Agrylin anagrelide hydrochloride .5 mg Capsule, 100-count — NDC 54092-063-01 (Billing 54092-0063-01)
This is a package of 100 capsules of Agrylin anagrelide hydrochloride .5 mg Capsule from Takeda Pharmaceuticals America, Inc., marketed since Mar 1997 and currently FDA-listed. It is this product's only package size.
NDC database record
One package, one record: these facts belong to NDC 54092-063-01 alone.
- Record
- FDA NDC Directory package listing · Human prescription drug
- Code segments
- 54092 labeler · 063 product · 01 package
- Package marketed since
- Mar 14, 1997
- Sample package
- No — commercial package
- Listing certified through
- Dec 31, 2027
- Billing quantity
- 100 EA per package
- Barcode (UPC)
- 0354092063017
- FDA record last changed
- Jul 24, 2026
Identity & classification
Regulatory identifiers FDA, NLM and CMS codes for this package
Drug-database identifiers Medi-Span GPI and First Databank GCN / HICL / AHFS classification
- GSN (GCN sequence number): 030949
- GCN: 22391
- GPI-14 (Medi-Span): 85156010100120
- HICL (First Databank): 012902
- AHFS class code: 20:12.14.00
- RxCUI (RxNorm): 597850
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 5, 2026
- RxNorm (NLM RxNav) · catalog refreshed Oct 1, 2026
- Medi-Span GPI (licensed)
- First Databank (licensed) · refreshed Oct 1, 2026
RxNorm drug class
This medicine belongs to the Platelet-reducing Agent class.
Where does this data come from?
- RxClass (NLM) · catalog refreshed Oct 1, 2026
Clinical
Anagrelide is used to decrease the number of platelets (a type of blood cell that is needed to control bleeding) in the blood of patients who have a bone marrow disorder, in which the body makes too many of one or more types of blood cells, such as essential thrombocythemia (condition in which the body makes too many platelets) or polycythemia vera (condition in which the body makes too many red blood cells and sometimes too many platelets). Anagrelide is in a class of medications called platelet-reducing agents. It works by slowing the production of platelets in the body.
Read the full MedlinePlus article ↗- Anagrelide is bringing down a platelet count that's dangerously high because of a bone marrow disorder. When you have too many platelets, your blood can form clots too easily — whi...
- What exactly is this medication doing for me?
- You can take anagrelide capsules with or without food — there's no strict requirement. Food does slow down how quickly the medication is absorbed, but it doesn't meaningfully chang...
- Can I take this with food, or does it need to be on an empty stomach?
Patient education
Supplement & herbal interactions
Where does this data come from?
- MedlinePlus (NLM) · refreshed Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 5, 2026
Ask a licensed pharmacist directly — free, answered by our team.
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 | $8.05 | $805.29 / 100 capsules |
Where does this data come from?
- CMS NADAC weekly file
- CMS ASP pricing files · refreshed Sep 20, 2026
- CMS Medicaid State Drug Utilization Data · refreshed Oct 5, 2026
- CMS Part D plan pricing files · refreshed Sep 24, 2026
- VA National Acquisition Center price file
Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Marketing end | Status |
|---|---|---|---|---|
| 54092-0063-01 You're viewing this Main listing | 100 CAPSULE in 1 BOTTLE | 1997-03-14 | — | Active |
Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| anagrelide .5 mg 13668-0453-01 | Torrent | 100 capsules | $0.729 | AB | Availability likely | — |
| Anagrelide .5 mg 62135-0312-12 | Chartwell | 120 capsules | $0.729 | — | Availability likely | — |
| Anagrelide .5 mg 70954-0879-10 | ANI | 100 capsules | $0.729 | AB | Availability likely | — |
| Agrylin .5 mgthis 54092-0063-01 | Takeda | 100 capsules | — | — | FDA listed | — |
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA Orange Book · refreshed Oct 3, 2026
- CMS NADAC weekly file
Availability & generic status
We did not find an FDA-approved generic match for this exact strength, form and route.
Where does this data come from?
- FDA Orange Book · refreshed Oct 3, 2026
What it looks like
Where does this data come from?
- FDA label on DailyMed · label index refreshed Oct 5, 2026
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 3SY5LH9PMK
Anhydrous lactose is a milk sugar with no water content. It acts as a filler and binder in tablets and capsules, adding bulk and helping ingredients stick together.
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UNII 2S7830E561
Crospovidone is a synthetic polymer derived from povidone. It acts as a disintegrant, helping the tablet or capsule break apart quickly in the stomach so the active ingredient can be absorbed.
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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 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 OP1R32D61U
Microcrystalline cellulose is a purified form of cellulose, a natural fiber from plant sources. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and give the medicine its shape and size.
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UNII U725QWY32X
Povidone K30 is a synthetic polymer made from petroleum. It acts as a binder to hold tablet ingredients together and as a disintegrant to help the tablet break apart in the stomach so the medicine can be absorbed.
6 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
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.- FDA label on DailyMed · label index refreshed Oct 5, 2026
- FDA openFDA NDC Directory · synced Oct 1, 2026
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Manufacturer & labeler
More NDCs from Takeda Pharmaceuticals America, Inc. labeler code 54092
- Mesalamine 1.2 g Tablet, Delayed Release NDC 54092-100-01
- Carbatrol carbamazepine 100 mg Capsule, Extended Release NDC 54092-171-12
- Carbatrol carbamazepine 200 mg Capsule, Extended Release NDC 54092-172-12
- Carbatrol carbamazepine 300 mg Capsule, Extended Release NDC 54092-173-12
- Pentasa mesalamine 250 mg Capsule NDC 54092-189-81
- Pentasa mesalamine 500 mg Capsule NDC 54092-191-12
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- Drugs@FDA
Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE AGRYLIN is indicated for the treatment of patients with thrombocythemia, secondary to myeloproliferative neoplasms, to reduce the elevated platelet count and the risk of thrombosis and to ameliorate associated symptoms including thrombo-hemorrhagic events. AGRYLIN is a platelet reducing agent indicated for the treatment of thrombocythemia, secondary to myeloproliferative neoplasms, to reduce the elevated platelet count and the risk of thrombosis and to ameliorate associated symptoms including thrombo-hemorrhagic events.
