Epirubicin is favoured over doxorubicin, the most popular anthracycline, in some chemotherapy regimens as it appears to cause fewer side-effects.

Epirubicin has a different spatial orientation of the hydroxyl group at the 4' carbon of the sugar - it has the opposite chirality - which may account for its faster elimination and reduced toxicity.

The aim of Epirubicin as adjuvanted therapy is to eradicate micro metastasis and prolong disease free survival.

The combination of Epirubicin and tamoxifen lead to an increase survival in node-positive postmenopausal women with hormone receptor-positive breast tumours.

Additionally the administration of more dose intensive epirubicin-containing regimens to patients with metastatic breast cancer has been associated with improved response rates, but not increased overall survival.

[4] Epirubicin first forms a complex with DNA by intercalation of its planar rings between nucleotide base pairs.

(Pharmacia & Upjohn Company LLC, 1999) This inhibits replication and transcription and triggers DNA cleavage by topoisomerase II.

Epirubicin then stabilizes the topoisomerase II-DNA complex, resulting in irreversible DNA strand breakage, leading to cell death.

[5] Epirubicin is also capable of generating cytotoxic free radicals, which are very reactive against DNA, cell membranes and mitochondria.

[6] Epirubicin is rapidly metabolized by the liver to relatively or totally inactive metabolites: epirubicinol, 2 glucuronides and 4 aglycones.

However, there is good evidence to suggest that cardiotoxicity is caused at least in part by the avid interaction of anthracyclines with iron, resulting in the formation of metal ion complexes.

Those could be related with radiation recall and local reactions such as cellulitis, which cause development of tissue necrosis and pain if extravasation damage occurs.

[3] Finally, the most adverse effect is secondary leukemia produced by breast cancer treated with epirubicin, particularly in those cases in which the patient receives concomitant alkylating agent therapy.

Due to numerous ionisable groups, it has multiple pka (pKa1 = 9.17 (phenol); pKa2 = 9.93 (amine); pKa3 = 12.67 (hydroxyl)) and is soluble in a variety of solvents (DMSO 125 mg/mL; Ethanol 120 mg/mL; In water, 93 mg/L at 25 °C (est)).

as the time it takes to degrade 10% from the initial concentration) has been documented as at least 14 and 180 days at 25 °C and 4 °C, respectively in a 0.9% sodium chloride solution in polypropylene syringes.

One pathway[19] starts from Daunorubicin, a common byproduct found in fermentation, since it is relatively easily available and already structurally similar to the product (only requiring minor alterations).

Secondly, the focus shifts to carbon number 13 where it is necessary to add a hydroxide group which is achieved by bromination followed by a reaction with an alkali salt of formic acid and water to give the final product.

There is an older variant of this pathway[20] which involves first splitting the Daunorubicin, into daunomycin one and daunosamine methyl ether, using methanol.

[21] Upjohn applied for approval by the U.S. Food and Drug Administration (FDA) in node-positive breast cancer in 1984, but was turned down because of lack of data.

In 1999 Pharmacia (who had by then merged with Upjohn) received FDA approval for the use of epirubicin as a component of adjuvant therapy in node-positive patients.