One case of deliberate overdosage with TICLID (ticlopidine hcl) has been reported by a foreign postmarketing surveillance program. A 38-year-old male took a single 6000-mg dose of TICLID (ticlopidine hcl) (equivalent to 24 standard 250-mg tablets). The only abnormalities reported were increased bleeding time and increased SGPT. No special therapy was instituted and the patient recovered without sequelae.
Single oral doses of ticlopidine at 1600 mg/kg and 500 mg/kg were lethal to rats and mice, respectively. Symptoms of acute toxicity were GI hemorrhage, convulsions, hypothermia, dyspnea, loss of equilibrium and abnormal gait.
Adverse reactions in stroke patients were relatively frequent with over 50% of patients reporting at least one. Most (30% to 40%) involved the gastrointestinal tract. Most adverse effects are mild, but 21% of patients discontinued therapy because of an adverse event, principally diarrhea, rash, nausea, vomiting, GI pain and neutropenia. Most adverse effects occur early in the course of treatment, but a new onset of adverse effects can occur after several months.
The incidence rates of adverse events listed in the following table were derived from multicenter, controlled clinical trials in stroke patients described above comparing TICLID (ticlopidine hcl) , placebo and aspirin over study periods of up to 5.8 years. Adverse events considered by the investigator to be probably drug-related that occurred in at least 1% of patients treated with TICLID (ticlopidine hcl) are shown in the following table:
Percent of Patients With Adverse Events in Controlled Studies
(TASS and CATS)
| Event | TICLID (ticlopidine hcl) (n = 2048) Incidence |
Aspirin (n = 1527) Incidence |
Placebo (n = 536) Incidence |
| Any Events | 60.0 (20.9) | 53.2 (14.5) | 34.3 (6.1) |
| Diarrhea | 12.5 (6.3) | 5.2 (1.8) | 4.5 (1.7) |
| Nausea | 7.0 (2.6) | 6.2 (1.9) | 1.7 (0.9) |
| Dyspepsia | 7.0 (1.1) | 9.0 (2.0) | 0.9 (0.2) |
| Rash | 5.1 (3.4) | 1.5 (0.8) | 0.6 (0.9) |
| GI Pain | 3.7 (1.9) | 5.6 (2.7) | 1.3 (0.4) |
| Neutropenia | 2.4 (1.3) | 0.8 (0.1) | 1.1 (0.4) |
| Purpura | 2.2 (0.2) | 1.6 (0.1) | 0.0 (0.0) |
| Vomiting | 1.9 (1.4) | 1.4 (0.9) | 0.9 (0.4) |
| Flatulence | 1.5 (0.1) | 1.4 (0.3) | 0.0 (0.0) |
| Pruritus | 1.3 (0.8) | 0.3 (0.1) | 0.0 (0.0) |
| Dizziness | 1.1 (0.4) | 0.5 (0.4) | 0.0 (0.0) |
| Anorexia | 1.0 (0.4) | 0.5 (0.3) | 0.0 (0.0) |
| Abnormal Liver Function Test | 1.0 (0.7) | 0.3 (0.3) | 0.0 (0.0) |
Incidence of discontinuation, regardless of relationship to therapy, is shown in parentheses.
Hematological: Neutropenia/thrombocytopenia, TTP, aplastic anemia (see BOXED WARNING and WARNINGS), leukemia, agranulocytosis, eosinophilia, pancytopenia, thrombocytosis and bone-marrow depression have been reported.
Gastrointestinal: TICLID (ticlopidine hcl) therapy has been associated with a variety of gastrointestinal complaints including diarrhea and nausea. The majority of cases are mild, but about 13% of patients discontinued therapy because of these. They usually occur within 3 months of initiation of therapy and typically are resolved within 1 to 2 weeks without discontinuation of therapy. If the effect is severe or persistent, therapy should be discontinued. In some cases of severe or bloody diarrhea, colitis was later diagnosed.
Hemorrhagic: TICLID (ticlopidine hcl) has been associated with increased bleeding, spontaneous posttraumatic bleeding and perioperative bleeding including, but not limited to, gastrointestinal bleeding. It has also been associated with a number of bleeding complications such as ecchymosis, epistaxis, hematuria and conjunctival hemorrhage.