( 1 )
⏱️ Dosage and Administration ▾
2 DOSAGE AND ADMINISTRATION The starting dose for adults is 0.5 mg four times a day or 1 mg twice a day. ( 2.1 ) The starting dose for pediatric patients is 0.5 mg per day. ( 2.1 ) Maintain the starting dose for at least one week and then titrate to maintain target platelet counts.
( 2.2 ) Do not exceed a dose increment of 0.5 mg/day in any one week. Do not exceed 10 mg/day or 2.5 mg in a single dose. ( 2.2 ) Moderate hepatic impairment: Start with 0.5 mg per day.
( 2.3 )
2.1Recommended Starting Dosage Adults: The recommended starting dosage of AGRYLIN is 0.5 mg four times daily or 1 mg twice daily. Pediatric Patients: The recommended starting dosage of AGRYLIN is 0.5 mg daily.
2.2Dose Titration Based Upon Platelet Response Continue the starting dose for at least one week and then titrate to reduce and maintain the platelet count below 600,000/µL, and ideally between 150,000/µL and 400,000/µL. The dose increment should not exceed 0.5 mg/day in any one week. Dosage should not exceed 10 mg/day or 2.5 mg in a single dose.
Most patients will experience an adequate response at a dose of 1.5 to 3.0 mg/day. Monitor platelet counts weekly during titration then monthly or as necessary.
2.3Dose Modifications for Hepatic Impairment In patients with moderate hepatic impairment (Child Pugh score 7-9) start AGRYLIN therapy at a dose of 0.5 mg/day and monitor frequently for cardiovascular events [see Warnings and Precautions (5.1) , Use in Specific Populations (8.6) and Clinical Pharmacology (12.3) ] . Patients with moderate hepatic impairment who have tolerated AGRYLIN therapy for one week may have their dose increased. The dose increase increment should not exceed 0.5 mg/day in any one week.
Avoid use of AGRYLIN in patients with severe hepatic impairment.
2.4Clinical Monitoring AGRYLIN therapy requires clinical monitoring, including complete blood counts, assessment of hepatic and renal function, and electrolytes. To prevent the occurrence of thrombocytopenia, monitor platelet counts every two days during the first week of treatment and at least weekly thereafter until the maintenance dosage is reached. Typically, platelet counts begin to respond within 7 to 14 days at the proper dosage.
In the clinical trials, the time to complete response, defined as platelet count ≤600,000/µL, ranged from 4 to 12 weeks. In the event of dosage interruption or treatment withdrawal, the rebound in platelet count is variable, but platelet counts typically will start to rise within 4 days and return to baseline levels in one to two weeks, possibly rebounding above baseline values. Monitor platelet counts frequently.
💊 Dosage Forms and Strengths ▾
3 DOSAGE FORMS AND STRENGTHS Capsules: White, opaque capsule, imprinted with " 063" in black ink. Each capsule contains 0.5 mg anagrelide equivalent to 0.61 mg anagrelide hydrochloride USP. Capsules: 0.5 mg. ( 3 ) Imprint
⛔ Contraindications ▾
4 CONTRAINDICATIONS None. None. ( 4 )
⚠️ Warnings and Cautions ▾
5 WARNINGS AND PRECAUTIONS Cardiovascular Toxicity: QT prolongation and ventricular tachycardia have been reported with AGRYLIN. Obtain a pre-treatment cardiovascular examination including an ECG in all patients. Monitor patients for cardiovascular effects.
( 5.1 ) Pulmonary Hypertension: Assess underlying cardiopulmonary disease prior to initiating therapy. ( 5.2 ) Bleeding Risk: Monitor patients for bleeding, including those receiving concomitant therapy with other drugs known to cause bleeding. ( 5.3 )
5.1Cardiovascular Toxicity Torsades de pointes and ventricular tachycardia have been reported with AGRYLIN. Obtain a pre-treatment cardiovascular examination including an ECG in all patients. During treatment with AGRYLIN monitor patients for cardiovascular effects and evaluate as necessary.
AGRYLIN increases the QTc interval of the electrocardiogram and increases the heart rate in healthy volunteers [ see Clinical Pharmacology (12.2) ] . Do not use AGRYLIN in patients with known risk factors for QT interval prolongation, such as congenital long QT syndrome, a known history of acquired QTc prolongation, medicinal products that can prolong QTc interval and hypokalemia [see Drug Interactions (7.1) ] . Hepatic impairment increases anagrelide exposure and could increase the risk of QTc prolongation.
Monitor patients with hepatic impairment for QTc prolongation and other cardiovascular adverse reactions. The potential risks and benefits of AGRYLIN therapy in a patient with mild and moderate hepatic impairment should be assessed before treatment is commenced. Reduce AGRYLIN dose in patients with moderate hepatic impairment.
Avoid use of AGRYLIN in patients with severe hepatic impairment. In patients with heart failure, bradyarrhythmias, or electrolyte abnormalities, consider periodic monitoring with electrocardiograms [see Clinical Pharmacology (12.2) ] . AGRYLIN is a phosphodiesterase 3 (PDE3) inhibitor and may cause vasodilation, tachycardia, palpitations, and congestive heart failure.
Other drugs that inhibit PDE3 have caused decreased survival when compared with placebo in patients with Class III-IV congestive heart failure [see Drug Interactions (7.2) ] . In patients with cardiac disease, use AGRYLIN only when the benefits outweigh the risks.
