Fenofibrate

RECENT MAJOR CHANGES Indications and Usage ( 1 ) 07/2024 Dosage and Administration ( 2 ) 07/2024 Warnings and Precautions, Mortality and Coronary Heart Disease Morbidity ( 5.1 ) 07/2024

INDICATIONS AND USAGE Treatment of Hypercholesterolemia Fenofibrate capsules are indicated as adjunctive therapy to diet for the reduction of LDL-C, total-C, Triglycerides and apo B in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb. Lipid altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and non-pharmacological interventions alone has been inadequate (see National Cholesterol Education Program [NCEP] Treatment Guidelines, below). Treatment of Hypertriglyceridemia Fenofibrate capsules are also indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. Markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dL) may increase the risk of developing pancreatitis. The effect of fenofibrate capsule therapy on reducing this risk has not been adequately studied. Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of very low density lipoprotein (VLDL). Inspection of plasma refrigerated for 14 hours is helpful in distinguishing Types I to IV and V hyperlipoproteinemia. The initial treatment for dyslipidemia is dietary therapy specific for the type of lipoprotein abnormality. Excess body weight and excess alcoholic intake may be important factors in hypertriglyceridemia and should be addressed prior to any drug therapy. Physical exercise can be an important ancillary measure. Diseases contributory to hyperlipidemia, such as hypothyroidism or diabetes mellitus should be looked for and adequately treated. Estrogen therapy, like thiazide diuretics and beta-blockers, is sometimes associated with massive rises in plasma triglycerides, especially in subjects with familial hypertriglyceridemia. In such cases, discontinuation of the specific etiologic agent may obviate the need for specific drug therapy of hypertriglyceridemia. The use of drugs should be considered only when reasonable attempts have been made to obtain satisfactory results with non-drug methods. If the decision is made to use drugs, the patient should be instructed that this does not reduce the importance of adhering to diet (See WARNINGS and PRECAUTIONS). Fredrickson Classification of Hyperlipoproteinemias Lipid Elevation Type Lipoprotein Elevated Major Minor I(rare) Chylomicrons TG ↑ ↔ C IIa LDL C --- IIb LDL, VLDL C TG III (rare) IDL C, TG --- IV VLDL TG ↑ ↔ C V(rare) chylomicrons, VLDL TG ↑ ↔ C = cholesterol TG = triglycerides LDL = low density lipoprotein VLDL = very low density lipoprotein IDL = intermediate density lipoprotein The NCEP Treatment Guidelines Two or More Other Risk Factors b LDL-Cholesterol mg/dL (mmoI/L) Definite Atherosclerotic Disease a Initiation Level Goal No No ≥190 (≥ 4.9) < 160 (< 4.1) No Yes ≥160 (≥ 4.1) <130 (< 3.4) Yes Yes or No ≥130 c (≥ 3.4) < 100 (< 2.6) a Coronary heart disease or peripheral vascular disease (including symptomatic carotid artery disease). b Other risk factors for coronary heart disease (CHD) include: age (males: ≥ 45 years; females: ≥ 55 years or premature menopause without estrogen replacement therapy); family history of premature CHD; current cigarette smoking; hypertension; confirmed HDL-C < 35 mg/dL (< 0.91 mmol/L); and diabetes mellitus. Subtract I risk favor if HDL-C is ≥ 60 mg/dL (≥ 1.6 mmol/L) c In CHD patients with LDL-C levels 100 to 129 mg/dL, the physician should exercise clinical judgment in deciding whether to initiate drug treatment.

