Pitavastatin 4 mg Tablet, Film Coated, 30-count
🆔 Identity & classification
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🏷️ RxNorm drug class
This medicine belongs to the HMG-CoA Reductase Inhibitor class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Pitavastatin is used to decrease the amount of cholesterol (a fatty substance that builds up in blood vessels causing heart attacks or strokes or other medical conditions). Pitavastatin is in a class of medications called HMG-CoA reductase inhibitors (statins). It works by slowing how much cholesterol your body makes. This lowers the amount of cholesterol that can build up on the walls of the arteries and block blood flow to the heart, brain, and other parts of the body.
Read the full MedlinePlus article ↗- Pitavastatin lowers LDL — that's the 'bad' cholesterol that can build up in your arteries. It works by blocking the main enzyme your liver uses to make cholesterol, so the liver en...
- What exactly is pitavastatin supposed to do for me?
- You can take pitavastatin with or without food — it won't cause stomach issues either way. Morning or evening both work, though evening dosing may give a slightly better LDL reduct...
- Does it matter what time of day I take it, or whether I eat first?
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Pitavastatin — tap one for details:
Pitavastatin may be associated with lower levels of 1 nutrient — worth a chat with your pharmacist, not a cause for alarm.
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Ask a licensed pharmacist directly — free, answered by our team.
💊 What it looks like
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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UNII RFW2ET671P
Hydroxypropyl cellulose is a plant-derived thickening agent made from cellulose. It acts as a binder to hold tablet ingredients together and as a film-former to coat tablets or control how fast the medicine releases.
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UNII 3NXW29V3WO
Hypromellose is a plant-based thickener made from cellulose. It's used in medicines as a binder to hold ingredients together, a coating for tablets, and a thickener for liquids.
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UNII EWQ57Q8I5X
Lactose monohydrate is a natural sugar derived from milk. It serves as a filler and binder in tablets and capsules, helping create the proper size, texture, and consistency of the medicine.
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UNII 8XK1039013
A clay-like mineral compound used as a glidant and anti-caking agent. It helps powder or granule ingredients flow smoothly during tablet or capsule manufacturing and prevents clumping in the finished product.
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UNII 70097M6I30
Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
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UNII ETJ7Z6XBU4
Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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UNII 15FIX9V2JP
Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.
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UNII 8Z96QXD6UM
Triethyl citrate is a clear liquid derived from citric acid. It acts as a plasticizer and solvent in tablet coatings and film formulations, helping the coating remain flexible and adhere properly to the medicine.
8 inactive ingredients listed in the exact product block matched to this NDC.
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ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per each | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | Not in the retail survey — common for institutional, discontinued, or low-volume packs. | |
| Medicaid paysCMS SDUD · 12 mo | No recent Medicaid claims on file for this NDC — rare and low-volume NDCs are suppressed in the public data. | |
| Medicare drug plans payPart D · Q2 2026 | $2.64 | $79.20 / 30 tablets |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Pitavastatin Calcium 4 mg 00378-5057-77 | Mylan | 90 tablets | $1.136 | AB | Availability likely | — |
| Pitavastatin 4.18 mg 00480-3633-98 | Teva | 90 tablets | $1.136 | AB | Availability likely | — |
| Pitavastatin 4 mg 00832-6050-90 | Upsher-Smith | 90 tablets | $1.136 | AB | Availability likely | — |
| pitavastatin calcium 4.18 mg 31722-0877-90 | Camber | 90 tablets | $1.136 | AB | Availability likely | — |
| pitavastatin calcium 4 mg 68382-0483-16 | Zydus | 90 tablets | $1.136 | AB | Availability likely | — |
| pitavastatin calcium 4.18 mg 72603-0480-01 | NorthStar | 90 tablets | $1.136 | AB | Availability likely | — |
| Pitavastatin 4.18 mg 42291-0907-90 | AvKARE | 90 tablets | — | AB | FDA listed | — |
| Pitavastatin 4 mg 51407-0958-90 | Golden | 90 tablets | — | AB | FDA listed | — |
| Pitavastatin 4 mgthis 65162-0031-03 | Amneal | 30 tablets | — | AB | FDA listed | — |
| Pitavastatin 4 mg 65862-0814-05 | Aurobindo | 500 tablets | — | AB | FDA listed | — |
| Livalo 4.18 mg 66869-0404-07 | Kowa | 7 tablets | — | AB | Discontinued | — |
| pitavastatin calcium 4 mg 70771-1786-09 | Zydus | 90 tablets | — | AB | FDA listed | — |
| pitavastatin calcium 4 mg 72865-0293-90 | XLCare | 90 tablets | — | AB | FDA listed | — |
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⏳ Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
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💊 Medicaid utilization by pack size
🔬 Reported adverse events (FAERS)
Top reported reactions
Age at onset
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📦 Packaging — all sizes for this product
| Package NDC | Description | Per unit | Per pack | Marketing start | Status |
|---|---|---|---|---|---|
| 65162-0031-03 You're viewing this | 30 TABLET, FILM COATED in 1 BOTTLE (65162-031-03) | — | — | 2024-08-21 | Active |
| 65162-0031-09 | 90 TABLET, FILM COATED in 1 BOTTLE (65162-031-09) | $1.14 / ea | $102.26 | 2024-08-21 | Active |
| 65162-0031-50 | 500 TABLET, FILM COATED in 1 BOTTLE (65162-031-50) | — | — | 2024-08-21 | Active |
You're viewing the smallest of 3 pack sizes for this product.