5.2Pulmonary Hypertension Cases of pulmonary hypertension have been reported in patients treated with AGRYLIN. Evaluate patients for signs and symptoms of underlying cardiopulmonary disease prior to initiating and during AGRYLIN therapy [see Adverse Reactions (6.1) ] .
5.3Bleeding Risk Use of concomitant AGRYLIN and aspirin increased major hemorrhagic events in a postmarketing study. Assess the potential risks and benefits for concomitant use of AGRYLIN with aspirin, since bleeding risks may be increased. Monitor patients for bleeding, including those receiving concomitant therapy with other drugs known to cause bleeding (e.g., anticoagulants, PDE3 inhibitors, NSAIDs, antiplatelet agents, selective serotonin reuptake inhibitors) [see Drug Interactions (7.3) , Clinical Pharmacology (12.3) ] .
5.4Pulmonary Toxicity Interstitial lung diseases (including allergic alveolitis, eosinophilic pneumonia and interstitial pneumonitis) have been reported to be associated with the use of AGRYLIN in post-marketing reports. Most cases presented with progressive dyspnea with lung infiltrations. The time of onset ranged from 1 week to several years after initiating AGRYLIN.
If suspected, discontinue AGRYLIN and evaluate. Symptoms may improve after discontinuation [see Adverse Reactions (6) ] .
🤒 Adverse Reactions ▾
6 ADVERSE REACTIONS The following clinically significant adverse reactions are discussed in greater detail in other sections of the labeling: Cardiovascular Toxicity [see Warnings and Precautions (5.1) ] Pulmonary Hypertension [see Warnings and Precautions (5.2) ] Bleeding Risk [see Warnings and Precautions (5.3) ] Pulmonary Toxicity [see Warnings and Precautions (5.4) ] The most common adverse reactions (incidence ≥ 5%) are headache, palpitations, diarrhea, asthenia, edema, nausea, abdominal pain, dizziness, pain, dyspnea, cough, flatulence, vomiting, fever, peripheral edema, rash, chest pain, anorexia, tachycardia, malaise, paresthesia, back pain, pruritus, and dyspepsia.
( 6.1 ) To report SUSPECTED ADVERSE REACTIONS, contact Takeda Pharmaceuticals U.S.A., Inc. at 1-877-TAKEDA-7 (1-877-825-3327)- or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
6.1Clinical 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 practice. Clinical Studies in Adult Patients In three single-arm clinical studies, 942 patients [see Clinical Trials (14) ] diagnosed with myeloproliferative neoplasms of varying etiology (ET: 551; PV: 117; OMPN: 274) were exposed to AGRYLIN with a mean duration of approximately 65 weeks.
Serious adverse reactions reported in these patients included the following: congestive heart failure, myocardial infarction, cardiomyopathy, cardiomegaly, complete heart block, atrial fibrillation, cerebrovascular accident, pericardial effusion [see Warnings and Precautions (5.1) ] , pleural effusion, pulmonary infiltrates, pulmonary fibrosis, pulmonary hypertension, and pancreatitis. Of the 942 patients treated with AGRYLIN, 161 (17%) were discontinued from the study because of adverse reactions or abnormal laboratory test results.
The most common adverse reactions resulting in treatment discontinuation were headache, diarrhea, edema, palpitations, and abdominal pain. The most frequently reported adverse reactions to AGRYLIN (in 5% or greater of 942 patients with myeloproliferative neoplasms) in clinical trials were listed in Table 1. Table 1 Adverse Reactions Reported in Clinical Studies of AGRYLIN in at least 5% of Patients Adverse Reactions AGRYLIN (N=942) (%) Cardiac disorders Palpitations 26% Tachycardia 8% Chest pain 8% General disorders and administration site conditions Asthenia 23% Edema 21% Pain 15% Fever 9% Peripheral edema 9% Malaise 6% Gastrointestinal disorders Diarrhea 26% Nausea 17% Abdominal pain 16% Vomiting 10% Flatulence 10% Anorexia 8% Dyspepsia 5% Respiratory, thoracic and mediastinal disorders Dyspnea 12% Cough 6% Skin and subcutaneous tissue disorders Rash 8% Pruritus 6% Musculoskeletal and connective tissue disorders Back pain 6% Nervous system disorders Headache 44% Dizziness 15% Paresthesia 6% Adverse Reactions (frequency 1% to < 5%) included: General disorders and administration site conditions : Flu symptoms, chills.
Cardiac disorders : Arrhythmia, angina pectoris, heart failure, syncope. Vascular disorders : Hemorrhage, hypertension, postural hypotension, vasodilatation. Gastrointestinal disorders : Constipation, gastrointestinal hemorrhage, gastritis.
Blood and lymphatic system disorders : Anemia, thrombocytopenia, ecchymosis. Hepatobiliary disorders : Elevated liver enzymes. Musculoskeletal and connective tissue disorders : Arthralgia, myalgia.
Psychiatric disorders : Depression, confusion, nervousness. Nervous system disorders : Somnolence, insomnia, amnesia, migraine headache. Respiratory, thoracic and mediastinal disorders : Epistaxis, pneumonia.
Skin and subcutaneous tissue disorders : Alopecia. Eye disorders : Abnormal vision, diplopia. Ear and labyrinth disorders : Tinnitus.
Renal and urinary disorders : Hematuria, renal failure. Other less frequent adverse reactions (<1%) were: C… [Excerpted — this section continues on DailyMed.]
