Percutaneous coronary intervention: IV: 30 mcg/kg bolus prior to percutaneous coronary intervention (PCI) followed immediately by an infusion of 4 mcg/kg/minute continued for at least 2 hours or for the duration of the PCI, whichever is longer.
Transitioning patients to oral P2Y12 antagonist therapy after percutaneous coronary intervention:
Conversion to clopidogrel: Administer 600 mg of clopidogrel immediately after discontinuing cangrelor infusion. Do not administer clopidogrel prior to cangrelor discontinuation.
Conversion to prasugrel: Administer 60 mg of prasugrel immediately after discontinuing cangrelor infusion. Do not administer prasugrel prior to cangrelor discontinuation.
Conversion to ticagrelor: Administer 180 mg of ticagrelor at any time during cangrelor infusion or immediately after discontinuing cangrelor infusion.
Bridging therapy prior to cardiac surgery (off-label use):
Note: Routine bridging is not recommended. However, exceptions can be made for high-risk patients (eg, coronary stenting in a critical vessel within the past 3 months) (Ref).
IV: 0.75 mcg/kg/min (without a bolus dose) following thienopyridine discontinuation for up to 7 days prior to surgery; discontinue 1 to 6 hours prior to surgical incision based on risk for thrombotic complications after antiplatelet therapy has been withheld. Cangrelor half-life is ~3 to 6 minutes, so for patients at high risk for thrombotic complications, consider minimizing the time between discontinuation and start of surgery (Ref).
No dosage adjustment necessary
No dosage adjustment necessary
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Hematologic & oncologic: Hemorrhage (GUSTO: 16%; TIMI: <1%)
Renal: Renal insufficiency (3%; severe; creatinine clearance <30 mL/minute)
Respiratory: Dyspnea (1%)
<1%, postmarketing, and/or case reports: Hypersensitivity reaction
Known hypersensitivity (eg, anaphylaxis) to cangrelor or any component of the formulation; significant active bleeding.
Canadian labeling: Additional contraindications (not in US labeling): Patients with increased risk for bleeding; patients who had an ischemic stroke or any previous hemorrhagic stroke.
Concerns related to adverse effects:
• Bleeding: Similar to other P2Y12 antagonists, the use of cangrelor increases the risk of bleeding; however, due to the short elimination half-life, no antiplatelet effect is observed an hour after discontinuation.
• Hypersensitivity: Although rare, serious cases of hypersensitivity (eg, anaphylaxis, anaphylactic shock, bronchospasm, angioedema, stridor) have been reported with cangrelor.
Concurrent drug therapy issues:
• Thienopyridines: If clopidogrel or prasugrel are administered prior to discontinuation of the cangrelor infusion, no antiplatelet effect will occur until the next dose is administered. Therefore, do not administer until after the cangrelor infusion is discontinued.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Reconstituted, Intravenous:
Kengreal: 50 mg (1 ea)
No
Solution (reconstituted) (Kengreal Intravenous)
50 mg (per each): $1,201.44
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Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Reconstituted, Intravenous:
Kengrexal: 50 mg (1 ea)
IV: Vial must be diluted prior to infusion. Administer via a dedicated IV line.
Obtain bolus volume from the prepared bag and administer rapidly over <1 minute via manual IV push or the infusion pump. Ensure the bolus is completely administered before the start of PCI. Start the infusion immediately after administration of the bolus.
Percutaneous coronary intervention (PCI): Adjunct to PCI to reduce the risk of periprocedural myocardial infarction, repeat coronary revascularization, and stent thrombosis in patients who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein IIb/IIIa inhibitor.
Bridging therapy prior to cardiac surgery
Cangrelor may be confused with ticagrelor.
None known.
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
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
Clopidogrel: Cangrelor may decrease antiplatelet effects of Clopidogrel. More specifically, while the use of Cangrelor is expected to increase total platelet inhibition in patients who have previously received Clopidogrel, Cangrelor is expected to decrease binding of Clopidogrel metabolites to P2Y12 receptors and thus reduce the extent of irreversible platelet inhibition. Management: Avoid administration of clopidogrel until cangrelor infusion is discontinued. Risk D: Consider Therapy Modification
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
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
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
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
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
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
Miscellaneous Antiplatelets: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
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
Prasugrel: Cangrelor may decrease antiplatelet effects of Prasugrel. More specifically, while the use of Cangrelor is expected to increase total platelet inhibition in patients who have previously received Prasugrel, Cangrelor is expected to decrease binding of Prasugrel metabolites to P2Y12 receptors and thus reduce the extent of irreversible platelet inhibition. Management: Avoid administration of prasugrel until cangrelor is discontinued. Risk D: Consider Therapy Modification
Selumetinib: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
Therapeutic Antiplatelets: May increase antiplatelet effects of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor
Thrombolytic Agents: Therapeutic Antiplatelets may increase adverse/toxic effects of Thrombolytic Agents. Specifically, the risk of bleeding may be increased. Risk C: Monitor
Tipranavir: May increase antiplatelet effects of Therapeutic Antiplatelets. Risk C: Monitor
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
Adverse events were observed in some animal reproduction studies.
It is not known if cangrelor is excreted in breast milk
Monitor for signs/symptoms of bleeding.
Cangrelor, a nonthienopyridine adenosine triphosphate analogue, is a direct P2Y12 platelet receptor inhibitor that blocks adenosine diphosphate (ADP)-induced platelet activation and aggregation. Cangrelor binds selectively and reversibly to the P2Y12 receptor, preventing further signaling and platelet activation.
Onset of action: Platelet inhibition occurs within 2 minutes
Duration of action: Antiplatelet effect is maintained throughout duration of infusion. After discontinuation, platelet function returns to normal within 1 hour
Distribution: Volume of distribution: 3.9 L
Protein binding: ~97% to 98%
Metabolism: Rapidly inactivated in the circulation by dephosphorylation to its primary metabolite, a nucleoside, which has negligible anti-platelet activity
Half-life elimination: ~3 to 6 minutes
Time to peak: Within 2 minutes
Excretion: Urine (58%); feces (35%)