Features and properties of decitabine/cedazuridine
| Alternative names | ASTX 727; ASTX727 LD; INQOVI®; |
| Class | Antineoplastics; aza compounds; deoxyribonucleosides; fluorinated hydrocarbons; pyrimidine nucleosides; ribonucleosides; small molecules; triazines |
| Mechanism of Action | Cedazuridine inhibits cytidine deaminase in the gastrointestinal tract and liver, thereby increasing systemic exposure of decitabine following oral administration |
| Route of Administration | Oral |
| Pharmacodynamics | In patients with MDS or CMML, there was no significant difference in LINE-1 DNA demethylation between oral decitabine/cedazuridine and intravenous decitabine |
| Pharmacokinetics | Oral decitabine/cedazuridine 35/100 mg fixed-dose combination achieved ≈ 99% of decitabine 5-day AUC systemic exposures compared with intravenous decitabine 20 mg/m2 |
| Cmax of decitabine and cedazuridine reached in median of 1 h and 3 h, respectively | |
| Steady state of decitabine and cedazuridine reached in 2 days | |
| Mean terminal half-life of decitabine and cedazuridine 1.5 h and 6.7 h, respectively | |
| Most frequent adverse reactions | |
| Any-grade | Fatigue, constipation, haemorrhage, myalgia, nausea, arthralgia |
| Grade 3/4 | Pneumonia, sepsis |
| Most frequent grade 3/4 laboratory abnormalities | Decreased leukocytes, decreased platelet count, decreased neutrophil count |
| ATC codes | |
| WHO ATC code | A (Alimentary Tract and Metabolism); L01B-C08 (Decitabine |
| EphMRA ATC code | A (Alimentary Tract and Metabolism); L1B (Antimetabolites) |
| Chemical Name | 4-amino-1-[(2R,4S,5R)-4-hydroxy-5(hydroxymethyl)oxolan-2-yl]-1,3,5-triazin-2(1H)-one |
AUC area under the concentration–time curve, Cmax peak plasma concentration, CMML chronic myelomonocytic leukaemia, LINE-1 long interspersed nuclear element-1, MDS myelodysplastic syndrome