This pack shows little to no recent Medicaid volume — the 90 tablets pack carries most fills. See all packs ↓
Pack size FAQ
What quantity is in NDC 65162-0031-03?
What is the difference between NDC 65162-0031-03 and NDC 65162-0031-09?
What NDC number is used to bill for this package of Pitavastatin 4 mg Tablet, Film Coated?
Prices are the latest CMS NADAC pharmacy acquisition cost per NDC; per-pack figures are per-unit × pack quantity, shown only when the pack is denominated in the same measure NADAC prices.
🧭 About this NDC listing & data coverage
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| NDC identity (package / product / labeler codes) | ✓ Available |
| Labeler | ✓ Available |
| Product & package description | ✓ Available |
| Marketing category & status | ✓ Available |
| Active ingredient / dosage form / route | ✓ Available |
| FDA label (SPL via DailyMed) | ✓ Available |
| Package photos | ✓ Available |
| Inactive ingredients (structured) | ✓ Available |
| NADAC pharmacy acquisition price (CMS) | — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey. |
| Orange Book / therapeutic-equivalence data | ✓ Available |
| HCPCS J-code billing crosswalk | — Not published for this NDC Most self-administered / retail products have no J-code — that is normal. |
| Medicaid utilization (CMS SDUD) | — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold. |
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📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE Pitavastatin tablets are indicated as an adjunct to diet to reduce low-density lipoprotein cholesterol (LDL-C) in: Adults with primary hyperlipidemia. Adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH). Pitavastatin tablets are a HMG-CoA reductase inhibitor (statin) indicated as an adjunct to diet to reduce low-density lipoprotein cholesterol (LDL-C) in: ( 1 ) Adults with primary hyperlipidemia.
Adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH).
⏱️ Dosage and Administration ▾
2 DOSAGE AND ADMINISTRATION Take orally once daily with or without food at the same time each day. ( 2.1 ) For patients requiring a high-intensity statin or are unable to achieve their LDL-C goal receiving pitavastatin tablets 4 mg daily, prescribe alternative LDL-C-lowering treatment. ( 2.1 ) Assess LDL-C when clinically appropriate, as early as 4 weeks after initiation of pitavastatin tablets, and adjust the dosage if necessary.
( 2.1 ) Recommended dosage is 2 mg to 4 mg once daily. Maximum recommended dosage is 4 mg once daily. ( 2.2 ) Recommended starting dosage for patients with moderate and severe renal impairment and end-stage renal disease on hemodialysis is 1 mg once daily.
Maximum recommended dosage is 2 mg once daily. ( 2.3 ) See full prescribing information for pitavastatin tablets dosage modifications due to drug interactions. ( 2.4 )
2.1Important Dosage and Administration Information Take pitavastatin tablets orally once daily with or without food at the same time each day. For patients that require a high-intensity statin or are unable to achieve their LDL-C goal receiving pitavastatin tablets 4 mg daily, prescribe alternative LDL-C-lowering treatment. Assess LDL-C when clinically appropriate, as early as 4 weeks after initiating pitavastatin tablets, and adjust the dosage if necessary.
2.2Recommended Dosage for Adults and Pediatric Patients Aged 8 Years and Older The recommended dosage range of pitavastatin tablets is 2 mg to 4 mg daily. The maximum recommended dosage is pitavastatin tablets 4 mg once daily.
