Epirubicin HCl

Systematic Name: (7S,9S)-7-[(2R,4S,5R,6S)-4-amino-5-hydroxy-6-methyloxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione;hydrochloride

Trade Name(s): Ellence

Molecular Formula: C27H30ClNO11

Molecular Weight: 579.98 g/mol

Physical Properties: red-orange powder

Therapeutic Category: antineoplastic agent (anthracycline) 

The API expertise for producing Epirubicin hcl is High Potent.

For more information about High Potency please click here

Epirubicin HCl belongs to a class of drugs termed anthracyclines and is primarily used for the treatment of breast cancers after surgical resection. Anthracyclines are a type of antibiotic isolated from the gram-positive bacteria Streptomyces.

They are commonly used as chemotherapy agents and exert their antineoplastic effects by targeting the replication of DNA. Epirubicin HCl is often preferred over the anthracycline doxorubicin as it has been shown to have fewer side effects.

Epirubicin HCl became FDA approved as an adjuvant therapy for the treatment of axillary node positive breast cancers following resection under the trade name Ellence in 1999.

It is currently manufactured through large-scale semi-synthetic methods using daunorubicin as starting material for its preparation. Semi-synthesis is a type of chemical synthesis that uses compounds isolated from abundant, natural sources as starting material.

Although the exact mechanism for how epirubicin HCl targets cancer cells is unknown, there is evidence for how it may interfere with biological processes essential for cell survival.

First, epirubicin can intercalate between nucleotide bases of DNA, resulting in inhibition of DNA, RNA, and protein synthesis. Intercalation of this drug can also lead to cleavage of DNA by topoisomerase II, resulting in activation of cell death. Epirubicin can also inhibit DNA helicase, an enzyme that separates double-stranded DNA during both replication and transcription.

Lastly, this drug can generate cytotoxic free radicals through the induction of oxidation/reduction reactions. These effects, along with others unknown, may contribute to both inhibition of cancer cell growth and induction of cell death.