• IBRANCE® has a convenient, once daily, oral regimen.
• The recommended starting dose is 125 mg of IBRANCE® once daily for 21 consecutive days followed by 7 days off treatment (schedule 3/1) to comprise a complete cycle of 28 days.¹
• IBRANCE should be given in combination with either an AI, or in combination with fulvestrant in women who have received prior endocrine therapy
• When co-administered with IBRANCE, the AI should be administered according to the dose schedule reported in the SmPC.
• When co-administered with IBRANCE, the recommended dose of fulvestrant is 500 mg administered intramuscularly on Days 1, 15, 29, and once monthly thereafter. Please refer to the SmPC of fulvestrant.
• In pre- or perimenopausal women, the endocrine therapy should be combined with a LHRH agonist.
• For patients with severe hepatic impairment (Child-Pugh class C), the recommended dose of IBRANCE is 75 mg once daily on Schedule 3/1
• Treatment with IBRANCE® should be continued as long as the patient is deriving clinical benefit from therapy or until unacceptable toxicity occurs.¹

IBRANCE 125 mg (starting dose) once daily PO with or without food

Patients with absolute neutrophil counts of ≥1000/mm³ and platelet counts of ≥50,000/mm³ are recommended to receive IBRANCE¹

Patients should be encouraged to take their dose at approximately the same time each day. If the patient vomits or misses a dose, an additional dose should not be taken that day. The next prescribed dose should be taken at the usual time.

IBRANCE® can be taken with or without food. No additional dose should be taken if a dose is missed, and the next prescribed dose should be taken at the usual time. IBRANCE® should be swallowed whole, not chewed, crushed or opened prior to swallowing.¹
 

As with all medications, IBRANCE may interact with certain drugs.

CYP3A4 inducers or inhibitors 
• Palbociclib is primarily metabolised by CYP3A and sulphotransferase (SULT) enzyme SULT2A1. In vivo, palbociclib is a weak, time-dependent inhibitor of CYP3A.
• Strong inhibitors of CYP3A4 may lead to increased toxicity.
• Concomitant use of strong CYP3A inhibitors during treatment with palbociclib should be avoided. Coadministration should only be considered after careful evaluation of the potential benefits and risks.
• If coadministration with a strong CYP3A inhibitor is unavoidable, reduce the palbociclib dose to 75 mg once daily. When the strong inhibitor is discontinued, the dose of palbociclib should be increased (after 3-5 half-lives of the inhibitor) to the dose used prior to the initiation of the strong CYP3A inhibitor.
• Coadministration of CYP3A inducers may lead to decreased palbociclib exposure and consequently a risk for lack of efficacy. Therefore, concomitant use of palbociclib with strong CYP3A4 inducers should be avoided. No dose adjustments are required for coadministration of palbociclib with moderate CYP3A inducers.

Effects on the PK of other medicines
• The dose of sensitive CYP3A substrates with a narrow therapeutic index (e.g., alfentanil, cyclosporine, dihydroergotamine, ergotamine, everolimus, fentanyl, pimozide, quinidine, sirolimus, and tacrolimus) may need to be reduced when coadministered with palbociclib, as palbociclib may increase their exposure.

Drug-drug interaction between palbociclib and statins 
• Concomitant use of palbociclib with statins may increase the risk of rhabdomyolysis. Cases of rhabdomyolysis including fatal cases have been reported following coadministration of palbociclib with simvastatin or atorvastatin.

In vitro studies with transporters 
• Based on in vitro data, palbociclib is predicted to inhibit intestinal P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) mediated transport. Therefore, administration of palbociclib with medicinal products that are substrates of P-gp (e.g., digoxin, dabigatran, colchicine) or BCRP (e.g., pravastatin, rosuvastatin, sulfasalazine) may increase their therapeutic effect and adverse reactions.
• Based on in vitro data, palbociclib may inhibit the uptake transporter organic cationic transporter OCT1 and then may increase the exposure of medical product substrates of this transporter (e.g. metformin)