2.3Recommended Dosage in Patients with Renal Impairment The recommended starting dosage for patients with moderate and severe renal impairment (estimated glomerular filtration rate 30 to 59 mL/minute/1.73 m 2 and 15 to 29 mL/minute/1.73 m 2 , respectively) and patients with end-stage renal disease receiving hemodialysis is pitavastatin tablets 1 mg once daily. The maximum recommended dose for these patients is pitavastatin tablets 2 mg once daily [see Use in Specific Populations (8.5) ] . There are no dosage adjustment recommendations for patients with mild renal impairment.
2.4Dosage Modifications Due to Drug Interactions In patients taking erythromycin, do not exceed pitavastatin tablets 1 mg once daily [see Drug Interactions (7) ] . In patients taking rifampin, do not exceed pitavastatin tablets 2 mg once daily [see Drug Interactions (7) ] .
💊 Dosage Forms and Strengths ▾
3 DOSAGE FORMS AND STRENGTHS Tablets: 1 mg: White to off-white colored, round shaped, beveled edges, film-coated tablet, debossed with “AN” on one side and “029” on the other side. 2 mg: White to off-white colored, round shaped, beveled edges, film-coated tablet, debossed with “AN” on one side and “030” on the other side. 4 mg: White to off-white colored, round shaped, film-coated tablet, debossed with “AN” on one side and “031” on the other side.
Tablets: 1 mg, 2 mg, and 4 mg. ( 3 )
⛔ Contraindications ▾
4 CONTRAINDICATIONS Pitavastatin tablets are contraindicated in the following conditions: Concomitant use of cyclosporine [see Drug Interactions (7) ]. Acute liver failure or decompensated cirrhosis [see Warnings and Precautions (5.3) ]. Hypersensitivity to pitavastatin or any excipents in pitavastatin tablets.
Hypersensitivity reactions including angioedema, rash, pruritus, and urticaria have been reported with pitavastatin tablets [see Adverse Reactions (6) ] . Cyclosporine. ( 4 , 7 ) Active liver failure or decompensated cirrhosis.
( 4 , 5.3 ) Hypersensitivity to pitavastatin or any excipients in pitavastatin tablets. ( 4 )
⚠️ Warnings and Cautions ▾
5 WARNINGS AND PRECAUTIONS Myopathy and Rhabdomyolysis: Risk factors include age 65 or greater, uncontrolled hypothyroidism, renal impairment, concomitant use with certain other drugs, and higher pitavastatin dosage. Discontinue pitavastatin if markedly elevated CK levels occur or myopathy is diagnosed or suspected. Temporarily discontinue pitavastatin in patients experiencing an acute or serious condition at high risk of developing renal failure secondary to rhabdomyolysis.
Inform patients of the risk of myopathy and rhabdomyolysis when starting or increasing the pitavastatin dosage. Instruct patients to promptly report unexplained muscle pain, tenderness or weakness particularly if accompanied by malaise or fever. ( 5.1 , 7 , 8.5 , 8.6 ) Immune-Mediated Necrotizing Myopathy (IMNM): Rare reports of IMNM, an autoimmune myopathy, have been reported.
Discontinue pitavastatin if IMNM is suspected. ( 5.2 ) Hepatic Dysfunction: Increases in serum transaminases have occurred, some persistent. Rare reports of fatal and non-fatal hepatic failure have occurred.
Consider testing liver enzymes before initiating therapy and as clinically indicated thereafter. If serious hepatic injury with clinical symptoms and/or hyperbilirubinemia or jaundice occurs, promptly discontinue pitavastatin. ( 5.3 )
5.1Myopathy and Rhabdomyolysis Pitavastatin may cause myopathy (muscle pain, tenderness, or weakness associated with elevated creatine kinase [CK]) and rhabdomyolysis. Acute kidney injury secondary to myoglobinuria and rare fatalities have occurred as a result of rhabdomyolysis in patients treated with statins, including pitavastatin. Risk Factors for Myopathy Risk factors for myopathy include age 65 years or greater, uncontrolled hypothyroidism, renal impairment, concomitant use of certain drugs (including other lipid-lowering therapies), and higher pitavastatin dosage [see Dosage and Administration (2.2) , Drug Interactions (7) , and Use in Specific Populations (8.5 , 8.6) ] .