🔄 Drug Interactions ▾
7 DRUG INTERACTIONS Other PDE3 inhibitors: Exacerbation of inotropic effects. ( 7.2 ) Aspirin and Drugs that Increase Bleeding Risk : Increased risk of bleeding with concomitant use. ( 7.3 )
7.1Drugs that Prolong QT Avoid use of AGRYLIN in patients taking medications that may prolong QT interval (including, but not limited to, chloroquine, clarithromycin, haloperidol, methadone, moxifloxacin, amiodarone, disopyramide, procainamide, and pimozide) [see Warnings and Precautions (5.1) and Clinical Pharmacology (12.2) ] .
7.2PDE3 Inhibitors AGRYLIN is a phosphodiesterase 3 (PDE3) inhibitor. Avoid use of drug products with similar properties such as inotropes and other PDE3 inhibitors (e.g., cilostazol, milrinone) [see Warnings and Precautions (5.1) and Clinical Pharmacology (12.2) ] .
7.3Aspirin and Drugs that Increase Bleeding Risk Co-administration of single-dose or repeat-dose AGRYLIN and aspirin showed greater ex vivo anti-platelet aggregation effects than administration of aspirin alone [see Clinical Pharmacology (12.3) ] . Results from an observational study in patients with essential thrombocythemia suggest the rate of major hemorrhagic events (MHEs) in patients treated with AGRYLIN is higher than in those subjects treated with another cytoreductive treatment. The majority of the major hemorrhagic events occurred in patients who were also receiving concomitant anti-aggregatory treatment (primarily, aspirin).
Therefore, the potential risks of the concomitant use of AGRYLIN with aspirin should be assessed, particularly in patients with a high-risk profile for hemorrhage, before treatment is initiated [see Warnings and Precautions (5.3) ] . Monitor patients for bleeding, particularly those receiving concomitant therapy with other drugs known to cause bleeding (e.g., anticoagulants, PDE3 inhibitors, NSAIDs, antiplatelet agents, selective serotonin reuptake inhibitors).
7.4CYP450 Interactions CYP1A2 inhibitors: AGRYLIN and its active metabolite are primarily metabolized by CYP1A2. Drugs that inhibit CYP1A2 (e.g., fluvoxamine, ciprofloxacin) could increase the exposure of AGRYLIN. Monitor patients for cardiovascular events and titrate doses accordingly when CYP1A2 inhibitors are co-administered.
CYP1A2 inducers: CYP1A2 inducers could decrease the exposure of AGRYLIN. Patients taking concomitant CYP1A2 inducers (e.g., omeprazole) may need to have their dose titrated to compensate for the decrease in AGRYLIN exposure. CYP1A2 substrates: AGRYLIN demonstrates limited inhibitory activity towards CYP1A2 in vitro and may alter the exposure of concomitant CYP1A2 substrates (e.g., theophylline, fluvoxamine, ondansetron).
👥 Use in Specific Populations ▾
8 USE IN SPECIFIC POPULATIONS Lactation: Advise not to breastfeed. ( 8.2 )
8.1Pregnancy Risk Summary Available data from case reports with AGRYLIN use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. In animal embryo-fetal studies, delayed fetal development (delayed skeletal ossification and reduced body weight) was observed in rats administered anagrelide hydrochloride during organogenesis at doses approximately 97 times the maximum clinical dose (10 mg/day) based on body surface area (see Data ) . There are adverse effects on maternal and fetal outcomes associated with thrombocythemia in pregnancy (see Clinical Considerations ).
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defect and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.
Clinical Considerations Disease-associated maternal and/or embryo/fetal risk Thrombotic events, such as stroke, deep vein thrombosis, or myocardial infarction, can be complications of thrombocythemia. Thrombocythemia in pregnancy is associated with an increased risk for miscarriage, stillbirth, and other maternal outcomes, such as preeclampsia. Data Animal Data Anagrelide hydrochloride was administered orally to pregnant rats and rabbits during the period of organogenesis at doses up to 900 mg/kg/day in rats and up to 20 mg/kg/day in rabbits (875 and 39 times, respectively, the maximum clinical dose of 10 mg/day based on body surface area).
In rats, developmental delays were observed including reductions in fetal weight at 300 and 900 mg/kg/day and delays in skeletal ossification at doses of 100 mg/kg/day and higher. The dose of 100 mg/kg/day (600 mg/m 2 /day) in rats is approximately 97 times the maximum clinical dose based on body surface area. No adverse embryo-fetal effects were detected in rabbits at the highest dose of 20 mg/kg/day (39 times the maximal clinical dose based on body surface area).
In a pre- and post-natal study conducted in female rats, anagrelide hydrochloride administered at oral doses of 60 mg/kg/day (58 times the maximum clinical dose based on body surface area) or higher during organogenesis through lactation produced delay or blockage of parturition, deaths of non-delivering pregnant dams and their fully developed fetuses, and increased mortality in the pups born. In a placental transfer study, a single oral dose of [ 14 C]-anagrelide hydrochloride (3 mg/kg) was administered to pregnant rats on gestation Day 17.
Drug-related radioactivity was detected in maternal and fetal tissue.
8.2Lactation Risk Summary There is no information regarding the presence of anagrelide in human milk, the effect on the breastfed child, or the effects on milk production. Anagrelide or its metabolites have been detected in the milk of lactating rats (see Data ) . Because of the potential for serious adverse reactions, including thrombocytopenia, in a breastfed child, advise patients that breastfeeding is not recommended during treatment with AGRYLIN, and for one week following the last dose.
Data In a rat milk secretion study, a single oral dose of [ 14 C]-anagrelide hydrochloride (3 mg/kg) was administered to lactating female rats on postnatal Day 10. Drug-related radioactivity was detected in the maternal milk and blood.
8.3Females and Males of Reproductive Potential Infertility Females Based on findings from animal studies, AGRYLIN may impair female fertility [see Nonclinical Toxicology (13.1) ] .
8.4Pediatric Use The safety and effectiveness of AGRYLIN have been established in pediatric patients 7 years of age and older. There are no data for pediatric patients less than 7 years of age. Use of AGRYLIN in these pediatric patients is… [Excerpted — this section continues on DailyMed.]