Intracerebral bleeding was rare in clinical trials in stroke patients with TICLID (ticlopidine hcl) , with an incidence no greater than that seen with comparator agents (ticlopidine 0.5%, aspirin 0.6%, placebo 0.75%). It has also been reported postmarketing.
Rash: Ticlopidine has been associated with a maculopapular or urticarial rash (often with pruritus). Rash usually occurs within 3 months of initiation of therapy with a mean onset time of 11 days. If drug is discontinued, recovery occurs within several days. Many rashes do not recur on drug rechallenge. There have been rare reports of severe rashes, including Stevens-Johnson syndrome, erythema multiforme and exfoliative dermatitis.
Less Frequent Adverse Reactions (Probably Related): Clinical adverse experiences occurring in 0.5% to 1.0% of stroke patients in controlled trials include: Digestive System: GI fullness
Skin and Appendages: urticaria
Nervous System: headache
Body as a Whole: asthenia, pain
Hemostatic System: epistaxis
Special Senses: tinnitus
In addition, rarer, relatively serious and potentially fatal events associated with the use of TICLID (ticlopidine hcl) have also been reported from postmarketing experience: Hemolytic anemia with reticulocytosis, immune thrombocytopenia, hepatitis, hepatocellular jaundice, cholestatic jaundice, hepatic necrosis, hepatic failure, peptic ulcer, renal failure, nephrotic syndrome, hyponatremia, vasculitis, sepsis, allergic reactions (including angioedema, allergic pneumonitis, and anaphylaxis), systemic lupus (positive ANA), peripheral neuropathy, serum sickness, arthropathy and myositis.
Hematological Adverse Reactions: Neutropenia: Neutropenia may occur suddenly. Bone-marrow examination typically shows a reduction in white blood cell precursors. After withdrawal of ticlopidine, the neutrophil count usually rises to !1200/mm³ within 1 to 3 weeks.
Thrombocytopenia: Rarely, thrombocytopenia may occur in isolation or together with neutropenia.
Thrombotic Thrombocytopenic Purpura (TTP): TTP is characterized by thrombocytopenia, microangiopathic hemolytic anemia (schistocytes [fragmented RBCs] seen on peripheral smear), neurological findings, renal dysfunction, and fever. The signs and symptoms can occur in any order, in particular, clinical symptoms may precede laboratory findings by hours or days. With prompt treatment (often including plasmapheresis), 70% to 80% of patients will survive with minimal or no sequelae. Because platelet transfusions may accelerate thrombosis in patients with TTP on ticlopidine, they should, if possible, be avoided.
Aplastic Anemia: Aplastic anemia is characterized by anemia, thrombocytopenia and neutropenia together with a bone marrow examination that shows decreases in the precursor cells for red blood cells, white blood cells, and platelets. Patients may present with signs or symptoms suggestive of infection, in association with low white blood cell and platelet counts. Prompt treatment, which may include the use of drugs to stimulate the bone marrow, can minimize the mortality associated with aplastic anemia.
Monitoring for Hematologic Adverse Reactions: Starting just before initiating treatment and continuing through the third month of therapy, patients receiving TICLID (ticlopidine hcl) must be monitored every 2 weeks. Because of discontinue ticlopidine during this 3-month period should continue to be monitored for 2 weeks after discontinuation. More frequent monitoring, and monitoring after the first 3 months of therapy, is necessary only in patients with clinical signs (eg, signs or symptoms suggestive of infection) or laboratory signs (eg, neutrophil count less than 70% of the baseline count, decrease in hematocrit or platelet count) that suggest incipient hematological adverse reactions.
Clinically, fever might suggest neutropenia, TTP, or aplastic anemia; TTP might also be suggested by weakness, pallor, petechiae or purpura, dark urine (due to blood, bile pigments, or hemoglobin) or jaundice, or neurological changes. Patients should be told to discontinue TICLID (ticlopidine hcl) and to contact the physician immediately upon the occurrence of any of these findings.
