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Agrylin (Anagrelide HCl)
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Pharmacology
The mechanism by which anagrelide reduces blood platelet count is still under investigation. Studies in patients support a hypothesis of dose-related reduction in platelet production resulting from a decrease in megakaryocyte hypermaturation. In blood withdrawn from normal volunteers treated with anagrelide, a disruption was found in the postmitotic phase of megakaryocyte development and a reduction in megakaryocyte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. Platelet aggregation is inhibited in humans at doses higher than those required to reduce platelet count. Anagrelide inhibits cyclic AMP phosphodiesterase, as well as ADP- and collagen-induced platelet aggregation.
Following oral administration of 14C-anagrelide in humans, more than 70% of the radioactivity was recovered in urine. Based on limited data, there appears to be a trend toward dose linearity between doses of 0.5and 2mg. At fasting and at a dose of 0.5mg of anagrelide, the plasma half-life is 1.3hours. The available plasma concentration time data at steady-state in patients showed that anagrelide does not accumulate in plasma after repeated administration. The drug is extensively metabolized; less than 1% is recovered in the urine as anagrelide.
When a 0.5mg dose of anagrelide was taken after food, its bioavailability (based on AUC values) was modestly reduced by an average of 13.8% and its plasma half-life slightly increased (to 1.8hours), when compared with drug administered to the same subjects in the fasted state. The peak plasma level was lowered by an average of 45% and delayed by 2hours.
The mechanism by which anagrelide reduces blood platelet count is still under investigation. Studies in patients support a hypothesis of dose-related reduction in platelet production resulting from a decrease in megakaryocyte hypermaturation. In blood withdrawn from normal volunteers treated with anagrelide, a disruption was found in the postmitotic phase of megakaryocyte development and a reduction in megakaryocyte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. Platelet aggregation is inhibited in humans at doses higher than those required to reduce platelet count. Anagrelide inhibits cyclic AMP phosphodiesterase, as well as ADP- and collagen-induced platelet aggregation.
Following oral administration of 14C-anagrelide in humans, more than 70% of the radioactivity was recovered in urine. Based on limited data, there appears to be a trend toward dose linearity between doses of 0.5and 2mg. At fasting and at a dose of 0.5mg of anagrelide, the plasma half-life is 1.3hours. The available plasma concentration time data at steady-state in patients showed that anagrelide does not accumulate in plasma after repeated administration. The drug is extensively metabolized; less than 1% is recovered in the urine as anagrelide.
When a 0.5mg dose of anagrelide was taken after food, its bioavailability (based on AUC values) was modestly reduced by an average of 13.8% and its plasma half-life slightly increased (to 1.8hours), when compared with drug administered to the same subjects in the fasted state. The peak plasma level was lowered by an average of 45% and delayed by 2hours.
Indications
The Mechanism By Which Anagrelide Reduces Blood Platelet Count Is Still Under Investigation. Studies In Patients Support A Hypothesis Of Dose-related Reduction In Platelet Production Resulting From A Decrease In Megakaryocyte Hypermaturation. 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. Platelet Aggregation Is Inhibited In Humans At Doses Higher Than Those Required To Reduce Platelet Count. Anagrelide Inhibits Cyclic AMP Phosphodiesterase, As Well As ADP- And Collagen-induced Platelet Aggregation.
Following Oral Administration Of 14C-anagrelide In Humans, More Than 70% Of The Radioactivity Was Recovered In Urine. Based On Limited Data, There Appears To Be A Trend Toward Dose Linearity Between Doses Of 0.5and 2mg. At Fasting And At A Dose Of 0.5mg Of Anagrelide, The Plasma Half-life Is 1.3hours. The Available Plasma Concentration Time Data At Steady-state In Patients Showed That Anagrelide Does Not Accumulate In Plasma After Repeated Administration. The Drug Is Extensively Metabolized; Less Than 1% Is Recovered In The Urine As Anagrelide.
