuation (17-18%) or in rare specific events (<1%). The following adverse events, mostly related to ACE inhibition, were reported more commonly in …

Drug Interactions Hypotension – Patients on Diuretic Therapy: Patients on diuretics and especially those in whom diuretic therapy was recently instituted, may occasionally experience an excessive reduction of blood pressure after initiation of therapy with lisinopril. The possibility of hypotensive effects with lisinopril can be minimized by either discontinuing the diuretic or increasing the salt intake prior to initiation of treatment with lisinopril. If it is necessary to continue the diuretic, initiate therapy with lisinopril at a dose of 5 mg daily, and provide close medical supervision after the initial dose until blood pressure has stabilized (See WARNINGS , and DOSAGE AND ADMINISTRATION ). When a diuretic is added to the therapy of a patient receiving lisinopril, an additional antihypertensive effect is usually observed. Studies with ACE inhibitors in combination with diuretics indicate that the dose of the ACE inhibitor can be reduced when it is given with a diuretic (See DOSAGE AND ADMINISTRATION ). Antidiabetics: Epidemiological studies have suggested that concomitant administration of ACE inhibitors and antidiabetic medicines (insulins, oral hypoglycemic agents) may cause an increased blood-glucose-lowering effect with risk of hypoglycemia. This phenomenon appeared to be more likely to occur during the first weeks of combined treatment and in patients with renal impairment. In diabetic patients treated with oral antidiabetic agents or insulin, glycemic control should be closely monitored for hypoglycemia, especially during the first month of treatment with an ACE inhibitor. Non-Steroidal Anti-Inflammatory Agents including Selective Cyclooxygenase-2 Inhibitors (COX-2 Inhibitors): In patients who are elderly, volume-depleted (including those on diuretic therapy), or with compromised renal function, co-administration of NSAIDs, including selective COX-2 inhibitors, with ACE inhibitors, including lisinopril, may result in deterioration of renal function, including possible acute renal failure. These effects are usually reversible. Monitor renal function periodically in patients receiving lisinopril and NSAID therapy. The antihypertensive effect of ACE inhibitors, including lisinopril, may be attenuated by NSAIDs. Dual Blockade of the Renin-Angiotensin System (RAS) Dual blockade of the RAS with angiotensin receptor blockers, ACE inhibitors, or aliskiren is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure) compared to monotherapy. Closely monitor blood pressure, renal function and electrolytes in patients on lisinopril and other agents that affect the RAS. Do not co-administer aliskiren with lisinopril in patients with diabetes. Avoid use of aliskiren with lisinopril in patients with renal impairment (GFR <60 ml/min). Other Agents: Lisinopril has been used concomitantly with nitrates and/or digoxin without evidence of clinically significant adverse interactions. This included post myocardial infarction patients who were receiving intravenous or transdermal nitroglycerin. No clinically important pharmacokinetic interactions occurred when lisinopril was used concomitantly with propranolol or hydrochlorothiazide. The presence of food in the stomach does not alter the bioavailability of lisinopril. Agents Increasing Serum Potassium: Lisinopril attenuates potassium loss caused by thiazide-type diuretics. Use of lisinopril with potassium-sparing diuretics (e.g., spironolactone, eplerenone, triamterene or amiloride), potassium supplements, or potassium-containing salt substitutes may lead to significant increases in serum potassium. Therefore, if concomitant use of these agents is indicated because of demonstrated hypokalemia, they should be used with caution and with frequent monitoring of serum potassium. Potassium-sparing agents should generally not be used in patients with heart failure who are receiving lisinopril. Lithium: Lithium toxicity has been …

