There is no known antidote for overdose of apalutamide. General supportive measures should be undertaken until clinical toxicity, if any, diminishes or resolves.
Interactions
Apalutamide has a high potential for drug interactions. In terms of effects of apalutamide on other drugs, the exposure of substrates of CYP3A4, CYP2C19, CYP2C9, UDP-glucuronosyltransferase, P-glycoprotein, ABCG2, or OATP1B1 may be reduced to varying extents. In terms of effects of other drugs on apalutamide, strong CYP2C8 or CYP3A4 inhibitors may increase levels of apalutamide or its major active metaboliteN-desmethylapalutamide, while mild to moderate CYP2C8 or CYP3A4 inhibitors are not expected to affect their exposure.
Pharmacology
Pharmacodynamics
Antiandrogenic activity
Apalutamide acts as a selectivecompetitivesilent antagonist of the androgen receptor, via the ligand-binding domain, and hence is an antiandrogen. It is similar both structurally and pharmacologically to the second-generation NSAA enzalutamide, but shows some advantages, including higher antiandrogenic activity as well as several-fold reduced central nervous systemdistribution. The latter difference may reduce its comparative risk of seizures and other central side effects. Apalutamide has 5- to 10-fold greater affinity for the AR than bicalutamide, a first-generation NSAA. The acquired F876L mutation of the AR identified in advanced prostate cancer cells has been found to confer resistance to both enzalutamide and apalutamide. A newer NSAA, darolutamide, is not affected by this mutation, nor has it been found to be affected by any other tested/well-known AR mutations. Apalutamide may be effective in a subset of prostate cancer patients with acquired resistance to abiraterone acetate.
Other activities
Apalutamide shows potent induction potential of cytochrome P450 enzymes similarly to enzalutamide. It is a strong inducer of CYP3A4 and CYP2C19 and a weak inducer of CYP2C9, as well as an inducer of UDP-glucuronosyltransferase. In addition, apalutamide is an inducer of P-glycoprotein, ABCG2, and OATP1B1. Apalutamide binds weakly to and inhibits the GABAA receptor in vitro similarly to enzalutamide, but due to its relatively lower central concentrations, may have a lower risk of seizures in comparison. Apalutamide has been found to significantly and concentration-dependently increase QT interval.
Pharmacokinetics
The mean absolute oral bioavailability of apalutamide is 100%. Mean peak levels of apalutamide occur 2 hours following administration, with a range of 1 to 5 hours. Food delays the median time to peak levels of apalutamide by approximately 2 hours, with no significant changes in the peak levels themselves or in area-under-curve levels. Steady-state levels of apalutamide are achieved following 4 weeks of administration, with an approximate 5-fold accumulation. Peak concentrations for 160 mg/day apalutamide at steady-state are 6.0 µg/mL, relative to peak levels of 16.6 μg/mL for 160 mg/day enzalutamide and mean -bicalutamide levels of 21.6 μg/mL for 150 mg/day bicalutamide. The mean volume of distribution of apalutamide at steady-state is approximately 276 L. The plasma protein binding of apalutamide is 96%, while that of its major metabolite N-desmethylapalutamide is 95%, both irrespective of concentration. Apalutamide is metabolized in the liver by CYP2C8 and CYP3A4. A major active metabolite, N-desmethylapalutamide, is formed by these enzymes, with similar contribution of each of these enzymes to its formation at steady-state. Following a single oral dose of 200 mg apalutamide, apalutamide represented 45% and N-desmethylapalutamide 44% of total area-under-curve levels. The mean elimination half-life of apalutamide at steady-state is 3 to 4 days. Fluctuations in apalutamide exposure are low and levels are stable throughout the day, with mean peak-to-trough ratios of 1.63 for apalutamide and 1.27–1.3 for N-desmethylapalutamide. After a single dose of apalutamide, its clearance rate was 1.3 L/h, while its clearance rate increased to 2.0 L/h at steady-state. This change is considered to be likely due to CYP3A4 auto-induction. Approximately 65% of apalutamide is excreted in urine while 24% is excreted in feces.
Chemistry
Apalutamide is a structural analogue of enzalutamide and RD-162. It is a pyridyl variant of RD-162. Enzalutamide and RD-162 were derived from the nonsteroidal androgenRU-59063, which itself was derived from the first-generation NSAA nilutamide and by extension from flutamide.