Not a Member?
Email this page
Send the page ""
to a friend, relative, colleague or yourself.
Separate multiple email address with a comma
We do not record any personal information entered above.
Thank you. Your email has been sent.
ADP (adenosine Diphosphate) Receptor Antagonist Platelet Aggregation Inhibitors
Injectable P2Y12 platelet inhibitor indicated as an adjunct to PCI in patients not already receiving an oral P2Y12 inhibitor or glycoprotein IIb/IIIa inhibitorOnset of platelet inhibitor occurs within 2 minutes of initiation of therapy and returns to normal within 1 hour of discontinuationContraindicated in patients with active significant bleeding
Cangrelor/Kengreal Intravenous Inj Pwd F/Sol: 50mg
30 mcg/kg single dose IV bolus followed immediately by 4 mcg/kg/minute continuous IV infusion. The bolus should be administered prior to PCI and the maintenance infusion should be continued for at least 2 hours or for the duration of PCI, whichever is longer. An oral P2Y12 platelet inhibitor (e.g., either ticagrelor, prasugrel or clopidogrel) should be administered to maintain platelet inhibition; choose one to administer. Prasugrel 60 mg PO or clopridogrel 600 mg PO may be administered after discontinuation of the cangrelor infusion. Do not administer prasugrel or clopidogrel prior to discontinuation of cangrelor. Ticagrelor 180 mg PO may be administered at any time during or immediately after discontinuation of cangrelor infusion.
30 mcg/kg IV bolus; 4 mcg/kg/minute IV infusion.
Safety and efficacy have not been established.
Because the metabolism of cangrelor is not dependent on hepatic function, no dosage adjustment is required for patients with hepatic impairment.
No dosage adjustment is required for patients with mild, moderate, or severe renal impairment.
Visually inspect parenteral products for particulate matter and discoloration prior to administration.Cangrelor is for intravenous use only.
Reconstitution:Reconstitute by adding 5 mL Sterile Water for Injection to a 50 mg cangrelor vial. Swirl gently until all material is dissolved. Do not mix vigorously. Allow foam to settle.Ensure contents of the vial are fully dissolved. Reconstituted solution should be clear and colorless or pale yellow.Withdraw contents of one reconstituted 50 mg vial and add to one 250 mL bag of 0.9% Sodium Chloride Injection or Dextrose 5% Injection resulting in a final infusion concentration of 200 mcg/mL.One bag should be sufficient for most patients for at least 2 hours of dosing. Patients weighing more than 100 kg will require a minimum of 2 bags.Administer diluted cangrelor immediately. When stored at room temperature, diluted cangrelor is stable for up to 12 hours in Dextrose 5% Injection and 24 hours in 0.9% Sodium Chloride Injection. Intravenous Administration:Administer cangrelor via a dedicated IV line.Bolus injection should be administered rapidly (< 1 minute). The bolus volume may be withdrawn from the diluted infusion bag and administered via manual IV push or may be administered via infusion pump.Ensure the bolus dose is completely administered prior to start of percutaneous coronary intervention (PCI).Start the continuous IV infusion immediately after administration of the bolus; an infusion pump should be used for the continuous IV infusion.
Kengreal:- Discard unused portion. Do not store for later use.- Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
Cangrelor is contraindicated in patients with a known cangrelor hypersensitivity (e.g., anaphylaxis) or hypersensitivity to any component of the product.
Cangrelor is contraindicated in patients with significant active bleeding. Cangrelor increases the risk of bleeding. In clinical studies, the use of cangrelor was associated with a higher incidence of bleeding compared to clopidogrel. After discontinuation of cangrelor infusion, the effect on platelet inhibition decreases rapidly and platelet function returns to normal within 1 hour.
Although cangrelor dose adjustments are not required for patients with renal impairment, decreased renal function has been reported in patients with severe renal impairment (creatinine clearance < 30 mL/minute).