When A 0.5mg Dose Of Anagrelide Was Taken After Food, Its Bioavailability (based On AUC Values) Was Modestly Reduced By An Average Of 13.8% And Its Plasma Half-life Slightly Increased (to 1.8hours), When Compared With Drug Administered To The Same Subjects In The Fasted State. The Peak Plasma Level Was Lowered By An Average Of 45% And Delayed By 2hours.
The Mechanism By Which Anagrelide Reduces Blood Platelet Count Is Still Under Investigation. Studies In Patients Support A Hypothesis Of Dose-related Reduction In Platelet Production Resulting From A Decrease In Megakaryocyte Hypermaturation. 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. Platelet Aggregation Is Inhibited In Humans At Doses Higher Than Those Required To Reduce Platelet Count. Anagrelide Inhibits Cyclic AMP Phosphodiesterase, As Well As ADP- And Collagen-induced Platelet Aggregation.
Following Oral Administration Of 14C-anagrelide In Humans, More Than 70% Of The Radioactivity Was Recovered In Urine. Based On Limited Data, There Appears To Be A Trend Toward Dose Linearity Between Doses Of 0.5and 2mg. At Fasting And At A Dose Of 0.5mg Of Anagrelide, The Plasma Half-life Is 1.3hours. The Available Plasma Concentration Time Data At Steady-state In Patients Showed That Anagrelide Does Not Accumulate In Plasma After Repeated Administration. The Drug Is Extensively Metabolized; Less Than 1% Is Recovered In The Urine As Anagrelide.
When A 0.5mg Dose Of Anagrelide Was Taken After Food, Its Bioavailability (based On AUC Values) Was Modestly Reduced By An Average Of 13.8% And Its Plasma Half-life Slightly Increased (to 1.8hours), When Compared With Drug Administered To The Same Subjects In The Fasted State. The Peak Plasma Level Was Lowered By An Average Of 45% And Delayed By 2hours.
Contraindications
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Information not available
Safety Information / Warning
Cardiovascular: Anagrelide should be used with caution in patients with known or suspected heart disease, and only if the potential benefits of therapy outweigh the potential risks. Because of the positive inotropic effects and side effects of anagrelide, a pre-treatment cardiovascular examination is recommended along with careful monitoring during treatment. In humans, therapeutic doses of anagrelide may cause cardiovascular effects, including vasodilation, tachycardia, palpitations, and congestive heart failure.
Renal: It is recommended that patients with renal insufficiency (creatinine ³2mg/dL) receive anagrelide when, in the physician's judgment, the potential benefits of therapy outweigh the potential risks. These patients should be monitored closely for signs of renal toxicity while receiving anagrelide (see Adverse Effects, Urogenital).
Hepatic: It is recommended that patients with evidence of hepatic dysfunction (bilirubin, AST, or measures of liver function >1.5times the upper limit of normal) receive anagrelide when, in the physician's judgment, the potential benefits of therapy outweigh the potential risks. These patients should be monitored closely for signs of hepatic toxicity while receiving anagrelide (see Adverse Effects, Hepatic).
Children: The safety and efficacy of anagrelide in patients under the age of 16years have not been established.
Pregnancy: There are no adequate and well-controlled studies in pregnant women. Anagrelide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Anagrelide is not recommended in women who are or may become pregnant. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential harm to the fetus. Women of childbearing potential should be instructed that they must not be pregnant and that they should use contraception while taking anagrelide. Anagrelide may cause fetal harm when administered to a pregnant woman.
Lactation: It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reaction in nursing infants from anagrelide, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Cardiovascular: Anagrelide should be used with caution in patients with known or suspected heart disease, and only if the potential benefits of therapy outweigh the potential risks. Because of the positive inotropic effects and side effects of anagrelide, a pre-treatment cardiovascular examination is recommended along with careful monitoring during treatment. In humans, therapeutic doses of anagrelide may cause cardiovascular effects, including vasodilation, tachycardia, palpitations, and congestive heart failure.
Renal: It is recommended that patients with renal insufficiency (creatinine ³2mg/dL) receive anagrelide when, in the physician's judgment, the potential benefits of therapy outweigh the potential risks. These patients should be monitored closely for signs of renal toxicity while receiving anagrelide (see Adverse Effects, Urogenital).