2 DOSAGE AND ADMINISTRATION Severe hypertriglyceridemia : 43 mg to 130 mg orally once daily; the dosage should be adjusted according to patient response (2.2). Primary hyperlipidemia : 130 mg orally once daily (2.2). Administer as a single dose, at any time of day, with or without food (2.2). Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibrate capsules. Discontinue fenofibrate capsules in patients who do not have an adequate response after 2 months of treatment (2.2). Renal impairment : Initial dosage of 43 mg orally once daily (2.3). Geriatric patients : Select the dosage on the basis of renal function (2.4). 2.1 Prior to Initiation of Fenofibrate Capsules • Assess lipid levels before initiating therapy. Identify other causes (e.g., diabetes mellitus, hypothyroidism, or medications) of high TG levels and manage as appropriate. • Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibrate capsules and should continue this diet during treatment with fenofibrate capsules. • In patients with diabetes and fasting chylomicronemia, improve glycemic control prior to considering starting fenofibrate capsules. 2.2 Recommended Dosage and Administration • Severe hypertriglyceridemia: o The recommended dosage of fenofibrate capsules is 43 mg or 130 mg orally once daily. o Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. • Primary hyperlipidemia: o The recommended dosage of fenofibrate capsule is 130 mg orally once daily. • Administer fenofibrate capsules as a single dose at any time of day, with or without food. • Advise patients to swallow fenofibrate capsules whole. Do not crush, break, dissolve, or chew capsules. • Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibrate capsules. Discontinue fenofibrate capsules in patients who do not have an adequate response after 2 months of treatment. • If a dose is missed, advise patients not to take an extra dose. Resume treatment with the next dose. • Advise patients to take fenofibrate capsules at least 1 hour before or 4 hours to 6 hours after a bile acid binding resin to avoid impeding its absorption. 2.3 Recommended Dosage in Patients with Renal Impairment Assess renal function prior to initiation of fenofibrate capsules and periodically thereafter [see Warnings and Precautions (5.4)] . Treatment with fenofibrate capsules should be initiated at a dosage of 43 mg orally once daily in patients with mild to moderately impaired renal function (eGFR 30 to <60 mL/min/1.73m 2 ), and increased only after evaluation of the effects on renal function and TG levels at this dosage. Fenofibrate capsules are contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m 2 ), including those with end-stage renal disease (ESRD) and those receiving dialysis [see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3)] . 2.4 Recommended Dosage in Geriatric Patients Dosage selection for geriatric patients should be made on the basis of renal function [see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3)] .

3 DOSAGE FORMS AND STRENGTHS Fenofibrate capsules, 43 mg are white to off-white granular powder filled in size ‘4’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG78 ’ on cap and body in black ink. Fenofibrate capsules, 130 mg are white to off-white granular powder filled in size ‘0’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG79 ’ on cap and body in black ink. • Capsules: 43 mg and 130 mg (3)

4 CONTRAINDICATIONS Fenofibrate capsules are contraindicated in patients with: Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis [see Clinical Pharmacology (12.3)] . Active liver disease, including those with primary biliary cirrhosis and unexplained persistent liver function abnormalities [see Warnings and Precautions ( 5.2 )] . Pre-existing gallbladder disease [see Warnings and Precautions ( 5.5 )] . .Hypersensitivity to fenofibrate, fenofibric acid, or any of the excipients of fenofibrate capsules. Serious hypersensitivity reactions including anaphylaxis and angioedema have been reported with fenofibrate [see Warnings and Precautions (5.9)] . Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis ( 4 ) Active liver disease, including those with unexplained persistent liver function abnormalities ( 4 ) Pre-existing gallbladder disease ( 4 ) Hypersensitivity to fenofibrate fenofibric acid, or any of the excipients in fenofibrate capsules ( 4 )