🤰 Pregnancy ▾
8.1Pregnancy Risk Summary Available data from case reports with AGRYLIN use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. In animal embryo-fetal studies, delayed fetal development (delayed skeletal ossification and reduced body weight) was observed in rats administered anagrelide hydrochloride during organogenesis at doses approximately 97 times the maximum clinical dose (10 mg/day) based on body surface area (see Data ) . There are adverse effects on maternal and fetal outcomes associated with thrombocythemia in pregnancy (see Clinical Considerations ).
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defect and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.
Clinical Considerations Disease-associated maternal and/or embryo/fetal risk Thrombotic events, such as stroke, deep vein thrombosis, or myocardial infarction, can be complications of thrombocythemia. Thrombocythemia in pregnancy is associated with an increased risk for miscarriage, stillbirth, and other maternal outcomes, such as preeclampsia. Data Animal Data Anagrelide hydrochloride was administered orally to pregnant rats and rabbits during the period of organogenesis at doses up to 900 mg/kg/day in rats and up to 20 mg/kg/day in rabbits (875 and 39 times, respectively, the maximum clinical dose of 10 mg/day based on body surface area).
In rats, developmental delays were observed including reductions in fetal weight at 300 and 900 mg/kg/day and delays in skeletal ossification at doses of 100 mg/kg/day and higher. The dose of 100 mg/kg/day (600 mg/m 2 /day) in rats is approximately 97 times the maximum clinical dose based on body surface area. No adverse embryo-fetal effects were detected in rabbits at the highest dose of 20 mg/kg/day (39 times the maximal clinical dose based on body surface area).
In a pre- and post-natal study conducted in female rats, anagrelide hydrochloride administered at oral doses of 60 mg/kg/day (58 times the maximum clinical dose based on body surface area) or higher during organogenesis through lactation produced delay or blockage of parturition, deaths of non-delivering pregnant dams and their fully developed fetuses, and increased mortality in the pups born. In a placental transfer study, a single oral dose of [ 14 C]-anagrelide hydrochloride (3 mg/kg) was administered to pregnant rats on gestation Day 17.
Drug-related radioactivity was detected in maternal and fetal tissue.
🧒 Pediatric Use ▾
8.4Pediatric Use The safety and effectiveness of AGRYLIN have been established in pediatric patients 7 years of age and older. There are no data for pediatric patients less than 7 years of age. Use of AGRYLIN in these pediatric patients is supported by evidence from adequate and well controlled studies of AGRYLIN in adults with additional pharmacokinetic, pharmacodynamic, and safety data in 18 pediatric patients aged 7 through 16 years with thrombocythemia secondary to ET [see Dosage and Administration (2.1) , Clinical Pharmacology (12.3) , and Clinical Studies (14) ] .
There were no apparent trends or differences in the types of adverse events observed between the pediatric patients compared with those of the adult patients [see Adverse Reactions (6.1) ].
🧓 Geriatric Use ▾
8.5Geriatric Use Of the 942 subjects in clinical studies of AGRYLIN, 42.1% were 65 years and over, while 14.9% were 75 years and over. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in response between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.
🆘 Overdosage ▾
10 OVERDOSAGE At higher than recommended doses, AGRYLIN has been shown to cause hypotension. There have been postmarketing case reports of intentional overdose with AGRYLIN. Reported symptoms include sinus tachycardia and vomiting.
Symptoms resolved with supportive management. Platelet reduction from AGRYLIN therapy is dose-related; therefore, thrombocytopenia, which can potentially cause bleeding, is expected from overdosage. In case of overdosage, stop AGRYLIN dosing and monitor platelet counts for thrombocytopenia and observe for possible complications such as bleeding.
Consider resumption of AGRYLIN dosing once the platelet count returns to the normal range.
🧬 Clinical Pharmacology ▾
12 CLINICAL PHARMACOLOGY
12.1Mechanism of Action The precise mechanism by which anagrelide reduces blood platelet count is unknown. In cell culture studies, anagrelide suppressed expression of transcription factors including GATA-1 and FOG-1 required for megakaryocytopoiesis, ultimately leading to reduced platelet production.
12.2Pharmacodynamics In blood withdrawn from normal volunteers treated with anagrelide, a disruption was found in the postmitotic phase of megakaryocyte development and a reduction in megakaryocyte size and ploidy. At therapeutic doses, anagrelide does not produce significant changes in white cell counts or coagulation parameters, and may have a small, but clinically insignificant effect on red cell parameters. The active metabolite, 3-hydroxy anagrelide, has similar potency and efficacy to that of anagrelide in the platelet lowering effect; however, exposure (measured by plasma AUC) to 3-hydroxy anagrelide is approximately 2-fold higher compared to anagrelide.
Anagrelide and 3-hydroxy anagrelide inhibit cyclic AMP phosphodiesterase 3 (PDE3) and 3-hydroxy anagrelide is approximately forty times more potent than anagrelide (IC 50s = 0.9 and 36 nM, respectively). PDE3 inhibition does not alter platelet production. PDE3 inhibitors, as a class can inhibit platelet aggregation.
However, significant inhibition of platelet aggregation is observed only at doses of anagrelide higher than those typically required to reduce platelet count. PDE3 inhibitors have cardiovascular (CV) effects including vasodilation, positive inotropy and chronotropy. Cardiac Electrophysiology The effect of anagrelide dose (0.5 mg and 2.5 mg single doses) on the heart rate and QTc interval prolongation potential was evaluated in a double-blind, randomized, placebo- and active-controlled, cross-over study in 60 healthy adult men and women.