Laboratory monitoring should include a complete blood count, with special attention to the absolute neutrophil count (WBC x % neutrophils), platelet count, and the appearance of the peripheral smear. Ticlopidine is occasionally associated with thrombocytopenia unrelated to TTP or aplastic anemia. Any acute, unexplained reduction in hemoglobin or platelet count should prompt further investigation for a diagnosis of TTP, and the appearance of schistocytes (fragmented RBCs) on the smear should be treated as presumptive evidence of TTP. A simultaneous decrease in platelet count and WBC count should prompt further investigation for a diagnosis of aplastic anemia. If there are laboratory signs of TTP or aplastic anemia, or if the neutrophil count is confirmed to be < 1200/mm³, then TICLID (ticlopidine hcl) should be discontinued immediately.
Other Hematological Effects: Rare cases of agranulocytosis, pancytopenia, or leukemia have been reported in postmarketing experience, some of which have been fatal. All forms of hematological adverse reactions are potentially fatal.
Cholesterol Elevation: TICLID (ticlopidine hcl) therapy causes increased serum cholesterol and triglycerides. Serum total cholesterol levels are increased 8% to 10% within 1 month of therapy and persist at that level. The ratios of the lipoprotein subfractions are unchanged.
Anticoagulant Drugs: The tolerance and long-term safety of coadministration of TICLID (ticlopidine hcl) with heparin, oral anticoagulants or fibrinolytic agents have not been established. In trials for cardiac stenting, patients received heparin and TICLID (ticlopidine hcl) concomitantly for approximately 12 hours. If a patient is switched from an anticoagulant or fibrinolytic drug to TICLID (ticlopidine hcl) , the former drug should be discontinued prior to TICLID (ticlopidine hcl) administration.
PRECAUTIONSGeneral: TICLID (ticlopidine hcl) should be used with caution in patients who may be at risk of increased bleeding from trauma, surgery or pathological conditions. If it is desired to eliminate the antiplatelet effects of TICLID (ticlopidine hcl) prior to elective surgery, the drug should be discontinued 10 to 14 days prior to surgery. Several controlled clinical studies have found increased surgical blood loss in patients undergoing surgery during treatment with ticlopidine. In TASS and CATS it was recommended that patients have ticlopidine discontinued prior to elective surgery. Several hundred patients underwent surgery during the trials, and no excessive surgical bleeding was reported.
Prolonged bleeding time is normalized within 2 hours after administration of 20 mg methylprednisolone IV. Platelet transfusions may also be used to reverse the effect of TICLID (ticlopidine hcl) on bleeding. Because platelet transfusions may accelerate thrombosis in patients with TTP on ticlopidine, they should, if possible, be avoided.
GI Bleeding: TICLID (ticlopidine hcl) prolongs template bleeding time. The drug should be used with caution in patients who have lesions with a propensity to bleed (such as ulcers). Drugs that might induce such lesions should be used with caution in patients on TICLID (see CONTRAINDICATIONS).
Use in Hepatically Impaired Patients: Since ticlopidine is metabolized by the liver, dosing of TICLID (ticlopidine hcl) or other drugs metabolized in the liver may require adjustment upon starting or stopping concomitant therapy. Because of limited experience in patients with severe hepatic disease, who may have bleeding diatheses, the use of TICLID (ticlopidine hcl) is not recommended in this population (see CLINICAL PHARMACOLOGY and CONTRAINDICATIONS).
Use in Renally Impaired Patients: There is limited experience in patients with renal impairment. Decreased plasma clearance, increased AUC values and prolonged bleeding times can occur in renally impaired patients. In controlled clinical trials no unexpected problems have been encountered in patients having mild renal impairment, and there is no experience with dosage adjustment in patients with greater degrees of renal impairment. Nevertheless, for renally impaired patients, it may be necessary to reduce the dosage of ticlopidine or discontinue it altogether if hemorrhagic or hematopoietic problems are encountered (see CLINICAL PHARMACOLOGY).
Information for the Patient(See Patient Leaflet) Patients should be told that a decrease in the number of white blood cells (neutropenia) or platelets (thrombocytopenia) can occur with TICLID (ticlopidine hcl) , especially during the first 3 months of treatment and that neutropenia, if it is severe, can result in an increased risk of infection. They should be told it is critically important to obtain the scheduled blood tests to detect neutropenia or thrombocytopenia. Patients should also be reminded to contact their physicians if they experience any indication of infection such as fever, chills, or sore throat, any of which might be a consequence of neutropenia. Thrombocytopenia may be part of a syndrome called TTP. Symptoms and signs of TTP, such as fever, weakness, difficulty speaking, seizures, yellowing of skin or eyes, dark or bloody urine, pallor or petechiae (pinpoint hemorrhagic spots on the skin), should be reported immediately.