6 ADVERSE REACTIONS The following serious adverse reactions are described below and elsewhere in the labeling: Mortality and coronary heart disease morbidity [see Warnings and Precautions (5.1) ] Hepatoxicity [see Warnings and Precautions (5.2) ] Myopathy and Rhabdomyolysis [see Warnings and Precautions (5.3) ] Increases in Serum Creatinine [see Warnings and Precautions (5.4) ] Cholelithiasis [see Warnings and Precautions (5.5) ] Increased Bleeding Risk with Coumarin Anticoagulants [see Warnings and Precautions (5.6) ] Pancreatitis [see Warnings and Precautions (5.7) ] Hematologic Changes [see Warnings and Precautions (5.8) ] Hypersensitivity reactions [see Warnings and Precautions (5.9) ] Venothromboembolic disease [see Warnings and Precautions (5.10) ] Paradoxical Decreases in HDL Cholesterol Levels [see Warnings and Precautions (5.11) ] Adverse reactions (≥ 2% and greater than placebo): abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis ( 6.1 ). To report SUSPECTED ADVERSE REACTIONS, contact ANI Pharmaceuticals, Inc. at 1-855-204-1431 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. 6.1 Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice. The safety of fenofibrate capsules has been established in adults with hypertriglyceridemia or primary hyperlipidemia based on adequate and well-controlled trials of other formulations of fenofibrate, referenced below as "fenofibrate" [see Clinical Studies (14) ]. Dosages of fenofibrate used in these trials were comparable to fenofibrate capsules 150 mg per day [see Clinical Pharmacology (12.3) ]. Adverse reactions reported by 2% or more of patients treated with fenofibrate (and greater than placebo) during the double-blind, placebo-controlled trials are listed in Table 1 below. Adverse reactions led to discontinuation of treatment in 5% of patients treated with fenofibrate and in 3% treated with placebo. Increases in liver function tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double-blind trials. Table 1: Adverse Reactions Reported by 2% or More of Patients Treated with Fenofibrate and Greater than Placebo During the Double-Blind, Placebo-Controlled Trials Adverse Reaction Placebo (N =365) Fenofibrate (N = 439) Abnormal Liver Tests 1% 8% Abdominal Pain 4% 5% Increased ALT 2% 3% Increased AST 1% 3% Increased Creatine Phosphokinase 1% 3% Constipation 1% 2% Rhinitis 1% 2% Other Adverse Reactions Urticaria Urticaria was seen in 1.1% vs. 0% and rash in 1.4% vs. 0.8% of fenofibrate and placebo patients respectively in controlled trials. Increases in Liver Enzymes In a pooled analysis of 10 placebo controlled trials, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking either an intermediate or the maximum recommended daily dosage of fenofibrate versus 1.1% of patients treated with placebo. In an 8-week trial, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving an intermediate daily dosage or the maximum recommended daily dosage of fenofibrate and was 0% in those receiving the lowest recommended daily dosage of fenofibrate or placebo [see Warnings and Precautions (5.2) ] . 6.2 Postmarketing Experience The following adverse reactions have been identified during post-approval use of fenofibrate. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure: Blood: Anemia, white blood cell decreases Gastrointestinal: Pancreatitis General: Asthenia Hepatobiliary: Increased total bilirubin, hepatitis, cirrhosis Immune System: Anaphylaxis, …