There are no available data on cangrelor use in human pregnancy to assess for a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. In animal reproduction studies, continuous infusion of cangrelor throughout organogenesis at a dose approximately 2 times the maximum recommended human dose (MRHD) did not result in any fetal malformations. In rat studies, dose-related fetal growth retardation, characterized by increased incidences of incomplete ossification and unossified hind limb metatarsals, was observed at doses of 3 mcg/kg/minute or more. In rabbit studies, increased abortion and intrauterine loss were observed at doses of 12 mcg/kg/minute or more (3 times the MRHD). Fetal growth retardation, characterized by decreased fetal weights, slight reduction in ossification, and a slight increase in skeletal variants, was observed at 36 mcg/kg/minute (9 times the MRHD). Cangrelor did not produce malformations in embryofetal development studies and is not considered to be a teratogen. Cangrelor use during labor and obstetric delivery may increase the risk for maternal bleeding and hemorrhage. Performance of neuraxial blockade procedures is not recommended during cangrelor use due to the potential risk of spinal hematoma. When possible, discontinue use of cangrelor 1 hour prior to labor, delivery, or neuraxial blockade. Myocardial infarction is a medical emergency, which can be fatal to the pregnant woman and the fetus if left untreated. Do not withhold life-sustaining therapy due to the potential concerns about the effect of cangrelor on the fetus.
There are no data available on the presence of cangrelor in human or animal milk, the effects on the breast-fed infant, or the effects on milk production. However, due to its short half-life, cangrelor exposure is expected to very low in a breast-feeding infant.
Cangrelor has not been studied in pediatric patients. Safety and efficacy have not been established in adolescents, children, or infants.
bleeding / Early / 0.2-0.2intracranial bleeding / Delayed / 0.2-0.2GI bleeding / Delayed / Incidence not knownretroperitoneal bleeding / Delayed / Incidence not knownbronchospasm / Rapid / Incidence not knownanaphylactoid reactions / Rapid / Incidence not knownangioedema / Rapid / Incidence not knownanaphylactic shock / Rapid / Incidence not known
dyspnea / Early / 1.3-1.3hematuria / Delayed / Incidence not knownhematoma / Early / Incidence not knownwheezing / Rapid / Incidence not known
ecchymosis / Delayed / Incidence not known
Clopidogrel: (Major) Do not administer clopidogrel until the cangrelor infusion is discontinued. The expected antiplatelet effect of a 600 mg loading dose of clopidogrel will be blocked if administered during the cangrelor infusion. Clopidogrel therapy should be initiated immediately after cangrelor discontinuation. Defibrotide: (Contraindicated) Coadministration of defibrotide with antithrombotic agents like cangrelor is contraindicated. The pharmacodynamic activity and risk of hemorrhage with antithrombotic agents are increased if coadministered with defibrotide. If therapy with defibrotide is necessary, discontinue antithrombotic agents prior to initiation of defibrotide therapy. Consider delaying the onset of defibrotide treatment until the effects of the antithrombotic agent have abated. Prasugrel: (Major) Do not administer prasugrel until the cangrelor infusion is discontinued. The expected antiplatelet effect of a 60 mg loading dose of prasugrel will be blocked if administered during the cangrelor infusion. Prasugrel therapy should be initiated immediately after cangrelor discontinuation. Selective serotonin reuptake inhibitors: (Moderate) Platelet aggregation may be impaired by selective serotonin reuptake inhibitors (SSRIs) due to platelet serotonin depletion, possibly increasing the risk of a bleeding complication (e.g., gastrointestinal bleeding, ecchymosis, epistaxis, hematomas, petechiae, hemorrhage) in patients receiving platelet inhibitors (e.g., cangrelor). Patients should be instructed to monitor for signs and symptoms of bleeding while taking an SSRI concurrently with an antiplatelet medication and to promptly report any bleeding events to the practitioner.
Cangrelor is a direct competitive inhibitor of the P2Y12 platelet receptor. Inhibition of the PY12 receptor prevents further signaling and platelet activation and thus results in inhibition of platelet activation and aggregation. In contrast to clopidogrel or prasugrel, cangrelor does not require hepatic conversion to an active metabolite.
Cangrelor is administered intravenously. Cangrelor is approximately 97% protein bound and undergoes rapid deactivation in the circulation by dephosphorylation to its inactive metabolite. Hepatic enzymes are not involved in the metabolism of cangrelor. The majority of cangrelor is excreted in urine. The average terminal half-life is 3—6 minutes. Platelet inhibition occurs within 2 minutes after administration of a cangrelor 30 mcg/kg IV bolus followed by a 4 mcg/kg/minute IV infusion. Platelet inhibition is maintained throughout the duration of the infusion. After discontinuation of the cangrelor infusion, the anti-platelet effect decreases rapidly and platelet function returns to normal within 1 hour.
Cangrelor follows linear pharmacokinetics. It is rapidly distributed and metabolized. The maximum plasma concentration is achieved within 2 minutes after administration of an intravenous (IV) bolus followed by IV infusion.