A dose-related increase in heart rate was observed, with the maximum increase occurring around the time of maximal drug concentration (0.5 – 4 hours). The maximum change in mean heart rate occurred at 2 hours after administration and was +7.8 beats per minute (bpm) for 0.5 mg and +29.1 bpm for 2.5 mg. Dose-related increase in mean QTc was observed.
The maximum mean (95% upper confidence bound) change in QTcI (individual subject correction) from placebo after baseline-correction was 7.0 (9.8) ms and 13.0 (15.7) ms following anagrelide doses of 0.5 mg and 2.5 mg, respectively.
12.3Pharmacokinetics Dose proportionality has been found in the dose range 0.5 mg to 2.5 mg. Absorption Following oral administration of AGRYLIN, at least 70% is absorbed from the gastrointestinal tract. In fasted subjects, anagrelide peak plasma concentrations occur within about 1 hour after administration.
Pharmacokinetic data obtained from healthy volunteers comparing the pharmacokinetics of anagrelide in the fed and fasted states showed that administration of a 1 mg dose of anagrelide with food decreased the C max by 14%, but increased the AUC by 20%. Food decreased the C max of the active metabolite 3-hydroxy anagrelide by 29%, although it had no effect on the AUC. Elimination Anagrelide and 3 - hydroxy anagrelide are eliminated with plasma half-lives of approximately 1.5 and 2.5 hours, respectively.
Anagrelide and 3-hydroxy anagrelide do not accumulate in plasma when the clinical dose regimens are administered. Metabolism : Anagrelide is primarily metabolized by CYP1A2 to the active metabolite, 3-hydroxy anagrelide, which is subsequently metabolized by CYP1A2 to the inactive metabolite, RL603. Less than 1% of the administered dose is recovered in the urine as anagrelide, and approximately 3% and 16-20% of the administered dose is recovered as 3 - hydroxy anagrelide and RL603, respectively.
Drug Interactions Aspirin : In two pharmacodynamic interaction studies in healthy subjects, co-administration of single-dose anagrelide 1 mg and aspirin 900 mg or repeat-dose anagrelide 1 mg once daily and aspirin 75 mg once daily showed g… [Excerpted — this section continues on DailyMed.]
🧬 Mechanism of Action ▾
12.1Mechanism of Action The precise mechanism by which anagrelide reduces blood platelet count is unknown. In cell culture studies, anagrelide suppressed expression of transcription factors including GATA-1 and FOG-1 required for megakaryocytopoiesis, ultimately leading to reduced platelet production.
📦 How Supplied / Storage and Handling ▾
16 HOW SUPPLIED/STORAGE AND HANDLING AGRYLIN is available as: 0.5 mg, opaque, white capsules imprinted " 063" in black ink: NDC 54092-063-01 = bottle of 100 Store at 25°C (77°F) excursions permitted to 15°C to 30°C (59°F to 86°F), [See USP Controlled Room Temperature]. Store in a light resistant container. Imprint
📋 Description ▾
11 DESCRIPTION AGRYLIN (anagrelide hydrochloride) is a platelet-reducing agent. Its chemical name is 6,7-dichloro-1,5-dihydroimidazo[2,1-b]quinazolin-2(3H)-one monohydrochloride monohydrate. The molecular formula is C 10 H 7 Cl 2 N 3 O∙HCl∙H 2 O which corresponds to a molecular weight of 310.55.
The structural formula is: Anagrelide hydrochloride is an off-white powder. It is very slightly soluble in water and sparingly soluble in dimethyl sulfoxide and dimethylformamide. AGRYLIN is supplied as capsules for oral administration, containing 0.5 mg of anagrelide (equivalent to 0.61 mg of anagrelide hydrochloride USP).
The capsules also contain anhydrous lactose NF, crospovidone NF, lactose monohydrate NF, magnesium stearate NF, microcrystalline cellulose NF, and povidone NF as inactive ingredients. The capsule shell contains gelatin, titanium dioxide, and black iron oxide. chemical structure
💬 Information for Patients ▾
17 PATIENT COUNSELING INFORMATION Dose: Tell the patient that their dose will be adjusted on a weekly basis until they are on a dose that lowers their platelets to an appropriate level. This will also help the patient to adjust to common side effects. Tell the patient to contact their doctor if they experience tolerability issues, so the dose or dosing frequency can be adjusted [see Dosage and Administration (2) ] .
Cardiovascular effects: Tell the patient to contact a doctor immediately if they experience chest pain, palpitations, or feel their heartbeat is irregular [see Warnings and Precautions (5.1) ] . Risk of Pulmonary Hypertension: Tell the patient to contact a doctor immediately if they experience shortness of breath, swelling in legs or ankles, or lips and skin turn a bluish color [see Warnings and Precautions (5.2) ] . Risk of bleeding: Warn the patient that concomitant aspirin (or other medicines that affect blood clotting) may increase the risk of bleeding.
Tell the patient to contact a doctor immediately if they experience signs or symptoms of bleeding (e.g., vomit blood, pass bloody or black stools) or experience unexplained bruising/bruise more easily than usual [see Warnings and Precautions (5.3) , Drug Interactions (7.1) ] . Lactation: Advise patients not to breastfeed during treatment with AGRYLIN, and for one week following the last dose [see Use in Specific Populations (8.2) ] . Infertility: Advise females of reproductive potential treatment with AGRYLIN may impair fertility [see Use in Specific Populations (8.3) , Nonclinical Toxicology (13.1) ] .
🧬 Pharmacokinetics ▾
12.3Pharmacokinetics Dose proportionality has been found in the dose range 0.5 mg to 2.5 mg. Absorption Following oral administration of AGRYLIN, at least 70% is absorbed from the gastrointestinal tract. In fasted subjects, anagrelide peak plasma concentrations occur within about 1 hour after administration.
