Source: Registered Drug Product Database (NG) Revision Year: 2025 Publisher: Manufacturer: Huazhong Pharmaceutical Co., Ltd. Site of Manufacture: No.118, Xianshan Road, Xiangyang City, Hubei Province, China
Pharmacotherapeutic group: corticosteroids for systemic use, glucocorticoids
ATC code: H02AB02
Dexamethasone is a mono-fluorinated glucocorticoid with pronounced anti-allergic, anti-inflammatory and membrane-stabilizing properties and effects on carbohydrate, protein and fat metabolism.
Dexamethasone has an approximately 7.5 times greater glucocorticoid effect than prednisolone, and compared to hydrocortisone it is 30 times more effective, lacking mineralocorticoid effects.
Glucocorticoids, such as dexamethasone, exert their biological effects by activating the transcription of corticosteroid-sensitive genes. The anti-inflammatory, immunosuppressive and anti-proliferative effects are caused by decreased formation, release and activity of inflammatory mediators, by the inhibition of specific functions and the migration of inflammatory cells. In addition, the effect of sensitized T lymphocytes and macrophages on target cells may be prevented by corticosteroids.
When long-term corticoid treatment is required, the possibility of induction of transient adrenal insufficiency must be considered. The suppression of the hypothalamic-pituitary-adrenal axis also depends on individual factors.
After oral administration, dexamethasone is rapidly and almost completely absorbed in the stomach and small intestine. Its bioavailability is 80–90%. Maximum blood levels are reached between 60 and 120 minutes. The binding of dexamethasone to plasma albumins is dose-dependent. At very high doses, the largest portion circulates freely in the blood. In hypoalbuminaemia the proportion of the unbound (active) corticoid rises.
The average (serum) elimination half-life of dexamethasone in adults is 250 minutes (+ 80 minutes). Due to its long biological half-life of more than 36 hours, daily continuous administration of dexamethasone can lead to accumulation and overdosing.
The elimination is largely renal in the form of free dexamethasone alcohol. Dexamethasone is partly metabolised, the metabolites are excreted as glucuronates or sulfates, also mainly by the kidneys.
Renal function impairment has no relevant effect on the clearance of dexamethasone. However, the elimination half-life is prolonged in severe liver disease.
In mice and rats, the LD50 for dexamethasone after a single oral dose is 16 g/kg body and over 3 g/kg body weight, respectively, within the first 7 days. Following a single subcutaneous dose, the LD50 in mice is more than 700 mg/kg body weight and in rats about 120 mg/kg body weight, within the first 7 days.
Over a period of 21 days, these values become lower, which is interpreted as a consequence of serious infectious diseases caused by the hormone-induced immunosuppression.
There are no data on chronic toxicity in humans and animals. Corticoid-induced intoxications are not known. In longer-term treatment with doses above 1.5 mg/day, pronounced undesirable effects can be expected (see section 4.8).
The available study findings for glucocorticoids show no evidence of clinically relevant genotoxic properties.
In animal studies, cleft palate was observed in rats, mice, hamsters, rabbits, dogs and primates; not in horses and sheep. In some cases these divergences were combined with defects of the central nervous system and of the heart. In primates, effects in the brain were seen after exposure. Moreover, intrauterine growth can be delayed. All these effects were seen at high dosages.
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