Dosages of pitavastatin greater than 4 mg once daily were associated with an increased risk for severe myopathy in premarketing clinical studies. The maximum recommended dose of pitavastatin is 4 mg once daily . Steps to Prevent or Reduce the Risk of Myopathy and Rhabdomyolysis Pitavastatin is contraindicated in patients taking cyclosporine and not recommended in patients taking gemfibrozil [see Contraindications (4) and Drug Interactions (7) ].
There are pitavastatin dosage restrictions for patients taking erythromycin or rifampin [see Dosage and Administration (2.4) ]. The following drugs when used concomitantly with pitavastatin may also increase the risk of myopathy and rhabdomyolysis: lipid-modifying dosages of niacin (> 1 grams/day), fibrates, and colchicine [see Drug Interactions (7) ]. Discontinue pitavastatin if markedly elevated CK levels occur or if myopathy is either diagnosed or suspected.
Muscle symptoms and CK elevations may resolve if pitavastatin is discontinued. Temporarily discontinue pitavastatin in patients experiencing an acute or serious condition at high risk of developing renal failure secondary to rhabdomyolysis (e.g., sepsis; shock; severe hypovolemia; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; or uncontrolled epilepsy). Inform patients of the risk of myopathy and rhabdomyolysis when starting or increasing the pitavastatin dosage.
Instruct patients to promptly report any unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever.
5.2Immune-Mediated Necrotizing Myopathy There have been rare reports of immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, associated with statin use, including reports of recurrence when the same or a different statin was administered. IMNM is characterized by proximal muscle weakness and elevated serum creatine kinase that persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody; muscle biops…
🤒 Adverse Reactions ▾
6 ADVERSE REACTIONS The following serious adverse reactions are discussed in other sections of the labeling: Myopathy and Rhabdomyolysis [see Warnings and Precautions (5.1) ] Immune-Mediated Necrotizing Myopathy [see Warning and Precautions (5.2) ] Hepatic Dysfunction [see Warning and Precautions (5.3) ] Increases in HbA1c and Fasting Serum Glucose Levels [see Warning and Precautions (5.4) ]. The most frequent adverse reactions (rate ≥ 2%) were myalgia, constipation, diarrhea, back pain, and pain in extremity. ( 6 ) To report SUSPECTED ADVERSE REACTIONS, contact Amneal Pharmaceuticals. at 1-877-835-5472 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
6.1Clinical Studies Experience Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of one drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice. Adverse Reactions in Adults with Primary Hyperlipidemia In 10 controlled clinical studies and 4 subsequent open-label extension studies, 3,291 adult patients with primary hyperlipidemia were administered pitavastatin 1 mg to 4 mg daily.
The mean continuous exposure of pitavastatin (1 mg to 4 mg) was 36.7 weeks (median 51.1 weeks). The mean age of the patients was 60.9 years (range; 18 years to 89 years) and 52% were females. Approximately 93% of the patients were White, 7% were Asian/Indian, 0.2% were African American and 0.3% were Hispanic and other.
In controlled clinical studies and their open-label extensions, 3.9% (1 mg), 3.3% (2 mg), and 3.7% (4 mg) of pitavastatin-treated patients were discontinued due to adverse reactions. The most common adverse reactions that led to treatment discontinuation were: elevated creatine phosphokinase (0.6% on 4 mg) and myalgia (0.5% on 4 mg). Adverse reactions reported in ≥ 2% of patients in controlled clinical studies and at a rate greater than or equal to placebo are shown in Table 1.
These studies had treatment duration of up to 12 weeks. Table 1: Adverse Reactions (≥ 2% and ≥ placebo) in Adults with Primary Hyperlipidemia in Studies up to 12 Weeks Adverse Reactions Placebo (n=208) % Pitavastatin 1 mg (n=309) % Pitavastatin 2 mg (n=951) % Pitavastatin 4 mg (n=1540) % Myalgia 1.4 1.9 2.8
3.1Constipation 1.9 3.6 1.5
2.2Diarrhea 1.9 2.6 1.5
1.9Back pain 2.9 3.9 1.8
1.4Pain in extremity 1.9 2.3 0.6
0.9Other adverse reactions reported from clinical studies were arthralgia, headache, influenza, and nasopharyngitis. Hypersensitivity reactions including rash, pruritus, and urticaria have been reported with pitavastatin. The following laboratory abnormalities have been reported: elevated creatine phosphokinase, transaminases, alkaline phosphatase, bilirubin, and glucose.