DRUG INTERACTIONS Oral Anticoagulants: CAUTION SHOULD BE EXERCISED WHEN COUMARIN ANTICOAGULANTS ARE GIVEN IN CONJUNCTION WITH FENOFIBRATE CAPSULES. THE DOSAGE OF THE ANTICOAGULANTS SHOULD BE REDUCED TO MAINTAIN THE PROTHROMBIN TIME/INR AT THE DESIRED LEVEL TO PREVENT BLEEDING COMPLICATIONS. FREQUENT PROTHROMBIN TIME/INR DETERMINATIONS ARE ADVISABLE UNTIL IT HAS BEEN DEFINITELY DETERMINED THAT THE PROTHROMBIN TIME/INR HAS STABILIZED. HMG-CoA Reductase Inhibitors: The combined use of fenofibrate capsules and HMG-CoA reductase inhibitors should be avoided unless the benefit of further alterations in lipid levels is likely to outweigh the increased risk of this drug combination (see WARNINGS). Resins: Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate capsules at least 1 hour before or 4 to 6 hours after a bile acid binding resin to avoid impeding its absorption. Cyclosporine: Because cyclosporine can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibrate capsules, there is a risk that an interaction will lead to deterioration. The benefits and risks of using fenofibrate capsules with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose employed. Carcinogenesis, Mutagenesis, Impairment of Fertility: Two dietary carcinogenicity studies have been conducted in rats with fenofibrate. In the first 24-month study, rats were dosed with fenofibrate at 10, 45 and 200 mg/kg/day, approximately 0.3, 1 and 6 times the maximum recommended human dose (MRHD), based on body surface area comparisons (mg/m 2 ). At a dose of 200 mg/kg/day (at 6 times the MRHD), the incidence of liver carcinomas was significantly increased in both sexes. A statistically significant increase in pancreatic carcinomas was observed in males at 1 and 6 times the MRHD; an increase in pancreatic adenomas and benign testicular interstitial cell tumors was observed at 6 times the MRHD in males. In a second 24-month rat carcinogenicity study in a different strain of rats, doses of 10 and 60 mg/kg/day (0.3 and 2 times the MRHD) produced significant increases in the incidence of pancreatic acinar adenomas in both sexes and increases in testicular interstitial cell tumors in males at 2 times the MRHD. A 117-week carcinogenicity study was conducted in rats comparing three drugs: fenofibrate 10 and 60 mg/kg/day (0.3 and 2 times the MRHD), clofibrate (400 mg/kg/day; 2 times the human dose) and gemfibrozil (250 mg/kg/day; 2 times the human dose, based on mg/m 2 surface area). Fenofibrate increased pancreatic acinar adenomas in both sexes. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females. Gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumors in males. In a 21-month study in mice, fenofibrate 10, 45 and 200 mg/kg/day (approximately 0.2, 1 and 3 times the MRHD on the basis of mg/m 2 surface area) significantly increased the liver 23 carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10, 60 and 200 mg/kg/day, fenofibrate significantly increased the liver carcinomas in male mice and liver adenomas in female mice at 3 times the MRHD. Electron microscopy studies have demonstrated peroxisomal proliferation following fenofibrate administration to the rat. An adequate study to test for peroxisome proliferation in humans has not been done, but changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual. Fenofibrate has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, mou …

8 USE IN SPECIFIC POPULATIONS 8.1 Pregnancy Risk Summary Limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. In animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or comparable to the maximum recommended clinical dosage of 130 mg of fenofibrate capsules daily, based on body surface area (mg/m 2 ). Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data). Fenofibrate capsules should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. Data Animal Data In pregnant rats given oral dietary doses of 14 mg/kg/day, 127 mg/kg/day, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, comparable to 130 mg fenofibrate capsules daily, based on body surface area comparisons). Increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the MRHD) that significantly suppressed maternal body weight gain. In pregnant rabbits given oral gavage doses of 15 mg/kg/day, 150 mg/kg/day, and 300 mg/kg/day from gestation day 6 to 18 during the period of organogenesis and allowed to deliver, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the MRHD, based on body surface area comparisons). Aborted litters were observed at maternally toxic doses (≥150 mg/kg/day, corresponding to ≥10 times the clinical exposure at the MRHD) that suppressed maternal body weight gain. In pregnant rats given oral dietary doses of 15 mg/kg/day, 75 mg/kg/day, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the MRHD, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). Post-implantation loss was observed at ≥75 mg/kg/day (≥2 times the clinical exposure at the MRHD) in the presence of maternal toxicity (decreased weight gain). Decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the MRHD), which was associated with decreased maternal body weight gain/maternal neglect. 8.2 Lactation Risk Summary There is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. Fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. Because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate capsules and for 5 days after the final dose. 8.4 Pediatric Use The safety and effectiveness of fenofibrate capsules have not been established in pediatric patients with severe hypertriglyceridemia or primary hyperlipidemia. 8.5 Geriatric Use Assess renal function in geriatric patients and follow contraindications and dosing recommendations for patients with renal impairment [see Contraindications (4), Warnings and Precautions (5.3, 5.4), and Use in Specific Populations (8.6)] . While fenofibric acid exposure is not influenced by age, geriatric patients are more likely to have renal …

12.1 Mechanism of Action The active moiety of fenofibrate is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate. The lipid-lowering effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity). The resulting decrease in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation) to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPARα also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.