Hepatic: It is recommended that patients with evidence of hepatic dysfunction (bilirubin, AST, or measures of liver function >1.5times the upper limit of normal) receive anagrelide when, in the physician's judgment, the potential benefits of therapy outweigh the potential risks. These patients should be monitored closely for signs of hepatic toxicity while receiving anagrelide (see Adverse Effects, Hepatic).
Children: The safety and efficacy of anagrelide in patients under the age of 16years have not been established.
Pregnancy: There are no adequate and well-controlled studies in pregnant women. Anagrelide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Anagrelide is not recommended in women who are or may become pregnant. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential harm to the fetus. Women of childbearing potential should be instructed that they must not be pregnant and that they should use contraception while taking anagrelide. Anagrelide may cause fetal harm when administered to a pregnant woman.
Lactation: It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reaction in nursing infants from anagrelide, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Precautions
The decision to treat asymptomatic young adults with thrombocythemia secondary to myeloproliferative disorders should be individualized.
Sudden discontinuation or interruption of anagrelide treatment is followed by an increase in platelet count. Following discontinuation, an increase in platelet count can be observed within 4days.
Drug Interactions : Bioavailability studies evaluating possible interactions between anagrelide and other drugs have not been conducted. The most common medications used concomitantly with anagrelide have been ASA, acetaminophen, furosemide, iron, ranitidine, hydroxyurea, and allopurinol. The most frequently used concomitant cardiac medication has been digoxin. Although drug-to-drug interaction studies have not been conducted, there is no clinical evidence to suggest that anagrelide interacts with any of these compounds.
There is a single case report which suggests that sucralfate may interfere with anagrelide absorption.
Food has no clinically significant effect on the bioavailability of anagrelide.
Monitoring: Anagrelide therapy requires close clinical supervision of the patient. To monitor the effect of anagrelide and prevent the occurrence of thrombocytopenia, platelet counts should be performed every 2days during the first week of treatment and at least weekly thereafter, until the maintenance dosage is reached. Typically, platelet count begins to respond within 7to 14days at the proper dosage. The time to complete response, defined as platelet count £600000/µL, ranged from 4 to 12 weeks. Most patients will experience an adequate response at a dose of 1.5to 3mg/day. In case of overdose, close clinical supervision of the patient is required, including monitoring of the platelet count for thrombocytopenia. Dosage should be decreased or stopped as appropriate, until platelet count returns to within the normal range. However, in patients with hepatic insufficiency or renal insufficiency, liver function and kidney function tests should be performed at least once/month or when deemed necessary in the physician's judgment.
The decision to treat asymptomatic young adults with thrombocythemia secondary to myeloproliferative disorders should be individualized.
Sudden discontinuation or interruption of anagrelide treatment is followed by an increase in platelet count. Following discontinuation, an increase in platelet count can be observed within 4days.
Drug Interactions : Bioavailability studies evaluating possible interactions between anagrelide and other drugs have not been conducted. The most common medications used concomitantly with anagrelide have been ASA, acetaminophen, furosemide, iron, ranitidine, hydroxyurea, and allopurinol. The most frequently used concomitant cardiac medication has been digoxin. Although drug-to-drug interaction studies have not been conducted, there is no clinical evidence to suggest that anagrelide interacts with any of these compounds.
There is a single case report which suggests that sucralfate may interfere with anagrelide absorption.
Food has no clinically significant effect on the bioavailability of anagrelide.
Monitoring: Anagrelide therapy requires close clinical supervision of the patient. To monitor the effect of anagrelide and prevent the occurrence of thrombocytopenia, platelet counts should be performed every 2days during the first week of treatment and at least weekly thereafter, until the maintenance dosage is reached. Typically, platelet count begins to respond within 7to 14days at the proper dosage. The time to complete response, defined as platelet count £600000/µL, ranged from 4 to 12 weeks. Most patients will experience an adequate response at a dose of 1.5to 3mg/day. In case of overdose, close clinical supervision of the patient is required, including monitoring of the platelet count for thrombocytopenia. Dosage should be decreased or stopped as appropriate, until platelet count returns to within the normal range. However, in patients with hepatic insufficiency or renal insufficiency, liver function and kidney function tests should be performed at least once/month or when deemed necessary in the physician's judgment.