Adverse Reactions in Adult HIV-Infected Patients with Dyslipidemia In a double-blind, randomized, controlled, 52-week trial, 252 HIV-infected patients with dyslipidemia were treated with either pitavastatin 4 mg once daily (n=126) or another statin (n=126). All patients were taking antiretroviral therapy (excluding darunavir) and had HIV-1 RNA less than 200 copies/mL and CD4 count greater than 200 cell/μL for at least 3 months prior to randomization. The safety profile of pitavastatin was generally consistent with that observed in the clinical trials described above.
One patient (0.8%) treated with pitavastatin had a peak creatine phosphokinase value exceeding 10 times the upper limit of normal (ULN), which resolved spontaneously. Four patients (3%) treated with pitavastatin had at least one ALT value exceeding 3 times but less than 5 times the ULN, none of which led to drug discontinuation. Virologic failure was reported for four patients (3%) treated with pitavastatin, defined as a confirmed measurement of HIV-1 RNA exceeding 200 copies/mL that was also more than a 2-fold increase from baseline.
Adverse Reactions in Pediatric Patients Aged 8 Years and Older with HeFH In a 12-we…
🔄 Drug Interactions ▾
7 DRUG INTERACTIONS Table 2 includes a list of drugs that increase the risk of myopathy and rhabdomyolysis when administered concomitantly with pitavastatin and instructions for preventing or managing drug interactions [see Warnings and Precautions (5.1) , Clinical Pharmacology (12.3) ]. Table 2: Drug Interactions that Increase the Risk of Myopathy and Rhabdomyolysis with Pitavastatin Cyclosporine Clinical Impact: Cyclosporine significantly increases pitavastatin exposure and increases the risk of myopathy and rhabdomyolysis .
Intervention: Concomitant use of cyclosporine with pitavastatin is contraindicated [see Contraindications (4) ]. Gemfibrozil Clinical Impact: Gemfibrozil may cause myopathy when given alone. The risk of myopathy and rhabdomyolysis is increased with concomitant use of gemfibrozil with statins, including pitavastatin.
Intervention: Avoid concomitant use of gemfibrozil with pitavastatin. Erythromycin Clinical Impact: Erythromycin significantly increases pitavastatin exposure and increases the risk of myopathy and rhabdomyolysis . Intervention: In patients taking erythromycin, do not exceed pitavastatin 1 mg once daily [see Dosage and Administration (2.4) ].
Rifampin Clinical Impact: Rifampin significantly increases peak pitavastatin exposure and increases the risk of myopathy and rhabdomyolysis . Intervention: In patients taking rifampin, do not exceed pitavastatin 2 mg once daily [see Dosage and Administration (2.4) ]. Fibrates Clinical Impact: Fibrates may cause myopathy when given alone.
The risk of myopathy and rhabdomyolysis is increased with concomitant use of fibrates with statins, including pitavastatin. Intervention: Consider if the benefit of using fibrates concomitantly with pitavastatin outweighs the increased risk of myopathy and rhabdomyolysis. Niacin Clinical Impact: The risk of myopathy and rhabdomyolysis may be increased with concomitant use of lipid-modifying doses (≥ 1 g/day) of niacin with pitavastatin.
Intervention: Consider if the benefit of using lipid-modifying doses ( ≥ 1 g/day) of niacin concomitantly with pitavastatin outweighs the increased risk of myopathy and rhabdomyolysis. Colchicine Clinical Impact: Cases of myopathy and rhabdomyolysis have been reported with concomitant use of colchicine with statins, including pitavastatin. Intervention: Consider the risk/benefit of concomitant use of colchicine with pitavastatin.
See full prescribing information for details regarding concomitant use of pitavastatin with other drugs that increase the risk of myopathy and rhabdomyolysis. ( 2.4 , 7 )
👥 Use in Specific Populations ▾
8 USE IN SPECIFIC POPULATIONS Pregnancy: May cause fetal harm. ( 8.1 ) Lactation : Breastfeeding not recommended during treatment with pitavastatin. ( 8.2 )
8.1Pregnancy Risk Summary Discontinue pitavastatin when pregnancy is recognized. Alternatively, consider the ongoing therapeutic needs of the individual patient. Pitavastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, pitavastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action [see Clinical Pharmacology (12.1) ].
In addition, treatment of hyperlipidemia is not generally necessary during pregnancy. Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. Available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of major congenital malformations.