Pharmacokinetic data obtained from healthy volunteers comparing the pharmacokinetics of anagrelide in the fed and fasted states showed that administration of a 1 mg dose of anagrelide with food decreased the C max by 14%, but increased the AUC by 20%. Food decreased the C max of the active metabolite 3-hydroxy anagrelide by 29%, although it had no effect on the AUC. Elimination Anagrelide and 3 - hydroxy anagrelide are eliminated with plasma half-lives of approximately 1.5 and 2.5 hours, respectively.
Anagrelide and 3-hydroxy anagrelide do not accumulate in plasma when the clinical dose regimens are administered. Metabolism : Anagrelide is primarily metabolized by CYP1A2 to the active metabolite, 3-hydroxy anagrelide, which is subsequently metabolized by CYP1A2 to the inactive metabolite, RL603. Less than 1% of the administered dose is recovered in the urine as anagrelide, and approximately 3% and 16-20% of the administered dose is recovered as 3 - hydroxy anagrelide and RL603, respectively.
Drug Interactions Aspirin : In two pharmacodynamic interaction studies in healthy subjects, co-administration of single-dose anagrelide 1 mg and aspirin 900 mg or repeat-dose anagrelide 1 mg once daily and aspirin 75 mg once daily showed greater ex vivo anti-platelet aggregation effects than administration of aspirin alone. Co-administered anagrelide 1 mg and aspirin 900 mg single-doses had no effect on bleeding time, prothrombin time (PT) or activated partial thromboplastin time (aPTT). Digoxin or warfarin : In vivo interaction studies in humans have demonstrated that anagrelide does not affect the pharmacokinetic properties of digoxin or warfarin, nor does digoxin or warfarin affect the pharmacokinetic properties of anagrelide.
Specific Populations Pediatric : Dose-normalized C max and AUC of anagrelide were higher in children and adolescents (age range 7 through 16 years) with essential thrombocythemia, by 17% and 56%, respectively, than in adult patients (19 through 57 years). Geriatric : C max and AUC of anagrelide were 36% and 61% higher, respectively, in elderly patients (age range 65 through 75 years), than in younger adults (age range 22 through 50 years), but C max and AUC of the active metabolite, 3-hydroxy anagrelide, were 42% and 37% lower, respectively, in the elderly patients.
Renal Impairment : Pharmacokinetic study at a single dose of 1 mg anagrelide in subjects with severe renal impairment (creatinine clearance <30 mL/min) showed no significant effects on the pharmacokinetics of anagrelide. Hepatic Impairment : A pharmacokinetic study at a single dose of 1 mg anagrelide in subjects with moderate hepatic impairment (Child Pugh score 7-9) showed a 2-fold increase in mean anagrelide C max and an 8-fold increase in total exposure (AUC) to anagrelide compared with healthy subjects. Additionally, subjects with moderate hepatic impairment showed 24% lower mean 3-hydroxy anagrelide C max and 77% higher mean 3-hydroxy anagrelide AUC compared to healthy subjects.
🧬 Pharmacodynamics ▾
12.2Pharmacodynamics In blood withdrawn from normal volunteers treated with anagrelide, a disruption was found in the postmitotic phase of megakaryocyte development and a reduction in megakaryocyte size and ploidy. At therapeutic doses, anagrelide does not produce significant changes in white cell counts or coagulation parameters, and may have a small, but clinically insignificant effect on red cell parameters. The active metabolite, 3-hydroxy anagrelide, has similar potency and efficacy to that of anagrelide in the platelet lowering effect; however, exposure (measured by plasma AUC) to 3-hydroxy anagrelide is approximately 2-fold higher compared to anagrelide.
Anagrelide and 3-hydroxy anagrelide inhibit cyclic AMP phosphodiesterase 3 (PDE3) and 3-hydroxy anagrelide is approximately forty times more potent than anagrelide (IC 50s = 0.9 and 36 nM, respectively). PDE3 inhibition does not alter platelet production. PDE3 inhibitors, as a class can inhibit platelet aggregation.
However, significant inhibition of platelet aggregation is observed only at doses of anagrelide higher than those typically required to reduce platelet count. PDE3 inhibitors have cardiovascular (CV) effects including vasodilation, positive inotropy and chronotropy. Cardiac Electrophysiology The effect of anagrelide dose (0.5 mg and 2.5 mg single doses) on the heart rate and QTc interval prolongation potential was evaluated in a double-blind, randomized, placebo- and active-controlled, cross-over study in 60 healthy adult men and women.
A dose-related increase in heart rate was observed, with the maximum increase occurring around the time of maximal drug concentration (0.5 – 4 hours). The maximum change in mean heart rate occurred at 2 hours after administration and was +7.8 beats per minute (bpm) for 0.5 mg and +29.1 bpm for 2.5 mg. Dose-related increase in mean QTc was observed.
The maximum mean (95% upper confidence bound) change in QTcI (individual subject correction) from placebo after baseline-correction was 7.0 (9.8) ms and 13.0 (15.7) ms following anagrelide doses of 0.5 mg and 2.5 mg, respectively.
🔬 Clinical Studies ▾
14 CLINICAL STUDIES Clinical Studies in Adult Patients: A total of 942 patients with myeloproliferative neoplasms including 551 patients with Essential Thrombocythemia (ET), 117 patients with Polycythemia Vera (PV), 178 patients with Chronic Myelogenous Leukemia (CML), and 96 patients with other myeloproliferative neoplasms (OMPN), were treated with AGRYLIN in three clinical trials. Patients with OMPN included 87 patients who had Myeloid Metaplasia with Myelofibrosis (MMM), and 9 patients who had unclassified myeloproliferative neoplasms.
Patients were enrolled in clinical trials if their platelet count was ≥900,000/µL on two occasions or ≥650,000/µL on two occasions with documentation of symptoms associated with thrombocythemia. The mean duration of AGRYLIN therapy for ET, PV, CML, and OMPN patients was 65, 67, 40, and 44 weeks, respectively; 23% of patients received treatment for 2 years. Patients were treated with AGRYLIN starting at doses of 0.5-2.0 mg every 6 hours.