All patients should be told that it may take them longer than usual to stop bleeding when they take TICLID (ticlopidine hcl) and that they should report any unusual bleeding to their physician. Patients should tell physicians and dentists that they are taking TICLID (ticlopidine hcl) before any surgery is scheduled and before any new drug is prescribed.
Patients should be told to promptly report side effects of TICLID (ticlopidine hcl) such as severe or persistent diarrhea, skin rashes or subcutaneous bleeding or any signs of cholestasis, such as yellow skin or sclera, dark urine, or light-colored stools.
Patients should be told to take TICLID (ticlopidine hcl) with food or just after eating in order to minimize gastrointestinal discomfort.
Laboratory Tests: Liver Function: TICLID (ticlopidine hcl) therapy has been associated with elevations of alkaline phosphatase, bilirubin, and transaminases, which generally occurred within 1 to 4 months of therapy initiation. In controlled clinical trials in stroke patients, the incidence of elevated alkaline phosphatase (greater than two times upper limit of normal) was 7.6% in ticlopidine patients, 6% in placebo patients and 2.5% in aspirin patients. The incidence of elevated AST (SGOT) (greater than two times upper limit of normal) was 3.1% in ticlopidine patients, 4% in placebo patients and 2.1% in aspirin patients. No progressive increases were observed in closely monitored clinical trials (eg, no transaminase greater than 10 times the upper limit of normal was seen), but most patients with these abnormalities had therapy discontinued. Occasionally patients had developed minor elevations in bilirubin.
Postmarketing experience includes rare individuals with elevations in their transaminases and bilirubin to > 10X above the upper limits of normal. Based on postmarketing and clinical trial experience, liver function testing, including ALT, AST, and GGT, should be considered whenever liver dysfunction is suspected, particularly during the first 4 months of treatment.
Carcinogenesis, Mutagenesis, Impairment of Fertility: In a 2-year oral carcinogenicity study in rats, ticlopidine at daily doses of up to 100 mg/kg (610 mg/m²) was not tumorigenic. For a 70-kg person (1.73 m² body surface area) the dose represents 14 times the recommended clinical dose on a mg/kg basis and two times the clinical dose on body surface area basis. In a 78-week oral carcinogenicity study in mice, ticlopidine at daily doses up to 275 mg/kg (1180 mg/m²) was not tumorigenic. The dose represents 40 times the recommended clinical dose on a mg/kg basis and four times the clinical dose on body surface area basis.
Ticlopidine was not mutagenic in vitro in the Ames test, the rat hepatocyte DNA-repair assay, or the Chinese-hamster fibroblast chromosomal aberration test; or in vivo in the mouse spermatozoid morphology test, the Chinese-hamster micronucleus test, or the Chinese-hamster bone-marrow-cell sister-chromatid exchange test. Ticlopidine was found to have no effect on fertility of male and female rats at oral doses up to 400 mg/kg/day.
Pregnancy:Teratogenic Effects: Pregnancy: Category B. Teratology studies have been conducted in mice (doses up to 200 mg/kg/day), rats (doses up to 400 mg/kg/day) and rabbits (doses up to 200 mg/kg/day). Doses of 400 mg/kg in rats, 200 mg/kg/day in mice and 100 mg/kg in rabbits produced maternal toxicity, as well as fetal toxicity, but there was no evidence of a teratogenic potential of ticlopidine. There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of a human response, this drug should be used during pregnancy only if clearly needed.
Nursing Mothers: Studies in rats have shown ticlopidine is excreted in the milk. It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from ticlopidine, 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.
Pediatric Use: Safety and effectiveness in pediatric patients have not been established.
Geriatric Use: Clearance of ticlopidine is somewhat lower in elderly patients and trough levels are increased. The major clinical trials with TICLID (ticlopidine hcl) in stroke patients were conducted in an elderly population with an average age of 64 years. Of the total number of patients in the therapeutic trials, 45% of patients were over 65 years old and 12% were over 75 years old. No overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out.