Published data from prospective and retrospective observational cohort studies with statin use in pregnant women are insufficient to determine if there is a drug associated risk of miscarriage (see Data) . In animal reproduction studies, no embryo-fetal toxicity or congenital malformations were observed in pregnant rats and rabbits orally administered pitavastatin during the period of organogenesis at doses which were 22 and 4 times, respectively, the human exposure at the maximum recommended human dosage (MRHD) of 4 mg, based on AUC [see Data].
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. Adverse outcomes in pregnancy occur regardless of the health of the mother or the use of medications. 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 Human Data A Medicaid cohort linkage study of 1,152 statin-exposed pregnant women compared to 8,86,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential confounders – including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use – using propensity score-based methods. The relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus.
There were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for confounders. In the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. Study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births.
Animal Data Embryo-fetal developmental studies were conducted in pregnant rats administered 3, 10, 30 mg/kg/day pitavastatin by oral gavage during organogenesis (gestation days 7 to 17). No adverse effects were observed at 3 mg/kg/day, systemic exposures 22 times human systemic exposure at 4 mg/day based on AUC. Embryo-fetal developmental studies were conducted in pregnant rabbits administered 0.1, 0.3, 1 mg/kg/day pitavastatin by oral gavage during the period of fetal organogenesis (gestation days 6 to 18).
Maternal toxicity consisting of reduced body weight and abortion was observed at all doses tested (4 times human systemic exposure at 4 mg/day based on AUC). In per…
🤰 Pregnancy ▾
8.1Pregnancy Risk Summary Discontinue pitavastatin when pregnancy is recognized. Alternatively, consider the ongoing therapeutic needs of the individual patient. Pitavastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, pitavastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action [see Clinical Pharmacology (12.1) ].
In addition, treatment of hyperlipidemia is not generally necessary during pregnancy. Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. Available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of major congenital malformations.
Published data from prospective and retrospective observational cohort studies with statin use in pregnant women are insufficient to determine if there is a drug associated risk of miscarriage (see Data) . In animal reproduction studies, no embryo-fetal toxicity or congenital malformations were observed in pregnant rats and rabbits orally administered pitavastatin during the period of organogenesis at doses which were 22 and 4 times, respectively, the human exposure at the maximum recommended human dosage (MRHD) of 4 mg, based on AUC [see Data].
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. Adverse outcomes in pregnancy occur regardless of the health of the mother or the use of medications. 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 Human Data A Medicaid cohort linkage study of 1,152 statin-exposed pregnant women compared to 8,86,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential confounders – including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use – using propensity score-based methods. The relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus.
There were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for confounders. In the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. Study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births.
Animal Data Embryo-fetal developmental studies were conducted in pregnant rats administered 3, 10, 30 mg/kg/day pitavastatin by oral gavage during organogenesis (gestation days 7 to 17). No adverse effects were observed at 3 mg/kg/day, systemic exposures 22 times human systemic exposure at 4 mg/day based on AUC. Embryo-fetal developmental studies were conducted in pregnant rabbits administered 0.1, 0.3, 1 mg/kg/day pitavastatin by oral gavage during the period of fetal organogenesis (gestation days 6 to 18).
Maternal toxicity consisting of reduced body weight and abortion was observed at all doses tested (4 times human systemic exposure at 4 mg/day based on AUC). In perinatal/postnatal studies in pregnant rats given oral gavage doses of pitavastatin at 0.1, 0.3, 1, 3, 10, 30 mg/kg/day from organogenesis through weaning (ges…
🧒 Pediatric Use ▾
8.4Pediatric Use The safety and effectiveness of pitavastatin as an adjunctive therapy to diet to reduce elevated LDL-C in pediatric patients aged 8 years and older with HeFH have been established. Use of pitavastatin for this indication is supported by a 12-week, double-blind, placebo-controlled trial in 82 pediatric patients 8 to 16 years of age with HeFH [see Clinical Studies (14) ] and a 52-week open-label trial in 85 pediatric patients with HeFH. The safety and effectiveness of pitavastatin have not been established in pediatric patients younger than 8 years of age with HeFH or in pediatric patients with other types of hyperlipidemia (other than HeFH).
🧓 Geriatric Use ▾
8.5Geriatric Use In controlled clinical studies, 1,209 (43%) patients were 65 years and older. No overall differences in safety or effectiveness were observed between these patients and younger patients. Advanced age (≥ 65 years) is a risk factor for pitavastatin-associated myopathy and rhabdomyolysis.
