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): 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 (Angiolillo 2012).
No dosage adjustment necessary
No dosage adjustment necessary
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Reconstituted, Intravenous:
Kengreal: 50 mg (1 ea)
No
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.
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
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.
None known.
Abrocitinib: Agents with Antiplatelet Properties may enhance the antiplatelet effect 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 combination
Acalabrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Agents with Antiplatelet Properties (e.g., P2Y12 inhibitors, NSAIDs, SSRIs, etc.): May enhance the antiplatelet effect of other Agents with Antiplatelet Properties. Risk C: Monitor therapy
Anticoagulants: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy
Apixaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Apixaban. Specifically, the risk for bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Bemiparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin with antiplatelet agents. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Cephalothin: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Cephalothin. Specifically, the risk for bleeding may be increased. Risk C: Monitor therapy
Clopidogrel: Cangrelor may diminish the antiplatelet effect 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): Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and/or bleeding may be increased. Risk C: Monitor therapy
Dabigatran Etexilate: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Dabigatran Etexilate. Specifically, the risk of bleeding may be increased. Antiplatelet Agents (P2Y12 Inhibitors) may increase the serum concentration of Dabigatran Etexilate. Specifically, clopidogrel may increase dabigatran serum concentrations. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Dasatinib: May enhance the anticoagulant effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Deoxycholic Acid: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor therapy
Edoxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Edoxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider the anticipated risks and benefits of this combination. If combined, increased monitoring for bleeding is recommended. Risk D: Consider therapy modification
Enoxaparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue antiplatelet agents prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
FentaNYL: May diminish the antiplatelet effect of Antiplatelet Agents (P2Y12 Inhibitors). FentaNYL may decrease the serum concentration of Antiplatelet Agents (P2Y12 Inhibitors). Risk C: Monitor therapy
Heparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or agents with antiplatelet properties if coadministration is required. Risk D: Consider therapy modification
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Bleeding may occur. Risk C: Monitor therapy
Ibritumomab Tiuxetan: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab Tiuxetan. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy
Ibrutinib: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Icosapent Ethyl: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Inotersen: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Limaprost: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lipid Emulsion (Fish Oil Based): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Fluoride (with ADE): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with AE, No Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Obinutuzumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Risk C: Monitor therapy
Omega-3 Fatty Acids: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Prasugrel: Cangrelor may diminish the antiplatelet effect 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
Prostacyclin Analogues: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Rivaroxaban: Antiplatelet Agents (P2Y12 Inhibitors) may enhance the adverse/toxic effect of Rivaroxaban. Specifically, the risk of bleeding may be increased. Management: Carefully consider risks and benefits of this combination and monitor closely; Canadian labeling recommends avoiding prasugrel or ticagrelor. Risk D: Consider therapy modification
Salicylates: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Salicylates. Increased risk of bleeding may result. Risk C: Monitor therapy
Selumetinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Thrombolytic Agents: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy
Tipranavir: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Urokinase: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Urokinase. Risk X: Avoid combination
Vitamin E (Systemic): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Zanubrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
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%)
Solution (reconstituted) (Kengreal Intravenous)
50 mg (per each): $1,000.36
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