Catalog Product Name CAS Number Molecular Formula Molecular Weight
BADC-00042 Daunomycin 20830-81-3 C27H29NO10 527.52
BADC-00811 Duocarmycin DM (free base) 1116745-06-2 C26H26ClN3O3 463.96 g/mol
BADC-00041 Daunorubicin hydrochloride 23541-50-6 C27H30ClNO10 563.98
BADC-00038 Doxorubicin hydrochloride 25316-40-9 C27H30ClNO11 579.98
BADC-00028 DOXO-EMCH 151038-96-9 C37H42N4O13 750.75
BADC-00027 INNO-206 1361644-26-9 C37H42N4O13 750.75
BADC-00033 PNU-159682 202350-68-3 C32H37NO12 627.64
BADC-00043 Daun02 290304-24-4 C41H44N2O20 884.79
BADC-00363 Aldoxorubicin hydrochloride 480998-12-7 C37H43ClN4O13 787.21
BADC-00685 MCC-Modified Daunorubicinol 721945-30-8 C39H44N4O13 776.79

Since the first anthracycline anticancer drug Daunorubicins (DNRs) were isolated in 1957, anthracycline antibiotics have become one of the most effective chemotherapeutic drugs widely used in clinic. The anthracycline antibiotics, of which Daunorubicins (Daunomycin) and Doxorubicins (Adriamycin, DOXs) are the parent compounds, are widely used in cancer chemotherapy. As an anti-tumor antibiotic, Daunorubicins are the first-line drug for the treatment of acute leukemia, chronic myeloid leukemia, malignant lymphoma, non-small cell lung cancer, breast cancer. Doxorubicins were isolated from Str. peucetius var. caesius in 1969, which has strong anticancer activity and high chemotherapy index. Research have shown that there is a close relationship between the intercalation of anthracycline drugs into DNA strand and their anticancer activity. Daunorubicins and Doxorubicins are arguably the best characterized DNA intercalators. These compounds are important models for understanding how small molecules interact with DNA in a sequence-specific manner.

Chemical structure

Anthracycline antibiotics are composed of a tetracyclic chromophore (glycosidic ligand) linked to one or more glycosyl or glucosamine through glycosidic bonds. Different anthracyclines have different ligands or glycosyls. The structure of Doxorubicins is very similar to Daunorubicins, that is, the H atom at 14 C of Daunorubicins replaced by OH to obtain Doxorubicins. Therefore, Doxorubicins can also be prepared by chemical synthesis of Daunorubicins.

Mechanism of action

The mechanism of anthracycline antibiotics indicated that anthraquinone rings were inserted and paralleled between the base pairs of double-stranded DNA by non-specific insertion, thus forming a relatively stable anthracene ring-DNA complex. The long axis of anthracycline is basically perpendicular to the hydrogen bond of the base pair, and the amino group of the glucosamine is combined with the phosphate group of DNA by ionic bond. This embedding effect changes the distance between the base pairs, thus changing the template properties of DNA. Changes in nucleic acid structure inhibit DNA replication and RNA transcription and affect the proliferation of rapidly growing tumor cells.

Furthermore, anthracyclines are also involved in the redox process to generate free radicals and eventually form reactive oxygen species fragments (O-, -OH, 1O2, etc.). These fragments are very active and directly act on biological targets (DNA, cell membrane, etc.) without protein-mediated, which play a special role in destroying the structure and function of biological targets.

The anticancer mechanism of Daunorubicins is mainly that it can produce daunorubicinol through liver metabolism, which changes the DNA topology by embedding the DNA base pairs of cancer cells. It affects gene expression by inhibiting the activity of DNA polymerase and damaging DNA, so as to kill tumor cells and treat cancer.

Doxorubicins are cell cycle non-specific drug. It is mainly inserted between DNA base pairs and tightly bound to DNA, thereby preventing DNA replication, inhibiting the role of DNA-dependent polymerase and interfering with RNA transcription. This effect of preventing cell division cannot selectively distinguish tumor cells from normal cells, so as most chemotherapy drugs, Doxorubicins have many adverse reactions.


At present, the classic scheme for clinical treatment of acute myeloid leukemia (AML) is anthracycline combined with cytarabine (Ara-C). The clinical complete remission rate of AML (except M3) treated with cytarabine combined with anthracyclines is about 80%-90%. The clinical complete remission rate of Daunorubicins combined with cytarabines in the treatment of AML was about 65.0%. In recent years, with the increasing binding capacity of DNA to idarubicin (IDA) and its less toxic side effects on human heart, IDA has been widely used in clinical treatment.

To reduce cardiac toxicity, Doxorubicins is mainly used in combination with liposomes for clinical application. At present, two kinds of Doxorubicins-liposomes drugs were listed abroad. That is, polyethylene glycol (PEG) modified long-acting circulating liposomes (PLD) and non-PEG modified conventional liposomes (NPLD). PEG-modified Doxorubicins-liposomes are mainly used in the treatment of recurrent ovarian cancer and AIDS-related Kaposi’s. However, non-PEG modified Doxorubicins-liposomes are widely used in the treatment of metastatic breast cancer.


  1. Leng; et al. Base specific and regioselective chemical cross-linking of daunorubicin to DNA. J. Am. Chem. Soc., 1996, 118: 473-4728.
  2. Chegaev, K.; et al. Nitric oxide donor doxorubicins dccumulate into doxorubicin-resistant human colon cancer cells inducing cytotoxicity. ACS Med. Chem. Lett., 2011, 2: 494–497.
* Only for research. Not suitable for any diagnostic or therapeutic use.

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