Dose selection for a geriatric patient should be cautious, recognizing the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy and the higher risk of myopathy. Monitor geriatric patients receiving pitavastatin for the increased risk of myopathy [see Warnings and Precautions (5.1) ].
🆘 Overdosage ▾
10 OVERDOSAGE No specific treatment for pitavastatin overdose is known. Contact Poison Control (1-800-222-1222) for latest recommendations. Hemodialysis is unlikely to be of benefit due to high protein binding ratio of pitavastatin.
🧬 Clinical Pharmacology ▾
12 CLINICAL PHARMACOLOGY
12.1Mechanism of Action Pitavastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, a rate-limiting step in the biosynthetic pathway for cholesterol. As a result, the expression of LDL-receptors followed by the uptake of LDL from blood to liver is accelerated and then the plasma TC decreases. Sustained inhibition of cholesterol synthesis in the liver also decreases levels of very low density lipoproteins.
12.2Pharmacodynamics Cardiac Electrophysiology In a randomized, double-blind, placebo-controlled, 4-way parallel, active-comparator study with moxifloxacin in 174 healthy participants, pitavastatin was not associated with clinically meaningful prolongation of the QTc interval or heart rate at daily doses up to 16 mg (4 times the recommended maximum dose of 4 mg daily).
12.3Pharmacokinetics Absorption Pitavastatin peak plasma concentrations are achieved about 1 hour after oral administration. Both C max and AUC 0-inf increased in an approximately dose-proportional manner for single pitavastatin doses from 1 mg to 24 mg once daily. The absolute bioavailability of pitavastatin oral solution is 51%.
The C max and AUC of pitavastatin did not differ following evening or morning drug administration. In healthy volunteers receiving 4 mg pitavastatin, the percent change from baseline for LDL-C following evening dosing was slightly greater than that following morning dosing. Pitavastatin was absorbed in the small intestine but very little in the colon.
Effect of Food Administration of pitavastatin with a high fat meal (50% fat content) decreases pitavastatin C max by 43% but does not significantly reduce pitavastatin AUC. Distribution Pitavastatin is more than 99% protein bound in human plasma, mainly to albumin and alpha 1-acid glycoprotein, and the mean volume of distribution is approximately 148 L. Elimination Metabolism The principal route of pitavastatin metabolism is glucuronidation via liver uridine 5'-diphosphate glucuronosyltransferase (UGT) with subsequent formation of pitavastatin lactone.
There is only minimal metabolism by the cytochrome P450 system. Pitavastatin is marginally metabolized by CYP2C9 and to a lesser extent by CYP2C8. The major metabolite in human plasma is the lactone, which is formed via an ester-type pitavastatin glucuronide conjugate by UGTs (UGT1A3 and UGT2B7).
Excretion A mean of 15% of radioactivity of orally administered, single 32 mg 14 C-labeled pitavastatin dose was excreted in urine, whereas a mean of 79% of the dose was excreted in feces within 7 days. The mean plasma elimination half-life is approximately 12 hours. Specific Populations Geriatric Patients In a pharmacokinetic study which compared healthy young and geriatric (≥ 65 years) volunteers, pitavastatin C max and AUC were 10% and 30% higher, respectively, in the geriatric patients [see Use in Specific Populations (8.4) ] Pediatric Patients A 12-week study in pediatric patients 8 to 16 years of age treated with pitavastatin 1 mg, 2 mg and 4 mg administered once daily, showed a dose-dependent increase in pitavastatin plasma concentrations at trough (for 2 mg and 4 mg doses) and 1 hour post dose.
A dose-dependent increase in pitavastatin lactone plasma concentrations was observed at trough and 1 hour post dose. Male and Female Patients In a pharmacokinetic study, which compared healthy male and female volunteers, pitavastatin C max and AUC were 60% and 54% higher, respectively in females. Racial or Ethnic Groups In pharmacokinetic studies pitavastatin C max and AUC were 21% and 5% lower, respectively in Black or African American healthy volunteers compared with those of White healthy volunteers.
In pharmacokinetic comparison between White volunteers and Japanese volunteers, there were no significant differences in C max and AUC. Patients with Renal Impairment In patients with moderate renal impairment (estimated glome…
🧬 Mechanism of Action ▾
12.1Mechanism of Action Pitavastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, a rate-limiting step in the biosynthetic pathway for cholesterol. As a result, the expression of LDL-receptors followed by the uptake of LDL from blood to liver is accelerated and then the plasma TC decreases. Sustained inhibition of cholesterol synthesis in the liver also decreases levels of very low density lipoproteins.