The dose was increased if the platelet count was still high, but to no more than 12 mg each day. Efficacy was defined as reduction of platelet count to or near physiologic levels (150,000-400,000/µL). The criteria for defining subjects as "responders" were reduction in platelets for at least 4 weeks to ≤600,000/µL, or by at least 50% from baseline value.
Subjects treated for less than 4 weeks were not considered evaluable. The results are depicted graphically below: Time on Treatment Weeks Years Baseline 4 12 24 48 2 3 4 Mean x 10 3 /µL 1131 683 575 526 484 460 437 457 N 923 Nine hundred and forty-two subjects with myeloproliferative neoplasms were enrolled in three research studies. Of these, 923 had platelet counts measured over the duration of the studies.
868 814 662 530 407 207 55 AGRYLIN was effective in phlebotomized patients as well as in patients treated with other concomitant therapies including hydroxyurea, aspirin, interferon, radioactive phosphorus, and alkylating agents. Figure 1 Clinical Study in Pediatric Patients: An open-label safety and PK/PD study was conducted in 18 pediatric patients 7 through 16 years of age (8 children 7 through 11 years of age and 10 adolescents 12 through 16 years of age, mean age of 12 years; 8 males and 10 females) with thrombocythemia secondary to ET as compared to 17 adult patients (mean age of 66 years, 9 males and 8 females).
Prior to entry on to the study, 17 of 18 pediatric patients and 12 of 17 adult patients had received AGRYLIN treatment for an average of 2 years. The median starting total daily dose, determined by retrospective chart review, for pediatric and adult patients with ET who had received AGRYLIN prior to study entry was 1 mg for each of the three age groups (7 through 11 and 12 through 16 years of age and adults). The starting dose for 6 AGRYLIN-naive patients at study entry was 0.5 mg once daily.
At study completion, the median total daily maintenance doses were similar across age groups, median of 1.75 mg for children of 7 through 11 years of age, 2.25 mg in adolescents 12 through 16 years of age, and 1.5 mg for adults.
🧪 Nonclinical Toxicology ▾
13 NONCLINICAL TOXICOLOGY
13.1Carcinogenesis, Mutagenesis, Impairment of Fertility In a two-year rat carcinogenicity study a higher incidence of uterine adenocarcinoma, relative to controls, was observed in females receiving 30 mg/kg/day (at least 174 times human AUC exposure after a 1 mg twice daily dose). Adrenal pheochromocytomas were increased relative to controls in males receiving 3 mg/kg/day and above, and in females receiving 10 mg/kg/day and above (at least 10 and 18 times respectively human AUC exposure after a 1 mg twice daily dose).
Anagrelide hydrochloride was not mutagenic in the bacterial mutagenesis (Ames) assay or the mouse lymphoma cell (L5178Y, TK+/-) forward mutation assay, and was not clastogenic in the in vitro chromosome aberration assay using human lymphocytes or the in vivo mouse micronucleus test. Anagrelide hydrochloride at oral doses up to 240 mg/kg/day (233 times the recommended human dose of 10 mg/day based on body surface area) had no effect on fertility and reproductive function of male rats. However, in fertility studies in female rats, oral doses of 30 mg/kg/day (29 times the recommended maximum human dose based on body surface area) or higher resulted in increased pre- and post-implantation loss and a decrease in the number of live embryos.
13.2Animal Toxicology and/or Pharmacology In the 2-year rat study, a significant increase in non-neoplastic lesions was observed in anagrelide treated males and females in the adrenal (medullary hyperplasia), heart (myocardial hypertrophy and chamber distension), kidney (hydronephrosis, tubular dilation and urothelial hyperplasia), and bone (femur enostosis). Vascular effects were observed in tissues of the pancreas (arteritis/periarteritis, intimal proliferation, and medial hypertrophy), kidney (arteritis/periarteritis, intimal proliferation, and medial hypertrophy), sciatic nerve (vascular mineralization), and testes (tubular atrophy and vascular infarct) in anagrelide-treated males.
📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ▾
13.1Carcinogenesis, Mutagenesis, Impairment of Fertility In a two-year rat carcinogenicity study a higher incidence of uterine adenocarcinoma, relative to controls, was observed in females receiving 30 mg/kg/day (at least 174 times human AUC exposure after a 1 mg twice daily dose). Adrenal pheochromocytomas were increased relative to controls in males receiving 3 mg/kg/day and above, and in females receiving 10 mg/kg/day and above (at least 10 and 18 times respectively human AUC exposure after a 1 mg twice daily dose).
Anagrelide hydrochloride was not mutagenic in the bacterial mutagenesis (Ames) assay or the mouse lymphoma cell (L5178Y, TK+/-) forward mutation assay, and was not clastogenic in the in vitro chromosome aberration assay using human lymphocytes or the in vivo mouse micronucleus test. Anagrelide hydrochloride at oral doses up to 240 mg/kg/day (233 times the recommended human dose of 10 mg/day based on body surface area) had no effect on fertility and reproductive function of male rats. However, in fertility studies in female rats, oral doses of 30 mg/kg/day (29 times the recommended maximum human dose based on body surface area) or higher resulted in increased pre- and post-implantation loss and a decrease in the number of live embryos.
📄 Package Label / Principal Display Panel ▾
PRINCIPAL DISPLAY PANEL - 0.5 mg Capsule Bottle Label 063-01 NDC 54092-063-01 Agrylin (anagrelide) Capsules Platelet-reducing Agent 100 CAPSULES Rx only 0.5 mg Takeda PRINCIPAL DISPLAY PANEL - 0.5 mg Capsule Bottle Label
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