8 USE IN SPECIFIC POPULATIONS Lactation: Advise not to breastfeed. ( 8.2 ) Race: Less antihypertensive effect in blacks than non blacks (8.6) 8.1 Pregnancy Risk Summary Lisinopril can cause fetal harm when administered to a pregnant woman. Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. When pregnancy is detected, discontinue lisinopril as soon as possible. The estimated background risk of major birth defects and miscarriage for the indicated population(s) are unknown. In the general U.S. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. Clinical Considerations Disease-associated maternal and/or embryo/fetal risk Hypertension in pregnancy increases the maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications (e.g., need for cesarean section, and post-partum hemorrhage). Hypertension increases the fetal risk for intrauterine growth restriction and intrauterine death. Pregnant women with hypertension should be carefully monitored and managed accordingly. Fetal/Neonatal Adverse Reactions Oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and skeletal deformations, including skull hypoplasia, hypotension, and death. In the unusual case that there is no appropriate alternative to therapy with drugs affecting the renin-angiotensin system for a particular patient, apprise the mother of the potential risk to the fetus. Perform serial ultrasound examinations to assess the intra-amniotic environment. Fetal testing may be appropriate, based on the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury. Closely observe infants with histories of in utero exposure to lisinopril for hypotension, oliguria, and hyperkalemia. If oliguria or hypotension occur in neonates with a history of in utero exposure to lisinopril, support blood pressure and renal perfusion. Exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function. 8.2 Lactation Risk Summary No data are available regarding the presence of lisinopril in human milk or the effects of lisinopril on the breast fed infant or on milk production. Lisinopril is present in rat milk. Because of the potential for severe adverse reactions in the breastfed infant, advise women not to breastfeed during treatment with lisinopril. 8.3 Nursing Mothers Milk of lactating rats contains radioactivity following administration of 14 C lisinopril. It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from ACE inhibitors, a decision should be made whether to discontinue nursing or discontinue Lisinopril, taking into account the importance of the drug to the mother. 8.4 Pediatric Use Antihypertensive effects and safety of lisinopril have been established in pediatric patients aged 6 to 16 years [see Dosage and Administration (2.1) and Clinical Studies (14.1) ] . No relevant differences between the adverse reaction profile for pediatric patients and adult patients were identified. Safety and effectiveness of lisinopril have not been established in pediatric patients under the age 6 or in pediatric patients with …

12.1 Mechanism of Action Lisinopril inhibits angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. The beneficial effects of lisinopril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. Inhibition of ACE results in decreased plasma angiotensin II which leads to decreased vasopressor activity and to decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. In hypertensive patients with normal renal function treated with lisinopril alone for up to 24 weeks, the mean increase in serum potassium was approximately 0.1 mEq/L; however, approximately 15% of patients had increases greater than 0.5 mEq/L and approximately 6% had a decrease greater than 0.5 mEq/L. In the same study, patients treated with lisinopril and hydrochlorothiazide for up to 24 weeks had a mean decrease in serum potassium of 0.1 mEq/L; approximately 4% of patients had increases greater than 0.5 mEq/L and approximately 12% had a decrease greater than 0.5 mEq/L [see Warnings and Precautions (5.5)]. Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity. ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of lisinopril remains to be elucidated. While the mechanism through which lisinopril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, lisinopril is antihypertensive even in patients with low-renin hypertension. Although lisinopril was antihypertensive in all races studied, Black hypertensive patients (usually a low-renin hypertensive population) had a smaller average response to monotherapy than non Black patients. Concomitant administration of lisinopril and hydrochlorothiazide further reduced blood pressure in Black and non-Black patients and any racial differences in blood pressure response were no longer evident.

11 DESCRIPTION Lisinopril is an oral long-acting angiotensin converting enzyme (ACE) inhibitor. Lisinopril, a synthetic peptide derivative, 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 is a white to off-white, crystalline powder, with a molecular weight of 441.53. It is soluble in water and sparingly soluble in methanol and practically insoluble in ethanol. Lisinopril tablets, USP, are supplied as 2.5 mg, 5 mg, 10 mg, 20 mg, 30 mg and 40 mg tablets for oral administration. Inactive Ingredients: 2.5 mg tablets – Mannitol, dibasic calcium phosphate, pregelatinized starch * , corn starch, colloidal silicon dioxide, sodium starch glycolate and magnesium stearate. 5 mg tablets – Mannitol, dibasic calcium phosphate, pregelatinized starch * , corn starch, colloidal silicon dioxide, sodium starch glycolate, magnesium stearate and yellow ferric oxide. 10 mg tablets – Mannitol, dibasic calcium phosphate, pregelatinized starch * , corn starch, colloidal silicon dioxide, sodium starch glycolate, magnesium stearate and red ferric oxide. 20 and 30 mg tablets - Mannitol, dibasic calcium phosphate, pregelatinized starch * , corn starch, colloidal silicon dioxide, magnesium stearate and red ferric oxide. 40 mg tablets - Mannitol, dibasic calcium phosphate, pregelatinized starch * , corn starch, colloidal silicon dioxide, magnesium stearate and yellow ferric oxide. * : Pregelatinized starch is a physically modified corn (maize) starch. Chemical Structure