📦 How Supplied / Storage and Handling ▾
16 HOW SUPPLIED/STORAGE AND HANDLING Pitavastatin tablets, 1 mg are supplied as white to off-white colored, round shaped, beveled edges, film-coated tablets, debossed with “AN” on one side and “029” on the other side. They are available as follows: Bottles of 30: NDC 65162-029-03 Bottles of 90: NDC 65162-029-09 Bottles of 500: NDC 65162-029-50 Pitavastatin tablets, 2 mg are supplied as white to off-white colored, round shaped, beveled edges, film-coated tablets, debossed with “AN” on one side and “030” on the other side.
They are available as follows: Bottles of 30: NDC 65162-030-03 Bottles of 90: NDC 65162-030-09 Bottles of 500: NDC 65162-030-50 Pitavastatin tablets, 4 mg are supplied as white to off-white colored, round shaped, film-coated tablets, debossed with “AN” on one side and “031” on the other side. They are available as follows: Bottles of 30: NDC 65162-031-03 Bottles of 90: NDC 65162-031-09 Bottles of 500: NDC 65162-031-50 Store at 20° to 25°C (68° to 77°F); excursions permitted between 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature].
Protect from light.
📋 Description ▾
11 DESCRIPTION Pitavastatin tablets for oral use is an HMG-CoA reductase inhibitor. The chemical name for pitavastatin is (+)monocalcium bis{(3R,5S,6 E )-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxyhept-6-enoate} pentahydrate. The structural formula is: The molecular formula for pitavastatin is C 50 H 46 CaF 2 N 2 O 8 ∙ 5H 2 O and the molecular weight is 971.06 g/mol.
Pitavastatin is odorless and occurs as white to off-white powder. It is freely soluble in tetrahydrofuran, soluble in ethylene glycol, sparingly soluble in dimethyl sulphoxide and in 50 % aqueous acetonitrile, slightly soluble in methanol, very slightly soluble in water and in ethanol (96%), and insoluble in diethyl ether. Pitavastatin is hygroscopic and slightly unstable in light.
Each film-coated tablet of pitavastatin contains 1 mg, 2 mg, or 4 mg of pitavastatin, which is equivalent to 1.045 mg, 2.09 mg, or 4.18 mg, respectively, of pitavastatin calcium and the following inactive ingredients: hypromellose, lactose monohydrate, low-substituted hydroxypropyl cellulose, magnesium aluminometasilicate, and magnesium stearate. The film-coating contains the following inactive ingredients: colloidal silicon dioxide, hypromellose, titanium dioxide, and triethyl citrate. 1
💬 Information for Patients ▾
17 PATIENT COUNSELING INFORMATION Myopathy and Rhabdomyolysis Advise patients that pitavastatin may cause myopathy and rhabdomyolysis. Inform patients that the risk is increased when taking certain types of medication and they should discuss all medication, both prescription and over the counter, with their healthcare provider. Instruct patients to promptly report any unexplained muscle pain, tenderness or weakness particularly if accompanied by malaise or fever [see Warnings and Precautions (5.1) ] .
Hepatic Dysfunction Inform patients that pitavastatin may cause liver enzyme elevations and possibly liver failure. Advise patients to promptly report fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice [see Warnings and Precautions (5.3) ]. Increases in HbA1c and Fasting Serum Glucose Levels Inform patients that increases in HbA1c and fasting serum glucose levels may occur with pitavastatin.
Encourage patients to optimize lifestyle measures, including regular exercise, maintaining a healthy body weight, and making healthy food choices [see Warnings and Precautions (5.4) ]. Pregnancy Advise pregnant patients and patients who become pregnant of the potential risk to a fetus. Advise patients to inform their healthcare provider of a known or suspected pregnancy to discuss if pitavastatin should be discontinued [see Use in Specific Populations (8.1) ] .
Lactation Advise patients that breastfeeding is not recommended during treatment with pitavastatin [see Use in Specific Populations (8.2) ]. Manufactured by: Amneal Pharmaceuticals Pvt. Ltd.
Ahmedabad, 382220 INDIA Distributed by: Amneal Pharmaceuticals LLC Bridgewater, NJ 08807 Rev. 07-2024-00