Side Effects / Adverse Effects
Analysis of the adverse events in a population consisting of 942 patients diagnosed with myeloproliferative diseases of varying etiology (ET: 551; PV: 117; OMPD: 274) has shown that all disease groups have the same adverse event profile. While most reported adverse events during anagrelide therapy have been mild in intensity and have decreased in frequency with continued therapy, serious adverse events reported were reported in these patients. These include the following: congestive heart failure, myocardial infarction, cardiomyopathy, cardiomegaly, complete heart block, atrial fibrillation, cerebrovascular accident, pericarditis, pulmonary infiltrates, pulmonary fibrosis, pulmonary hypertension, pancreatitis, gastric/duodenal ulceration, and seizure.
The mean duration of anagrelide therapy for ET, PV, CML and OMPD patients was 65, 67, 40 and 44 weeks, respectively. Of the 942 patients treated with anagrelide, 161 (17%) were discontinued from the study because of adverse events or abnormal laboratory test results. The most common adverse events for treatment discontinuation were headache, diarrhea, edema, palpitation, and abdominal pain. Overall, the occurrence rate of all adverse events was 17.9 per 1000 treatment days. The occurrence rate of adverse events increased at higher dosages of anagrelide.
The most frequently reported adverse reactions to anagrelide (in 5% or greater of 942 patients with myeloproliferative disease) in clinical trials were: headache 43.5%; palpitations 26.1%; diarrhea 25.7%; asthenia 23.1%; edema, other 20.6%; nausea 17.1%; abdominal pain 16.5%; dizziness 15.4%; pain, other 15.0%; dyspnea 11.9%; flatulence 10.2%; vomiting 9.7%; fever 8.9%; peripheral edema 8.5%; rash, including urticaria 8.3%; chest pain 8.0%; anorexia 7.7%; tachycardia 7.5%; pharyngitis 6.8%; malaise 6.4%; cough 6.3%; paresthesia 5.9%; back pain 5.9%; pruritus 5.5%; dyspepsia 5.2%.
Adverse events with an incidence of 1% to <5% included the following:
Body as a Whole System: chills, flu symptoms, infection, neck pain, accidental injury, photosensitivity, cellulitis.
Cardiovascular: arrhythmia, hemorrhage, cardiovascular disease, angina pectoris, heart failure, congestive heart failure, vasodilatation, postural hypotension, migraine, syncope, hypotension.
Digestive: constipation, gastrointestinal hemorrhage, gastrointestinal distress, melena, nausea and vomiting, gastritis, dysphagia, eructation.
Hemic and Lymphatic: anemia, thrombocytopenia, ecchymosis, lymphadenoma. Platelet counts below 100000/µL occurred in 84 patients (ET: 35; PV: 9; OMPD: 40) and reduction below 50000/µL occurred in 44 patients (ET: 7; PV: 6; OMPD: 31) while on anagrelide therapy. Thrombocytopenia promptly recovered upon discontinuation of anagrelide.
Hepatic: Elevated liver enzymes were observed in 3 patients (ET: 2; OMPD: 1) during anagrelide therapy.
Musculoskeletal: arthralgia, myalgia, leg cramps, arthritis, bone pain.
Nervous: depression, somnolence, insomnia, confusion, hypertension, nervousness, amnesia.
Nutritional Disorders: weight Loss, weight gain, edema.
Respiratory: rhinitis, epistaxis, respiratory disease, sinusitis, pneumonia, bronchitis.
Skin and Appendages: sweating, skin disease, alopecia, skin ulcer, skin discoloration.
Special Senses: amblyopia, abnormal vision, ear disorder, conjunctivitis, visual field abnormality, tinnitus, eye disorder.