OVERDOSAGE Following a single oral dose of 20 g/kg no lethality occurred in rats, and death occurred in one of 20 mice receiving the same dose. The most likely manifestation of overdosage would be hypotension, for which the usual treatment would be intravenous infusion of normal saline solution. Lisinopril can be removed by hemodialysis (See WARNINGS , Anaphylactoid Reactions During Membrane Exposure ).

16 HOW SUPPLIED/STORAGE AND HANDLING 2.5 mg Tablets: white to off-white, capsule-shaped tablets, imprinted with ‘H 144’ on one side and plain on the other side. NDC 76420-340-30 Bottles of 30 tablets, with child-resistant closure (relabeled from NDC 43547-351-03) NDC 76420-340-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-351-XX) NDC 76420-340-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-351-XX) NDC 76420-340-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-351-10) NDC 76420-340-05 Bottles of 500 tablets, with child-resistant closure (relabeled from NDC 43547-351-50) 5 mg Tablets: yellow, capsule-shaped tablets, imprinted with ‘H 145’ on one side and plain on the other side. NDC 76420-341-30 Bottles of 30 tablets, with child-resistant closure (relabeled from NDC 43547-352-03) NDC 76420-341-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-352-XX) NDC 76420-341-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-352-XX) NDC 76420-341-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-352-10) NDC 76420-341-00 Bottles of 1000 tablets, with child-resistant closure (relabeled from NDC 43547-352-11) 10 mg Tablets: light pink, capsule-shaped tablets, imprinted with ‘H 146’ on one side and plain on the other side. NDC 76420-342-30 Bottles of 30 tablets, with child-resistant closure (relabeled from NDC 43547-353-03) NDC 76420-342-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-353-XX) NDC 76420-342-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-353-XX) NDC 76420-342-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-353-10) NDC 76420-342-00 Bottles of 1000 tablets, with child-resistant closure (relabeled from NDC 43547-353-11) 20 mg Tablets: dark pink, capsule-shaped tablets, imprinted with ‘H 147’ on one side and plain on the other side. NDC 76420-343-30 Bottles of 30 tablets, with child-resistant closure (relabeled from NDC 43547-354-03) NDC 76420-343-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-354-XX) NDC 76420-343-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-354-XX) NDC 76420-343-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-354-10) NDC 76420-343-00 Bottles of 1000 tablets (relabeled from NDC 43547-354-11) 30 mg Tablets: red, capsule-shaped tablets, imprinted with ‘H 148’ on one side and plain on the other side. NDC 76420-344-30 Bottles of 30 tablets, with child-resistant closure (relabeled from NDC 43547-355-03) NDC 76420-344-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-355-XX) NDC 76420-344-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-355-XX) NDC 76420-344-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-355-10) NDC 76420-344-05 Bottles of 500 tablets (relabeled from NDC 43547-355-50) NDC 76420-344-00 Bottles of 1000 tablets (relabeled from NDC 43547-355-11) 40 mg Tablets: yellow, capsule-shaped tablets, imprinted with ‘H 149’ on one side and plain on the other side. NDC 76420-345-30 Bottles of 30 tablets, with child-resistant closure ((repackaged from NDC 43547-355-XX) NDC 76420-345-60 Bottles of 60 tablets, with child-resistant closure (repackaged from NDC 43547-355-XX) NDC 76420-345-90 Bottles of 90 tablets, with child-resistant closure (repackaged from NDC 43547-355-XX) NDC 76420-345-01 Bottles of 100 tablets, with child-resistant closure (relabeled from NDC 43547-355-10) NDC 76420-345-00 Bottles of 1000 tablets (relabeled from NDC 43547-355-11)