57852-57-0

Orange Solid

Idarubicin HCl is a hydrochloride salt form of Idarubicin which is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL

Orally active anthracycline; analog of Daunorubicin. Antineoplastic

Idarubicin HCl(57852-57-0) is a hydrochloride salt form of Idarubicin which is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL

Orally active anthracycline; analog of Daunorubicin. Antineoplastic

Idarubicin hydrochloride(57852-57-0) is a derivative of daunorubicin indicated for acute nonlymphocytic leukemia, acute lymphocytic leukemia, and acute myeloid leukemia. Compared with daunorubicin, idarubicin hydrochloride is less cardiotoxic, has milder side effects, is orally active and more potent in experimental leukemias. Idarubicin hydrochloride is also reportedly active in daunorubicin-resistant patients, breast cancer,Hodgkin's and non-Hodgkin's lymphoma.

Erbamont (Italy)

ChEBI: Idarubicin hydrochloride is an anthracycline.

Zavedos

Idarubicin(57852-57-0) is available in 5-, 10-, and 20-mL vials for IV administrationin the treatment of acute myeloid leukemia andacute nonlymphocytic leukemia. The compound lacks the4-methoxy group and terminal side-chain alcohol of doxorubicinmaking it the most lipophilic of the four major anthracyclines(doxorubicin, daunorubicin, epirubicin, idarubicin),and it is considered less cardiotoxic than doxorubicin. Theremoval of the 4-methoxy group also increases inhibition oftopoisomerase II. The drug has a fast distributive phase anda high volume of distribution reflecting binding to tissue.Concentrations in blood and bone marrow cells are 100 timeshigher than those found in plasma, reflecting its use in treatingleukemias. Metabolism of the agent primarily occurs byconversion to idarubicinol via reduction of the side chain ketoneto the alcohol, which retains activity as an antineoplastic.Elimination occurs primarily in the bile. Adverse effectsare similar to those found for doxorubicin; however, there isa lower incidence of cardiotoxicity.

Idamycin PFS, Idamycin^?

Increased rates of remission have been noted with the use of idarubicin compared to other anthracyclines antineoplastic agents. Unlike its congeners, idarubicin shows significant oral bioavailability and is lipophilic enough to penetrate the blood-brain barrier. Currently, however, it is given only by the IV route and is not used in the treatment of brain cancer.

Its primary indication is in acute myeloid leukemia, and it is administered in combination with other antileukemic drug.

Common adverse reactions to Idarubicin hydrochloride(57852-57-0) may include nausea and vomiting, mucositis, and some patients may experience serious adverse reactions including transient elevation of hepatic aminotransferases and total bilirubin, alopecia, transient rash, urticaria at the site of injection, and skin toxicity^[1].

Potentially hazardous interactions with other drugs
Other myelosuppressant medication and radiotherapy: increased risk of myelosuppression.
Antipsychotics: avoid concomitant use with clozapine, increased risk of agranulocytosis.
Ciclosporin: concentration increased by ciclosporin.
Cytotoxics: possible increased cardiotoxicity with trastuzumab.
Live vaccines: risk of generalised infections - avoid.

Idarubicin is reduced by aldoketoreductases to idarubicinol, which is as active as the parent drug. Because there is no aromatic methoxy group, there is no O-dealkylation to the C4-phenol. The major metabolite is free, unconjugated idarubicinol. The half-lives of both idarubicin and idarubicinol are 22 and 45 hours, respectively. Idarubicin is administered IV at a dose of 10 to 12 mg/m2 /day for 3 to 4 days, and the idarubicinol metabolite can still be found in therapeutic concentrations in the blood 8 days after administration. Like other anthracyclines, excretion primarily is fecal, with a lesser dependence on renal elimination.

4°C, away from moisture and light

[1] h. dorota halicka, m. fevzi ozkaynak, oya levendoglu-tugal, claudio sandoval , karen seiter, malgorzata kajstura, frank traganos, somasunadaram jayabose, and zbigniew darzynkiewicz. dna damage response as a biomarker in treatment of leukemias. cell cycle. 2009, 8(11): 1720–1724.
[2] haydar ?elik and emel arin?. evaluation of the protective effects of quercetin, rutin, resveratrol, naringenin and trolox against idarubicin-induced dna damage. j pharm pharmaceut sci. 2010, 13(2): 231 – 241.
[3] ching-hon pui, siebold s. n. de graaf, lois w. dow, john h. rodman, william e. evans, bruce s. alpert and sharon b. murphy. phase i