Version July 2025
Ticlopidine HCl can cause life-threatening hematological adverse reactions, including neutropenia/agranulocytosis and thrombotic thrombocytopenic purpura (TTP) and aplastic anemia.
Among 2048 patients in clinical trials, there were 50 cases (2.4%) of neutropenia (less than 1200 neutrophils/mm3), and the neutrophil count was below 450/mm3 in 17 of these patients (0.8% of the total population).
One case of TTP was reported during clinical trials. Based on postmarketing data, US physicians reported about 100 cases between 1992 and 1997. Based on an estimated patient exposure of 2 million to 4 million, and assuming an event reporting rate of 10% (the true rate is not known), the incidence of ticlopidine-associated TTP may be as high as 1 case in every 2000 to 4000 patients exposed.
Aplastic anemia was not seen during clinical trials in stroke patients, but US physicians reported about 50 cases between 1992 and 1998. Based on an estimated patient exposure of 2 million to 4 million, and assuming an event reporting rate of 10% (the true rate is not known), the incidence of ticlopidine-associated aplastic anemia may be as high as 1 case in every 4000 to 8000 patients exposed.
Severe hematologic adverse reactions may occur within a few days of the start of therapy. The incidence of TTP peaks after about 3 to 4 weeks of therapy and neutropenia peaks at approximately 4 to 6 weeks. The incidence of aplastic anemia peaks after about 4 to 8 weeks of therapy. The incidence of the hematologic adverse reactions declines thereafter. Only a few cases of neutropenia, TTP, or aplastic anemia have arisen after more than 3 months of treatment.
Hematological adverse reactions cannot be reliably predicted by any identified demographic or clinical characteristics. During the first 3 months of treatment, patients receiving ticlopidine HCl must, therefore, be hematologically and clinically monitored for evidence of neutropenia or TTP. If any such evidence is seen, ticlopidine HCl should be immediately discontinued.
Note: Ticlopidine is no longer available in the United States.
Stroke prevention: Oral: 250 mg twice daily.
Note: Overall, the use of ticlopidine is no longer recommended for this indication and has largely been replaced by clopidogrel (Ref).
There are no dosage adjustment provided in the manufacturer's labeling. While there were no statistically significant differences in ADP-induced platelet aggregation, AUC increases and clearance decreases were seen in patients with mild to moderate renal impairment. However, bleeding time may be prolonged in patients with moderate renal impairment
Hemodialysis: Not dialyzable (Ref).
There are no dosage adjustment provided in the manufacturer's labeling. Use with caution. Use is contraindicated in severe hepatic impairment.
Oral: 250 mg twice daily with food; dosage in older patients has not been determined; however, in two large clinical trials, the average age of subjects was 63 and 66 years. A dosage decrease may be necessary if bleeding occurs.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. As with all drugs which may affect hemostasis, bleeding is associated with ticlopidine. Hemorrhage may occur at virtually any site. Risk is dependent on multiple variables, including the use of multiple agents which alter hemostasis and patient susceptibility.
>10%:
Endocrine & metabolic: Hyperlipidemia (8% to 10%; within 1 month of therapy), increased serum triglycerides
Gastrointestinal: Diarrhea (13%; may be chronic)
1% to 10%:
Central nervous system: Dizziness (1%)
Dermatologic: Skin rash (5%), pruritus (1%)
Gastrointestinal: Dyspepsia (7%), nausea (7%), gastrointestinal pain (4%), flatulence (2%), vomiting (2%), anorexia (1%)
Hematologic & oncologic: Neutropenia (2%), purpura (2%)
Hepatic: Increased serum alkaline phosphatase (>2 x upper limit of normal: 8%), abnormal hepatic function tests (1%)
<1%, postmarketing, and/or case reports: Agranulocytosis, anaphylaxis, angioedema, aplastic anemia, arthropathy, bone marrow depression, bronchiolitis obliterans organizing pneumonia, conjunctival hemorrhage, ecchymosis, eosinophilia, epistaxis, erythema multiforme, erythema nodosum, exfoliative dermatitis, gastrointestinal hemorrhage, headache, hematuria, hemolytic anemia, hepatic necrosis, hepatitis, hypermenorrhea, hypersensitivity pneumonitis, hyponatremia, increased serum bilirubin, intracranial hemorrhage, immune thrombocytopenia, increased serum creatinine, jaundice, maculopapular rash, myositis, nephrotic syndrome, pain, pancytopenia, peptic ulcer, peripheral neuropathy, positive ANA titer, renal failure, sepsis, serum sickness, Stevens-Johnson syndrome, systemic lupus erythematosus, thrombocythemia, thrombotic thrombocytopenic purpura (TTP), tinnitus, urticaria, vasculitis, weakness
Hypersensitivity to ticlopidine or any component of the formulation; active pathological bleeding such as peptic ulcer bleeding or intracranial hemorrhage; severe liver impairment; hematopoietic disorders (neutropenia, thrombocytopenia, or a past history of TTP or aplastic anemia); hemostatic disorders
Concerns related to adverse effects:
• Hematologic toxicity: [US Boxed Warning]: May cause life-threatening hematologic reactions, including neutropenia, agranulocytosis, thrombotic thrombocytopenic purpura (TTP), and aplastic anemia. Routine monitoring is required (see Monitoring Parameters). Monitor for signs and symptoms of neutropenia including WBC count. Discontinue if the absolute neutrophil count falls to <1,200/mm3 or if laboratory signs of TTP or aplastic anemia occur.
