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Cangrelor: Drug information

Cangrelor: Drug information
(For additional information see "Cangrelor: Patient drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
Brand Names: US
  • Kengreal
Pharmacologic Category
  • Antiplatelet Agent;
  • Antiplatelet Agent, Non-thienopyridine;
  • P2Y12 Antagonist
Dosing: Adult
Percutaneous coronary intervention

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

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).

Dosing: Kidney Impairment: Adult

No dosage adjustment necessary

Dosing: Hepatic Impairment: Adult

No dosage adjustment necessary

Dosing: Older Adult

Refer to adult dosing.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Solution Reconstituted, Intravenous:

Kengreal: 50 mg (1 ea)

Generic Equivalent Available: US

No

Administration: Adult

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.

Use: Labeled Indications

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.

Use: Off-Label: Adult

Bridging therapy prior to cardiac surgery

Medication Safety Issues
Sound-alike/look-alike issues:

Cangrelor may be confused with ticagrelor.

Adverse Reactions

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

Contraindications

Known hypersensitivity (eg, anaphylaxis) to cangrelor or any component of the formulation; significant active bleeding

Warnings/Precautions

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.

Metabolism/Transport Effects

None known.

Drug Interactions

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 Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.

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

Caplacizumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Caplacizumab. Specifically, the risk of bleeding may be increased. Management: Avoid coadministration of caplacizumab with antiplatelets if possible. If coadministration is required, monitor closely for signs and symptoms of bleeding. Interrupt use of caplacizumab if clinically significant bleeding occurs. 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

Pregnancy Considerations

Adverse events were observed in some animal reproduction studies.

Breastfeeding Considerations

It is not known if cangrelor is excreted in breast milk

Monitoring Parameters

Monitor for signs/symptoms of bleeding.

Mechanism of Action

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.

Pharmacokinetics

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%)

Pricing: US

Solution (reconstituted) (Kengreal Intravenous)

50 mg (per each): $1,000.36

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Brand Names: International
  • Kengrexal (AT, BE, CH, CZ, DE, DK, EE, ES, FI, FR, GB, HR, IE, LT, NL, NO, PL, PT, RO, SE, SI, SK)


For country code abbreviations (show table)
  1. Akers WS, Oh JJ, Oestreich JH, Ferraris S, Wethington M, Steinhubl SR. Pharmacokinetics and pharmacodynamics of a bolus and infusion of cangrelor: a direct, parenteral P2Y12 receptor antagonist. J Clin Pharmacol. 2010;50(1):27-35. doi: 10.1177/0091270009344986. [PubMed 19779037]
  2. Angiolillo DJ, Firstenberg MS, Price MJ, et al; BRIDGE Investigators. Bridging antiplatelet therapy with cangrelor in patients undergoing cardiac surgery: a randomized controlled trial. JAMA. 2012;307(3):265-274 [PubMed 22253393]
  3. Bhatt DL, Lincoff AM, Gibson CM, et al; CHAMPION PLATFORM Investigators. Intravenous platelet blockade with cangrelor during PCI. N Engl J Med. 2009;361(24):2330-2341. doi: 10.1056/NEJMoa0908629. [PubMed 19915222]
  4. Bhatt DL, Stone GW, Mahaffey KW, et al; CHAMPION PHOENIX Investigators. Effect of platelet inhibition with cangrelor during PCI on ischemic events. N Engl J Med. 2013;368(14):1303-1313. doi: 10.1056/NEJMoa1300815. [PubMed 23473369]
  5. Harrington RA, Stone GW, McNulty S, et al. Platelet inhibition with cangrelor in patients undergoing PCI. N Engl J Med. 2009;361(24):2318-2329. doi: 10.1056/NEJMoa0908628. [PubMed 19915221]
  6. Kengreal (cangrelor) [prescribing information]. Cary, NC: Chiesi USA Inc; September 2022.
  7. Schneider DJ, Agarwal Z, Seecheran N, Keating FK, Gogo P. Pharmacodynamic effects during the transition between cangrelor and ticagrelor. JACC Cardiovasc Interv. 2014;7(4):435-442. doi: 10.1016/j.jcin.2013.08.017. [PubMed 24656538]
  8. Steinhubl SR, Oh JJ, Oestreich JH, Ferraris S, Charnigo R, Akers WS. Transitioning patients from cangrelor to clopidogrel: pharmacodynamic evidence of a competitive effect. Thromb Res. 2008;121(4):527-534. [PubMed 17631948]
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