DESCRIPTION Fenofibrate, USP (micronized), is a lipid regulating agent available as capsules for oral administration. Each capsule contains 67 mg, 134 mg or 200 mg of micronized fenofibrate, USP. The chemical name for fenofibrate, USP is 2-[4-(4- chlorobenzoyl) phenoxy]-2-methyl-propanoic acid, 1-methylethyl ester with the following structural formula: The empirical formula is C 20 H 21 O 4 Cl and the molecular weight is 360.83; fenofibrate, USP is very soluble in methylene chloride; slightly soluble in alcohol; practically insoluble in water. The melting point is 79° to 82°C. Fenofibrate, USP is a white or almost white crystalline powder which is stable under ordinary conditions. Each 67 mg fenofibrate capsule, USP (micronized) contains the following inactive ingredients: sodium lauryl sulfate, croscarmellose sodium, pregelatinized starch, microcrystalline cellulose, colloidal silicon dioxide, sodium stearyl fumarate, titanium dioxide and gelatin. The capsule shell imprinting ink contains the following inactive ingredients: shellac, black iron oxide and potassium hydroxide. Each 134 mg fenofibrate capsule, USP (micronized) contains the following inactive ingredients: sodium lauryl sulfate, croscarmellose sodium, pregelatinized starch, microcrystalline cellulose, colloidal silicon dioxide, sodium stearyl fumarate, titanium dioxide, FD&C Yellow 6, D&C Yellow 10 and gelatin. The capsule shell imprinting ink contains the following inactive ingredients: shellac, black iron oxide and potassium hydroxide. Each 200 mg fenofibrate capsule, USP (micronized) contains the following inactive ingredients: sodium lauryl sulfate, croscarmellose sodium, pregelatinized starch, microcrystalline cellulose, colloidal silicon dioxide, sodium stearyl fumarate, titanium dioxide, FD&C Yellow 6, D&C Yellow 10 and gelatin. The capsule shell imprinting ink contains the following inactive ingredients: shellac, black iron oxide and potassium hydroxide. structure-fenofibrate

10 OVERDOSAGE In the event of an overdose of fenofibrate capsules, consider contacting the Poison Help line (1-800-222-1222) or a medical toxicologist for additional overdosage management recommendations. There is no specific treatment for overdose with fenofibrate. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway. Because fenofibric acid is highly bound to plasma proteins, hemodialysis should not be considered.

HOW SUPPLIED Fenofibrate capsules, USP (micronized) is available as hard gelatin capsules in three strengths: Fenofibrate capsules, USP (micronized),67 mg are Opaque pale Yellow / Opaque pale Yellow, Size “3” capsules imprinted with “A317” on cap with black ink, filled with white to off-white granular powder. Bottle of 30 capsules with child resistant closure, NDC 62332-084-30 Bottle of 100 capsules with child resistant closure, NDC 62332-084-31 Bottle of 500 capsules, NDC 62332-084-71 Fenofibrate capsules, USP (micronized), 134 mg are Opaque White / Opaque White, Size “1” capsules imprinted with “A318” on cap in black ink, filled with white to off-white granular powder. Bottle of 30 capsules with child resistant closure, NDC 62332-085-30 Bottle of 100 capsules with child resistant closure, NDC 62332-085-31 Bottle of 500 capsules, NDC 62332-085-71 Fenofibrate capsules, USP (micronized), 200 mg are Opaque orange / Opaque orange, Size “1” capsules imprinted with “A319” on cap in black ink, filled with white to off-white granular powder. Bottle of 30 capsules with child resistant closure, NDC 62332-086-30 Bottle of 100 capsules with child resistant closure, NDC 62332-086-31 Bottle of 500 capsules, NDC 62332-086-71 Storage Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature].Keep out of the reach of children. Protect from moisture.