• Thienopyridine hypersensitivity: Because of structural similarities, cross-reactivity is possible among the thienopyridines (clopidogrel, prasugrel, and ticlopidine); use with caution or avoid in patients with previous thienopyridine hypersensitivity. Use of ticlopidine is contraindicated in patients with hypersensitivity to ticlopidine.
Disease-related concerns:
• Bleeding disorders: Use with caution in patients with platelet disorders, bleeding disorders and/or at increased risk for bleeding (eg, PUD, trauma, or surgery).
• Hepatic impairment: Use with caution in patients with mild-to-moderate hepatic impairment. Use is contraindicated with severe hepatic impairment.
• Renal impairment: Use with caution in patients with moderate-to-severe renal impairment (experience is limited); bleeding times may be significantly prolonged and the risk of hematologic adverse events (eg, neutropenia) may be increased.
Concurrent drug therapy issues:
• Anticoagulants and platelet aggregation inhibitors: Use with caution in patients receiving either anticoagulants (eg, heparin, warfarin) or other platelet aggregation inhibitors; bleeding risk is increased.
Special populations:
• Lower GI bleed patients: An individualized and multidisciplinary approach should be utilized to determine therapy discontinuation and management in patients with acute lower GI bleed (LGIB) who are on antiplatelet medications; risk of ongoing bleeding should be weighed with risk of thromboembolic events. In patients receiving dual antiplatelet therapy (aspirin plus P2Y12 receptor blocker [eg, clopidogrel, prasugrel, ticagrelor, ticlopidine]) or thienopyridine monotherapy, the thienopyridine should generally be resumed as soon as possible and at least within 7 days, taking into account control of bleeding and cardiovascular risk (aspirin should not be discontinued); however, dual antiplatelet therapy should not be discontinued in the 90 days post-acute coronary syndrome or 30 days post-coronary stenting (Strate 2016).
Other warnings/precautions:
• Coronary artery stents: In patients who have received bare-metal or drug-eluting stents (sirolimus or paclitaxel), premature interruption of antiplatelet therapy may result in stent thrombosis with subsequent fatal and nonfatal myocardial infarction. If ticlopidine is used, duration of therapy, in general, is determined by the type of stent placed (bare metal or drug eluting) and whether an ACS event was ongoing at the time of placement (Levine, 2011).
• Elective surgery: Consider discontinuing 10 to 14 days before elective surgery (except in patients with cardiac stents that have not completed their full course of dual antiplatelet therapy; patient-specific situations need to be discussed with cardiologist; AHA/ACC/SCAI/ACS/ADA Science Advisory provides recommendations).
Ticlopidine is no longer available in the US.
Tablets (Ticlopidine HCl Oral)
250 mg (60): $111.97
Disclaimer: The pricing data provide a representative AWP and/or AAWP price from a single manufacturer of the brand and/or generic product, respectively. The pricing data should be used for benchmarking purposes only, and as such should not be used to set or adjudicate any prices for reimbursement or purchasing functions. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral, as hydrochloride:
Generic: 250 mg
Administer with food.
Platelet aggregation inhibitor that reduces the risk of thrombotic stroke in patients who have had a stroke or stroke precursors (Note: Due to its association with life-threatening hematologic disorders, ticlopidine should be reserved for patients who are intolerant to aspirin, who have failed aspirin therapy, or who are not eligible to receive other antiplatelet therapy.)
Pharmacy Quality Alliance (PQA): Ticlopidine is identified as a high-risk medication in patients 65 years and older on the PQA’s, Use of High-Risk Medications in the Elderly (HRM) performance measure, a safety measure used by the Centers for Medicare and Medicaid Services (CMS) for Medicare plans (PQA 2017).
