Immunomodulators and Antineoplastics

Glucocorticoid

Sedating antihistamine

Less sedating antihistamine

Less sedating antihistamine

Folic acid antagonist

IL-1 receptor antagonist

Anti-androgen

Synthetic corticosteroid

GnRH agonist

Selective oestrogen receptor modulator

Aromatase inhibitor

Synthetic corticosteroid

Corticosteroids regulate gene expression, which results in: • Glucocorticoid effects, e.g. gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses • Mineralocorticoid effects, e.g. hypertension, sodium and water retention, potassium loss

Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form They also have anticholinergic activity and some have alpha-blocking activity

Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form

Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form

Inhibits DNA synthesis and cell replication by competitively inhibiting the conversion of folic acid to folinic acid as it resembles the structure of folic acid It has cytotoxic, immunosuppressive and anti-inflammatory action

Recombinant form of human interleukin-1 (IL-1) receptor antagonist; it neutralises the activity of IL-1, which is involved in acute inflammatory response

Competitively inhibits the binding of androgen at androgen receptors Cyproterone (a steroidal anti-androgen) also has progestogenic effects that result in decreased production of testosterone

Regulates gene expression, which results in mainly glucocorticoid effects, but also some mineralocorticoid effects Acts as an anti-inflammatory and immunosuppressant, mimicking the effect of cortisol but with 20 to 30 times the potency. It is 4 to 5 times more potent than prednisone With steroid treatment, it is critical to progressively reduce dosage rather than stop administration abruptly. This is because the adrenal glands significantly reduce steroid production when levels are high (due to treatment) and it takes some weeks to recover from induced adrenal insufficiency

GnRH initially stimulates synthesis of FSH and LH, transiently increasing serum testosterone in males or serum oestrogen in females Continuous administration of GnRH agonists inhibits gonadotrophin production, suppressing ovarian and testicular steroidogenesis and inhibiting the growth of certain hormone-dependent tumours

Competes with oestrogen for receptor sites in breast tissue (anti-oestrogenic effect) inhibiting tumour growth Also have oestrogen agonist activity on endometrium, bone and lipids Suppression of other growth factors and cytokines may occur

Aromatase enzymes (in fat, liver, muscle and breast tissue of postmenopausal women) convert circulating androstenedione and testosterone to oestriol and oestradiol Aromatase inhibitors reduce tissue oestrogen concentration

Regulates gene expression, which results in both glucocorticoid and mineralocorticoid effects In the kidney, cortisol is a potent agonist of the mineralocorticoid receptor. However, these mineralocorticoid receptors are ‘shielded’ from cortisol by the action of 11β-HSD 2, which converts active cortisol into inactive cortisone. This mechanism ensures that, at physiologic levels, cortisol does not exert mineralocorticoid effects At high concentrations, however, cortisol can overwhelm the capacity of 11β-HSD 2, leading to stimulation of renal mineralocorticoid receptors