TICLID

Clinical safety rating: caution

Comprehensive clinical and safety monograph for TICLID (TICLID).

How it works

Ticlopidine is a thienopyridine ADP receptor antagonist that irreversibly inhibits the P2Y12 receptor on platelets, preventing ADP-induced platelet aggregation.

What the body does with it

Metabolism	Extensively metabolized in the liver via cytochrome P450 enzymes, primarily CYP3A4 and CYP2C19, with minor contributions from CYP1A2 and CYP2B6.
Excretion	Primarily hepatic metabolism; 60% renal as metabolites, 23% fecal. Minimal parent drug excreted unchanged.
Half-life	Terminal elimination half-life is approximately 30-50 hours (mean ~33 hours), with clinical effects lasting 7-10 days after discontinuation due to irreversible platelet binding.
Protein binding	98% bound, primarily to albumin; also binds to lipoproteins and alpha-1-acid glycoprotein.
Volume of Distribution	Approximately 1.2-1.8 L/kg; large Vd indicates extensive tissue distribution, including irreversible binding to platelets.
Bioavailability	Oral bioavailability is >80% (approximately 80-90%) with food increasing absorption; admin with meals to reduce GI irritation.
Onset of Action	Oral: 48-72 hours for detectable inhibition of platelet aggregation; maximal effect at 8-11 days.
Duration of Action	Duration of platelet inhibition persists for the lifespan of the platelet (7-10 days) after drug cessation; antiplatelet effect peaks at 8-11 days and gradually declines over 1-2 weeks.

Classification & Brands

Dosing & administration

250 mg orally twice daily

Dosage form	TABLET
Renal impairment	No dose adjustment required for mild to moderate renal impairment; avoid use in severe renal impairment (CrCl < 25 mL/min) due to limited data.
Liver impairment	Contraindicated in severe hepatic impairment (Child-Pugh class C); use with caution in moderate impairment (Child-Pugh class B) with dose reduction to 250 mg once daily.
Pediatric use	Safety and efficacy not established; not recommended for use in pediatric patients.
Geriatric use	No specific dose adjustment; monitor for increased bleeding risk and renal function in elderly patients.

Use during pregnancy

1st trimester	Consult provider
2nd trimester	Consult provider
3rd trimester	Consult provider

Clinical note

Comprehensive clinical and safety monograph for TICLID (TICLID).

Breastfeeding	Ticlopidine is excreted in human breast milk; the M/P ratio is unknown. Due to potential for adverse effects in the nursing infant, including bleeding risk, a decision should be made to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
Teratogenic Risk	Ticlopidine is FDA Pregnancy Category B. Animal studies have not revealed evidence of fetal harm, but there are no adequate and well-controlled studies in pregnant women. It should be used during pregnancy only if clearly needed. Potential risks include hemorrhage in the fetus due to maternal platelet inhibition.

Warnings & precautions

■ FDA Black Box Warning

Ticlopidine can cause life-threatening hematologic adverse reactions including neutropenia/agranulocytosis, thrombotic thrombocytopenic purpura (TTP), and aplastic anemia. Fatalities have occurred.

Side Effect Profile

Serious Effects

Absolute Contraindications

Hypersensitivity to ticlopidine; active bleeding such as peptic ulcer or intracranial hemorrhage; history of thrombotic thrombocytopenic purpura (TTP); severe liver impairment; concomitant use with other thienopyridines.

Clinical Precautions

Precautions

Hematologic toxicity (neutropenia, TTP, aplastic anemia) requires regular CBC monitoring. Use caution in patients with hepatic impairment, renal impairment, bleeding disorders, or those undergoing surgery.

Clinical Tips & Counseling

Drug interactions

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TICLID

Clinical safety rating: caution

Comprehensive clinical and safety monograph for TICLID (TICLID).

How it works

Ticlopidine is a thienopyridine ADP receptor antagonist that irreversibly inhibits the P2Y12 receptor on platelets, preventing ADP-induced platelet aggregation.

What the body does with it

Metabolism	Extensively metabolized in the liver via cytochrome P450 enzymes, primarily CYP3A4 and CYP2C19, with minor contributions from CYP1A2 and CYP2B6.
Excretion	Primarily hepatic metabolism; 60% renal as metabolites, 23% fecal. Minimal parent drug excreted unchanged.
Half-life	Terminal elimination half-life is approximately 30-50 hours (mean ~33 hours), with clinical effects lasting 7-10 days after discontinuation due to irreversible platelet binding.
Protein binding	98% bound, primarily to albumin; also binds to lipoproteins and alpha-1-acid glycoprotein.
Volume of Distribution	Approximately 1.2-1.8 L/kg; large Vd indicates extensive tissue distribution, including irreversible binding to platelets.
Bioavailability	Oral bioavailability is >80% (approximately 80-90%) with food increasing absorption; admin with meals to reduce GI irritation.
Onset of Action	Oral: 48-72 hours for detectable inhibition of platelet aggregation; maximal effect at 8-11 days.
Duration of Action	Duration of platelet inhibition persists for the lifespan of the platelet (7-10 days) after drug cessation; antiplatelet effect peaks at 8-11 days and gradually declines over 1-2 weeks.

Classification & Brands

Dosing & administration

250 mg orally twice daily

Dosage form	TABLET
Renal impairment	No dose adjustment required for mild to moderate renal impairment; avoid use in severe renal impairment (CrCl < 25 mL/min) due to limited data.
Liver impairment	Contraindicated in severe hepatic impairment (Child-Pugh class C); use with caution in moderate impairment (Child-Pugh class B) with dose reduction to 250 mg once daily.
Pediatric use	Safety and efficacy not established; not recommended for use in pediatric patients.
Geriatric use	No specific dose adjustment; monitor for increased bleeding risk and renal function in elderly patients.

Use during pregnancy

1st trimester	Consult provider
2nd trimester	Consult provider
3rd trimester	Consult provider

Clinical note

Comprehensive clinical and safety monograph for TICLID (TICLID).

Breastfeeding	Ticlopidine is excreted in human breast milk; the M/P ratio is unknown. Due to potential for adverse effects in the nursing infant, including bleeding risk, a decision should be made to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
Teratogenic Risk	Ticlopidine is FDA Pregnancy Category B. Animal studies have not revealed evidence of fetal harm, but there are no adequate and well-controlled studies in pregnant women. It should be used during pregnancy only if clearly needed. Potential risks include hemorrhage in the fetus due to maternal platelet inhibition.

Warnings & precautions

■ FDA Black Box Warning

Ticlopidine can cause life-threatening hematologic adverse reactions including neutropenia/agranulocytosis, thrombotic thrombocytopenic purpura (TTP), and aplastic anemia. Fatalities have occurred.