Urogenital: urinary tract disorder, urinary frequency, hematuria, urinary tract infection, dysuria, nocturia, urinary incontinence.
Renal abnormalities occurred in 15 patients (ET: 10; PV: 4; OMPD: 1). Six ET, 4 PV and 1 OMPD experienced renal failure (approximately 1%) while on anagrelide treatment; in 4 cases the renal failure was considered to be possibly related to anagrelide treatment. The remaining 11 were found to have pre-existing renal impairment and were successfully treated with anagrelide. Doses ranged from 1.5to 6 mg/day, with exposure periods of 2 to 12 months. No dose adjustment was required because of renal insufficiency.
Analysis of the adverse events in a population consisting of 942 patients diagnosed with myeloproliferative diseases of varying etiology (ET: 551; PV: 117; OMPD: 274) has shown that all disease groups have the same adverse event profile. While most reported adverse events during anagrelide therapy have been mild in intensity and have decreased in frequency with continued therapy, serious adverse events reported were reported in these patients. These include the following: congestive heart failure, myocardial infarction, cardiomyopathy, cardiomegaly, complete heart block, atrial fibrillation, cerebrovascular accident, pericarditis, pulmonary infiltrates, pulmonary fibrosis, pulmonary hypertension, pancreatitis, gastric/duodenal ulceration, and seizure.
The mean duration of anagrelide therapy for ET, PV, CML and OMPD patients was 65, 67, 40 and 44 weeks, respectively. Of the 942 patients treated with anagrelide, 161 (17%) were discontinued from the study because of adverse events or abnormal laboratory test results. The most common adverse events for treatment discontinuation were headache, diarrhea, edema, palpitation, and abdominal pain. Overall, the occurrence rate of all adverse events was 17.9 per 1000 treatment days. The occurrence rate of adverse events increased at higher dosages of anagrelide.
The most frequently reported adverse reactions to anagrelide (in 5% or greater of 942 patients with myeloproliferative disease) in clinical trials were: headache 43.5%; palpitations 26.1%; diarrhea 25.7%; asthenia 23.1%; edema, other 20.6%; nausea 17.1%; abdominal pain 16.5%; dizziness 15.4%; pain, other 15.0%; dyspnea 11.9%; flatulence 10.2%; vomiting 9.7%; fever 8.9%; peripheral edema 8.5%; rash, including urticaria 8.3%; chest pain 8.0%; anorexia 7.7%; tachycardia 7.5%; pharyngitis 6.8%; malaise 6.4%; cough 6.3%; paresthesia 5.9%; back pain 5.9%; pruritus 5.5%; dyspepsia 5.2%.
Adverse events with an incidence of 1% to <5% included the following:
Body as a Whole System: chills, flu symptoms, infection, neck pain, accidental injury, photosensitivity, cellulitis.
Cardiovascular: arrhythmia, hemorrhage, cardiovascular disease, angina pectoris, heart failure, congestive heart failure, vasodilatation, postural hypotension, migraine, syncope, hypotension.
Digestive: constipation, gastrointestinal hemorrhage, gastrointestinal distress, melena, nausea and vomiting, gastritis, dysphagia, eructation.
Hemic and Lymphatic: anemia, thrombocytopenia, ecchymosis, lymphadenoma. Platelet counts below 100000/µL occurred in 84 patients (ET: 35; PV: 9; OMPD: 40) and reduction below 50000/µL occurred in 44 patients (ET: 7; PV: 6; OMPD: 31) while on anagrelide therapy. Thrombocytopenia promptly recovered upon discontinuation of anagrelide.
Hepatic: Elevated liver enzymes were observed in 3 patients (ET: 2; OMPD: 1) during anagrelide therapy.
Musculoskeletal: arthralgia, myalgia, leg cramps, arthritis, bone pain.
Nervous: depression, somnolence, insomnia, confusion, hypertension, nervousness, amnesia.
Nutritional Disorders: weight Loss, weight gain, edema.
Respiratory: rhinitis, epistaxis, respiratory disease, sinusitis, pneumonia, bronchitis.