Inhibits CYP1A2 (Weak), CYP2B6 (Weak), CYP2C19 (Weak), CYP2D6 (Weak);
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Abrocitinib: Therapeutic Antiplatelets may increase antiplatelet effects of Abrocitinib. Management: Do not use antiplatelet drugs with abrocitinib during the first 3 months of abrocitinib therapy. The abrocitinib prescribing information lists this combination as contraindicated. This does not apply to low dose aspirin (81 mg/day or less). Risk X: Avoid
Acalabrutinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Aducanumab: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Agents with Antiplatelet Effects: May increase antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
Anagrelide: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Anticoagulants (Miscellaneous Agents): Therapeutic Antiplatelets may increase anticoagulant effects of Anticoagulants (Miscellaneous Agents). Risk C: Monitor
Antiplatelet Agents (P2Y12 Inhibitors): Therapeutic Antiplatelets may increase antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
BuPROPion: CYP2B6 Inhibitors (Weak) may increase serum concentration of BuPROPion. Risk C: Monitor
Caplacizumab: May increase antiplatelet effects of Therapeutic Antiplatelets. Management: Avoid this combination if possible. If coadministration is required, monitor closely for bleeding. Interrupt caplacizumab if clinically significant bleeding occurs and administer von Willebrand factor concentrate to rapidly correct hemostasis, if needed. Risk D: Consider Therapy Modification
Cilostazol: Ticlopidine may increase serum concentration of Cilostazol. Ticlopidine may increase active metabolite exposure of Cilostazol. Risk C: Monitor
CloBAZam: CYP2C19 Inhibitors (Weak) may increase serum concentration of CloBAZam. CYP2C19 Inhibitors (Weak) may increase active metabolite exposure of CloBAZam. Risk C: Monitor
CloZAPine: CYP1A2 Inhibitors (Weak) may increase serum concentration of CloZAPine. Risk C: Monitor
Collagenase (Systemic): Therapeutic Antiplatelets may increase adverse/toxic effects of Collagenase (Systemic). Specifically, the risk of injection site bruising and or bleeding may be increased. Risk C: Monitor
CycloSPORINE (Systemic): Ticlopidine may decrease serum concentration of CycloSPORINE (Systemic). Risk C: Monitor
Dabigatran Etexilate: Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Dabigatran Etexilate. Risk C: Monitor
Dasatinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Deoxycholic Acid: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Desirudin: Therapeutic Antiplatelets may increase anticoagulant effects of Desirudin. Risk C: Monitor
Diamorphine: May decrease antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Diamorphine may decrease serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
Direct Oral Anticoagulants (DOACs): Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Direct Oral Anticoagulants (DOACs). Risk C: Monitor
Donanemab: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
FentaNYL: May decrease antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). FentaNYL may decrease serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
Fezolinetant: CYP1A2 Inhibitors (Weak) may increase serum concentration of Fezolinetant. Risk X: Avoid
Fondaparinux: Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Fondaparinux. Management: Discontinue antiplatelet agents, such as P2Y12 inhibitors, prior to fondaparinux therapy, if possible. If co-administration is required use caution and monitor for bleeding. Risk D: Consider Therapy Modification
Fosphenytoin-Phenytoin: CYP2C19 Inhibitors (Weak) may increase serum concentration of Fosphenytoin-Phenytoin. Risk C: Monitor
Glycoprotein IIb/IIIa Inhibitors: Therapeutic Antiplatelets may increase anticoagulant effects of Glycoprotein IIb/IIIa Inhibitors. Risk C: Monitor
Heparin: Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Heparin. Risk C: Monitor
Heparins (Low Molecular Weight): Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Heparins (Low Molecular Weight). Risk C: Monitor
Herbal Products with Anticoagulant/Antiplatelet Effects: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Ibritumomab Tiuxetan: Therapeutic Antiplatelets may increase antiplatelet effects of Ibritumomab Tiuxetan. Risk C: Monitor
Ibrutinib: Therapeutic Antiplatelets may increase adverse/toxic effects of Ibrutinib. Specifically, the risks of bleeding and hemorrhage may be increased. Risk C: Monitor
Icosapent Ethyl: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Inotersen: Therapeutic Antiplatelets may increase adverse/toxic effects of Inotersen. Specifically, the risk of bleeding may be increased. Risk C: Monitor
Ketamine: Ticlopidine may increase serum concentration of Ketamine. Risk C: Monitor
Lecanemab: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Limaprost: May increase adverse/toxic effects of Therapeutic Antiplatelets. Specifically, the risk of bleeding may be increased. Risk C: Monitor
Lipid Emulsion (Fish Oil Based): May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Mavacamten: CYP2C19 Inhibitors (Weak) may increase serum concentration of Mavacamten. Management: Start mavacamten at 5 mg/day if stable on a weak CYP2C19 inhibitor, and reduce the mavacamten dose by one dose level if initiating a weak CYP2C19 inhibitor. Avoid initiating weak CYP2C19 inhibitors in patients on mavacamten 2.5 mg/day. Risk D: Consider Therapy Modification
