Duocarmycin A 

Duocarmycin A is an antitumor antibiotic and DNA alkylating agent with broad-spectrum antibacterial activity, which can serve as a payload for synthesizing antibody-drug conjugates (ADCs). Duocarmycin A selectively binds to the AT-rich minor groove of DNA, forms covalent adducts by alkylating the adenine N3 residue, thereby disrupting DNA structure and inhibiting its replication and transcription. Duocarmycin A induces apoptosis, sub-G1 phase accumulation and chromatin condensation, reduces the levels of pro-caspase-3/9, and induces p53-independent p21 expression. Duocarmycin A is widely used in the research of various malignancies, including leukemia, sarcoma, glioblastoma, as well as multiple solid tumor models such as lung cancer, breast cancer, and colorectal cancer^[1][2][3].

Duocarmycin A (0.0016-0.0064 μg/ml; 0.032-42 μg/ml) potently inhibits the growth of Gram-positive bacterial strains (MIC 0.0016-0.0064 μg/ml) and exhibits variable inhibitory activity against Gram-negative bacterial and fungal strains (MIC 0.032-42 μg/ml)^[1].
Duocarmycin A (0.003-0.03 μg/mL) induces intrinsic pathway apoptosis and G₁ phase cell cycle arrest in HLC-2 cells in vitro in a dose-dependent manner, with altered expression of key apoptotic proteins (caspase-3, caspase-9, Bax) at 0.03 μg/mL^[2].
Duocarmycin A (0.003-0.03 μg/ml; 72 h) induces concentration-dependent apoptosis in HLC-2 cells, with 27% apoptosis at 0.003 μg/ml and 51% apoptosis at 0.03 μg/ml after 72 h of treatment, accompanied by characteristic apoptotic nuclear morphology^[3].
Duocarmycin A (0.003-0.03 μg/ml; 24-72 h) induces time- and concentration-dependent accumulation of apoptotic sub-G1 phase cells in HLC-2 cultures, with higher sub-G1 populations observed at 0.03 μg/ml compared to 0.003 μg/ml across 24, 48, and 72 h treatments^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Duocarmycin A (0.0075-0.04 mg/kg; i.p., i.v.; single dose) exhibits potent in vivo anti-tumor activity against murine sarcoma 180 in ddY mice; at a single intravenous (i.v.) dose of 0.03 mg/kg, its T/C ratio can be as low as 0.26^[1].
Duocarmycin-based B2M-ADC selectively targets senescent cancer cells and reduces their viability in in vivo models, with its activity exhibiting senescence phenotype specificity^[2].
Galactose-modified Duocarmycin can selectively induce cell death in senescent cancer cells in mice by targeting SA-β-gal activity^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

507.49

C₂₆H₂₅N₃O₈

118292-34-5

O=C([C@@](N1)(C)C(C([C@@]23[C@@](C3)([H])CN(C(C(N4)=CC5=C4C(OC)=C(OC)C(OC)=C5)=O)C2=C6)=C1C6=O)=O)OC

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. TAKAHASHI I, et al. Duocarmycin A, a new antitumor antibiotic from Streptomyces[J]. The Journal of antibiotics, 1988, 41(12): 1915-1917.

  [2]. Morcos A, et al. A Comprehensive Review of the Antitumor Properties and Mechanistic Insights of Duocarmycin Analogs. Cancers (Basel). 2024;16(19):3293. Published 2024 Sep 27.  [Content Brief]

  [3]. Hirota M, et al. Distamycin A enhances the cytotoxicity of duocarmycin A and suppresses duocarmycin A-induced apoptosis in human lung carcinoma cells. Int J Biochem Cell Biol. 2007;39(5):988-996.  [Content Brief]