Adverse reactions in stroke patients were relatively frequent with over 50% of patients reporting at least one. Most (30% to 40%) involved the gastrointestinal tract. Most adverse effects are mild, but 21% of patients discontinued therapy because of an adverse event, principally diarrhea, rash, nausea, vomiting, GI pain and neutropenia. Most adverse effects occur early in the course of treatment, but a new onset of adverse effects can occur after several months.
The incidence rates of adverse events listed in the following table were derived from multicenter, controlled clinical trials in stroke patients described above comparing TICLID (ticlopidine hcl) , placebo and aspirin over study periods of up to 5.8 years. Adverse events considered by the investigator to be probably drug-related that occurred in at least 1% of patients treated with TICLID (ticlopidine hcl) are shown in the following table:
Percent of Patients With Adverse Events in Controlled Studies
(TASS and CATS)
| Event | TICLID (ticlopidine hcl) (n = 2048) Incidence |
Aspirin (n = 1527) Incidence |
Placebo (n = 536) Incidence |
| Any Events | 60.0 (20.9) | 53.2 (14.5) | 34.3 (6.1) |
| Diarrhea | 12.5 (6.3) | 5.2 (1.8) | 4.5 (1.7) |
| Nausea | 7.0 (2.6) | 6.2 (1.9) | 1.7 (0.9) |
| Dyspepsia | 7.0 (1.1) | 9.0 (2.0) | 0.9 (0.2) |
| Rash | 5.1 (3.4) | 1.5 (0.8) | 0.6 (0.9) |
| GI Pain | 3.7 (1.9) | 5.6 (2.7) | 1.3 (0.4) |
| Neutropenia | 2.4 (1.3) | 0.8 (0.1) | 1.1 (0.4) |
| Purpura | 2.2 (0.2) | 1.6 (0.1) | 0.0 (0.0) |
| Vomiting | 1.9 (1.4) | 1.4 (0.9) | 0.9 (0.4) |
| Flatulence | 1.5 (0.1) | 1.4 (0.3) | 0.0 (0.0) |
| Pruritus | 1.3 (0.8) | 0.3 (0.1) | 0.0 (0.0) |
| Dizziness | 1.1 (0.4) | 0.5 (0.4) | 0.0 (0.0) |
| Anorexia | 1.0 (0.4) | 0.5 (0.3) | 0.0 (0.0) |
| Abnormal Liver Function Test | 1.0 (0.7) | 0.3 (0.3) | 0.0 (0.0) |
Incidence of discontinuation, regardless of relationship to therapy, is shown in parentheses.
Hematological: Neutropenia/thrombocytopenia, TTP, aplastic anemia (see BOXED WARNING and WARNINGS), leukemia, agranulocytosis, eosinophilia, pancytopenia, thrombocytosis and bone-marrow depression have been reported.
Gastrointestinal: TICLID (ticlopidine hcl) therapy has been associated with a variety of gastrointestinal complaints including diarrhea and nausea. The majority of cases are mild, but about 13% of patients discontinued therapy because of these. They usually occur within 3 months of initiation of therapy and typically are resolved within 1 to 2 weeks without discontinuation of therapy. If the effect is severe or persistent, therapy should be discontinued. In some cases of severe or bloody diarrhea, colitis was later diagnosed.
Hemorrhagic: TICLID (ticlopidine hcl) has been associated with increased bleeding, spontaneous posttraumatic bleeding and perioperative bleeding including, but not limited to, gastrointestinal bleeding. It has also been associated with a number of bleeding complications such as ecchymosis, epistaxis, hematuria and conjunctival hemorrhage.
Intracerebral bleeding was rare in clinical trials in stroke patients with TICLID (ticlopidine hcl) , with an incidence no greater than that seen with comparator agents (ticlopidine 0.5%, aspirin 0.6%, placebo 0.75%). It has also been reported postmarketing.
Rash: Ticlopidine has been associated with a maculopapular or urticarial rash (often with pruritus). Rash usually occurs within 3 months of initiation of therapy with a mean onset time of 11 days. If drug is discontinued, recovery occurs within several days. Many rashes do not recur on drug rechallenge. There have been rare reports of severe rashes, including Stevens-Johnson syndrome, erythema multiforme and exfoliative dermatitis.