Miscellaneous Antiplatelets: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Morphine (Systemic): May decrease antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Morphine (Systemic) may decrease serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Management: Consider alternative anti-ischemic/analgesic therapies (eg, beta-blockers, nitroglycerin) in patients with acute coronary syndromes treated with a P2Y12 inhibitor when possible. The risks associated with other opioids are unknown. Risk D: Consider Therapy Modification
Multivitamins/Fluoride (with ADE): May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Multivitamins/Minerals (with ADEK, Folate, Iron): May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Multivitamins/Minerals (with AE, No Iron): May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Obinutuzumab: Therapeutic Antiplatelets may increase adverse/toxic effects of Obinutuzumab. Specifically, the risk of bleeding may be increased. Management: Consider avoiding coadministration of obinutuzumab and therapeutic antiplatelets, especially during the first cycle of obinutuzumab therapy. Risk D: Consider Therapy Modification
Omega-3 Fatty Acids: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Pentosan Polysulfate Sodium: Therapeutic Antiplatelets may increase adverse/toxic effects of Pentosan Polysulfate Sodium. Specifically, the risk of hemorrhage may be increased. Risk C: Monitor
Pirtobrutinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Selumetinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Theophylline Derivatives: CYP1A2 Inhibitors (Weak) may increase serum concentration of Theophylline Derivatives. Risk C: Monitor
Therapeutic Antiplatelets: May increase antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
Thioridazine: CYP2D6 Inhibitors (Weak) may increase serum concentration of Thioridazine. Management: Consider avoiding concomitant use of thioridazine and weak CYP2D6 inhibitors. If combined, monitor closely for QTc interval prolongation and arrhythmias. Some weak CYP2D6 inhibitors list use with thioridazine as a contraindication. Risk D: Consider Therapy Modification
Thrombolytic Agents: Therapeutic Antiplatelets may increase adverse/toxic effects of Thrombolytic Agents. Specifically, the risk of bleeding may be increased. Risk C: Monitor
Ticagrelor: Antiplatelet Agents (P2Y12 Inhibitors) may increase antiplatelet effects of Ticagrelor. Risk X: Avoid
Tipranavir: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
TiZANidine: CYP1A2 Inhibitors (Weak) may increase serum concentration of TiZANidine. Management: Avoid the use of tizanidine with weak CYP1A2 inhibitors when possible. If combined, monitor closely for increased tizanidine toxicities (eg, hypotension, bradycardia, drowsiness). Tizanidine dose reduction or discontinuation may be necessary. Risk D: Consider Therapy Modification
Vitamin E (Systemic): May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Vitamin K Antagonists: Antiplatelet Agents (P2Y12 Inhibitors) may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor
Volanesorsen: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Zanubrutinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Ticlopidine bioavailability may be increased (20%) if taken with food. High-fat meals increase absorption, antacids decrease absorption. May cause upset stomach. Management: Take with food to reduce stomach upset.
Teratogenic effects have not been observed in animal reproduction studies. Information related to ticlopidine use in a pregnant woman has been noted in a case report (Ueno 2001).
It is not known if ticlopidine is excreted in breast milk. Due to the potential for serious adverse reactions in the nursing infant, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of treatment to the mother.
Signs of bleeding; CBC with differential at baseline prior to treatment initiation and then weekly for the first 3 months of therapy; more frequent monitoring is recommended for patients whose absolute neutrophil counts have been consistently declining or are 30% less than baseline values. The peak incidence of TTP occurs between 3-4 weeks, the peak incidence of neutropenia occurs at approximately 4-6 weeks, and the incidence of aplastic anemia peaks after 4-8 weeks of therapy. Few cases have been reported after 3 months of treatment. Liver function tests (alkaline phosphatase and transaminases) should be performed in the first 4 months of therapy if liver dysfunction is suspected.
Ticlopidine requires in vivo biotransformation to an unidentified active metabolite. This active metabolite irreversibly blocks the P2Y12 component of ADP receptors, which prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation. Platelets blocked by ticlopidine are affected for the remainder of their lifespan.
Onset of action: ~6 hours
Peak effect: 3-5 days; serum levels do not correlate with clinical antiplatelet activity
Absorption: Well absorbed
Protein binding: Parent drug: 98%; <15% bound to alpha1-acid glycoprotein
Metabolism: Extensively hepatic; has at least 1 active metabolite
Half-life elimination: 13 hours
Time to peak, serum: ~2 hours
Excretion: Urine (60%); feces (23%)
Hepatic function impairment: Average plasma concentration is slightly higher in cirrhosis.
