QT time prolongation
Adverse drug events
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Explanations of the substances for patients
We have no additional warnings for the combination of abarelix and cyclophosphamide. Please also consult the relevant specialist information.
The reported changes in exposure correspond to the changes in the plasma concentration-time curve [ AUC ]. We do not expect any change in exposure for abarelix, when combined with cyclophosphamide (100%). We do not expect any change in exposure for cyclophosphamide, when combined with abarelix (100%).
The pharmacokinetic parameters of the average population are used as the starting point for calculating the individual changes in exposure due to the interactions.
The bioavailability of abarelix is unknown. The terminal half-life [ t12 ] is rather long at 316.8 hours and constant plasma levels [ Css ] are only reached after more than 1267.2 hours. The protein binding [ Pb ] is 97.5% strong. The metabolism via cytochromes is currently still being worked on.
Cyclophosphamide has a mean oral bioavailability [ F ] of 75%, which is why the maximum plasma levels [Cmax] tend to change with an interaction. The terminal half-life [ t12 ] is 7.5 hours and constant plasma levels [ Css ] are reached after approximately 30 hours. The therapeutic window is narrow and the safety margin is therefore small. Even small changes in exposure can increase the risk of toxicity. The protein binding [ Pb ] is rather weak at 60%. The metabolism takes place via CYP2B6, CYP2C19, CYP2C9 and CYP3A4, among others and the active transport takes place partly via MRP4 and PGP.
|Serotonergic Effects a||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor cyclophosphamide increase serotonergic activity.
|Kiesel & Durán b||0||Ø||Ø|
Rating: According to our knowledge, neither abarelix nor cyclophosphamide increase anticholinergic activity.
QT time prolongation
Rating: In combination, abarelix and cyclophosphamide can potentially trigger ventricular arrhythmias of the torsades de pointes type.
General adverse effects
|Side effects||∑ frequency||aba||cyc|
|Hemorrhagic cystitis||1.0 %||n.a.||+|
Hearing loss: cyclophosphamide
Heart failure: cyclophosphamide
Pericardial effusion: cyclophosphamide
Stevens johnson syndrome: cyclophosphamide
Toxic epidermal necrolysis: cyclophosphamide
Loss of appetite: cyclophosphamide
Acute myeloid leukemia: cyclophosphamide
Febrile neutropenia: cyclophosphamide
Cholestatic hepatitis: cyclophosphamide
Anaphylactic reaction: cyclophosphamide
Peripheral neuropathy: cyclophosphamide
Based on your answers and scientific information, we assess the individual risk of undesirable side effects. These recommendations are intended to advise professionals and are not a substitute for consultation with a doctor. In the restricted test version (alpha), the risk of all substances has not yet been conclusively assessed.
Abstract: No useful predictor of risk of acute heart failure in peripheral-blood stem-cell transplantation (PBSCT) regimens, Including high-dose cyclophosphamide, has previously been available. Corrected QT dispersion can predict acute heart failure after high-dose cyclophosphamide chemotherapy used in PBSCT.
Abstract: Transporters in proximal renal tubules contribute to the disposition of numerous drugs. Furthermore, the molecular mechanisms of tubular secretion have been progressively elucidated during the past decades. Organic anions tend to be secreted by the transport proteins OAT1, OAT3 and OATP4C1 on the basolateral side of tubular cells, and multidrug resistance protein (MRP) 2, MRP4, OATP1A2 and breast cancer resistance protein (BCRP) on the apical side. Organic cations are secreted by organic cation transporter (OCT) 2 on the basolateral side, and multidrug and toxic compound extrusion (MATE) proteins MATE1, MATE2/2-K, P-glycoprotein, organic cation and carnitine transporter (OCTN) 1 and OCTN2 on the apical side. Significant drug-drug interactions (DDIs) may affect any of these transporters, altering the clearance and, consequently, the efficacy and/or toxicity of substrate drugs. Interactions at the level of basolateral transporters typically decrease the clearance of the victim drug, causing higher systemic exposure. Interactions at the apical level can also lower drug clearance, but may be associated with higher renal toxicity, due to intracellular accumulation. Whereas the importance of glomerular filtration in drug disposition is largely appreciated among clinicians, DDIs involving renal transporters are less well recognized. This review summarizes current knowledge on the roles, quantitative importance and clinical relevance of these transporters in drug therapy. It proposes an approach based on substrate-inhibitor associations for predicting potential tubular-based DDIs and preventing their adverse consequences. We provide a comprehensive list of known drug interactions with renally-expressed transporters. While many of these interactions have limited clinical consequences, some involving high-risk drugs (e.g. methotrexate) definitely deserve the attention of prescribers.