Less Frequent Adverse Reactions (Probably Related): Clinical adverse experiences occurring in 0.5% to 1.0% of stroke patients in controlled trials include: Digestive System: GI fullness
Skin and Appendages: urticaria
Nervous System: headache
Body as a Whole: asthenia, pain
Hemostatic System: epistaxis
Special Senses: tinnitus
In addition, rarer, relatively serious and potentially fatal events associated with the use of TICLID (ticlopidine hcl) have also been reported from postmarketing experience: Hemolytic anemia with reticulocytosis, immune thrombocytopenia, hepatitis, hepatocellular jaundice, cholestatic jaundice, hepatic necrosis, hepatic failure, peptic ulcer, renal failure, nephrotic syndrome, hyponatremia, vasculitis, sepsis, allergic reactions (including angioedema, allergic pneumonitis, and anaphylaxis), systemic lupus (positive ANA), peripheral neuropathy, serum sickness, arthropathy and myositis.
DRUG INTERACTIONSTherapeutic doses of TICLID (ticlopidine hcl) caused a 30% increase in the plasma half-life of antipyrine and may cause analogous effects on similarly metabolized drugs. Therefore, the dose of drugs metabolized by hepatic microsomal enzymes with low therapeutic ratios or being given to patients with hepatic impairment may require adjustment to maintain optimal therapeutic blood levels when starting or stopping concomitant therapy with ticlopidine. Studies of specific drug interactions yielded the following results:
Aspirin and Other NSAIDs: Ticlopidine potentiates the effect of aspirin or other NSAIDs on platelet aggregation. The safety of concomitant use of ticlopidine and NSAIDs has not been established. The safety of concomitantuse of ticlopidine and aspirin beyond 30 days has not been established (see Clinical Trials : Stent Patients). Aspirin did not modify the ticlopidine-mediated inhibition of ADP-induced platelet aggregation, but ticlopidine potentiated the effect of aspirin on collagen-induced platelet aggregation. Caution should be exercised in patients who have lesions with a propensity to bleed, such as ulcers. Long-term concomitant use of aspirin and ticlopidine is not recommended (see PRECAUTIONS: GI Bleeding).
Antacids: Administration of TICLID (ticlopidine hcl) after antacids resulted in an 18% decrease in plasma levels of ticlopidine.
Cimetidine: Chronic administration of cimetidine reduced the clearance of a single dose of TICLID (ticlopidine hcl) by 50%.
Digoxin: Coadministration of TICLID (ticlopidine hcl) with digoxin resulted in a slight decrease (approximately 15%) in digoxin plasma levels. Little or no change in therapeutic efficacy of digoxin would be expected.
Theophylline: In normal volunteers, concomitant administration of TICLID (ticlopidine hcl) resulted in a significant increase in the theophylline elimination half-life from 8.6 to 12.2 hours and a comparable reduction in total plasma clearance of theophylline.
Phenobarbital: In 6 normal volunteers, the inhibitory effects of TICLID (ticlopidine hcl) on platelet aggregation were not altered by chronic administration of phenobarbital.
Phenytoin: In vitro studies demonstrated that ticlopidine does not alter the plasma protein binding of phenytoin. However, the protein binding interactions of ticlopidine and its metabolites have not been studied in vivo. Several cases of elevated phenytoin plasma levels with associated somnolence and lethargy have been reported following coadministration with TICLID (ticlopidine hcl). Caution should be exercised in coadministering this drug with TICLID (ticlopidine hcl) , and it may be useful to remeasure phenytoin blood concentrations.
Propranolol: In vitro studies demonstrated that ticlopidine does not alter the plasma protein binding of propranolol. However, the protein binding interactions of ticlopidine and its metabolites have not been studied in vivo. Caution should be exercised in coadministering this drug with TICLID (ticlopidine hcl).
Other Concomitant Therapy: Although specific interaction studies were not performed, in clinical studies TICLID (ticlopidine hcl) was used concomitantly with beta blockers, calcium channel blockers and diuretics without evidence of clinically significant adverse interactions (see PRECAUTIONS).
Food Interaction: The oral bioavailability of ticlopidine is increased by 20% when taken after a meal. Administration of TICLID (ticlopidine hcl) with food is recommended to maximize gastrointestinal tolerance. In controlled trials in stroke patients, TICLID (ticlopidine hcl) was taken with meals.