Skin and Appendages: sweating, skin disease, alopecia, skin ulcer, skin discoloration.
Special Senses: amblyopia, abnormal vision, ear disorder, conjunctivitis, visual field abnormality, tinnitus, eye disorder.
Urogenital: urinary tract disorder, urinary frequency, hematuria, urinary tract infection, dysuria, nocturia, urinary incontinence.
Renal abnormalities occurred in 15 patients (ET: 10; PV: 4; OMPD: 1). Six ET, 4 PV and 1 OMPD experienced renal failure (approximately 1%) while on anagrelide treatment; in 4 cases the renal failure was considered to be possibly related to anagrelide treatment. The remaining 11 were found to have pre-existing renal impairment and were successfully treated with anagrelide. Doses ranged from 1.5to 6 mg/day, with exposure periods of 2 to 12 months. No dose adjustment was required because of renal insufficiency.
Overdose
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Information not available
Recommended Dosage
Treatment should be initiated under close medical supervision. The recommended starting dose is 0.5mg q.i.d. or 1mg b.i.d., which should be maintained for at least 1week.
Dosage should then be adjusted to the lowest effective dosage required to reduce and maintain platelet count below 600000/µL, and ideally to the normal range. The dosage should be increased by not more than 0.5mg/day in any 1week. Dosage should not exceed 10mg/day or 2.5mg in a single dose (see Precautions).
The decision to treat asymptomatic young adults with thrombocythemia secondary to myeloproliferative disorders should be individualized.
To monitor the effect of anagrelide and prevent the occurrence of thrombocytopenia, platelet counts should be performed every 2days during the first week of treatment and at least weekly thereafter until the maintenance dosage is reached.
Typically, platelet count begins to respond within 7to 14days at the proper dosage.
The time to complete response, defined as platelet count £600000/µL, ranged from 4 to 12 weeks. Most patients will experience an adequate response at a dose of 1.5 to 3mg/day. Patients with known or suspected heart disease, renal insufficiency, or hepatic dysfunction should be monitored closely.
Treatment should be initiated under close medical supervision. The recommended starting dose is 0.5mg q.i.d. or 1mg b.i.d., which should be maintained for at least 1week.
Dosage should then be adjusted to the lowest effective dosage required to reduce and maintain platelet count below 600000/µL, and ideally to the normal range. The dosage should be increased by not more than 0.5mg/day in any 1week. Dosage should not exceed 10mg/day or 2.5mg in a single dose (see Precautions).
The decision to treat asymptomatic young adults with thrombocythemia secondary to myeloproliferative disorders should be individualized.
To monitor the effect of anagrelide and prevent the occurrence of thrombocytopenia, platelet counts should be performed every 2days during the first week of treatment and at least weekly thereafter until the maintenance dosage is reached.
Typically, platelet count begins to respond within 7to 14days at the proper dosage.
The time to complete response, defined as platelet count £600000/µL, ranged from 4 to 12 weeks. Most patients will experience an adequate response at a dose of 1.5 to 3mg/day. Patients with known or suspected heart disease, renal insufficiency, or hepatic dysfunction should be monitored closely.
Supplied / Packaging
Each white, opaque capsule, imprinted with “ROBERTS 063” in black ink, contains: anagrelide base 0.5mg (as anagrelide HCl). Nonmedicinal ingredients: black iron oxide, crospovidone, gelatin, lactose, magnesium stearate, microcrystalline cellulose, povidone, silicon dioxide, sodium lauryl sulfate and titanium oxide. Bottles of100. Store from 15to 25°C in a light-resistant container.
Each white, opaque capsule, imprinted with “ROBERTS 063” in black ink, contains: anagrelide base 0.5mg (as anagrelide HCl). Nonmedicinal ingredients: black iron oxide, crospovidone, gelatin, lactose, magnesium stearate, microcrystalline cellulose, povidone, silicon dioxide, sodium lauryl sulfate and titanium oxide. Bottles of100. Store from 15to 25°C in a light-resistant container.
