Dp44mT is an iron chelator, possessing DNA-damaging activity mediated by top2a inhibition.
Chemical Formula: C14H15N5S
Exact Mass: 285.1048
Molecular Weight: 285.369
Elemental Analysis: C, 58.93; H, 5.30; N, 24.54; S, 11.23
Iron Chelator, Dp44mT
Dp44mT, >=98% (HPLC)
di-2-pyridyl ketone 4,4-dimethylthiosemicarbazone
Appearance: Solid powder
Purity: >98% (or refer to the Certificate of Analysis)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility: Soluble in DMSO
Shelf Life: >2 years if stored properly
Drug Formulation: This drug may be formulated in DMSO
Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code: 2934.99.9001
Dp44mT is cytotoxic to breast cancer cells, at least in part, due to selective inhibition of top2α. Dp44mT alone induced selective cell killing in the breast cancer cell line MDA-MB-231 when compared with healthy mammary epithelial cells (MCF-12A). It induces G1 cell cycle arrest and reduces cancer cell clonogenic growth at nanomolar concentrations. Dp44mT, but not the iron chelator desferal, induces DNA double-strand breaks quantified as S139 phosphorylated histone foci (γ-H2AX) and Comet tails induced in MDA-MB-231 cells. Doxorubicin-induced cytotoxicity and DNA damage are both enhanced significantly in the presence of low concentrations of Dp44mT. The chelator caused selective poisoning of DNA topoisomerase IIα (top2α) as measured by an in vitro DNA cleavage assay and cellular topoisomerase-DNA complex formation. Dp44mT targets lysosome integrity through copper binding. Copper binding is essential for the potent antitumor activity of Dp44mT, as coincubation with nontoxic copper chelators markedly attenuated its cytotoxicity.
Al-Akra L, Bae DH, Sahni S, Huang MLH, Park KC, Lane DJR, Jansson PJ, Richardson DR. Tumor stressors induce two mechanisms of intracellular p-glycoprotein-mediated resistance that are overcome by lysosomal-targeted thiosemicarbazones. J Biol Chem. 2018 Jan 5. pii: jbc.M116.772699. doi: 10.1074/jbc.M116.772699. [Epub ahead of print] PubMed PMID: 29305422.
Kang YJ, Kuo CF, Majd S. Nanoparticle-based delivery of an anti-proliferative metal chelator to tumor cells. Conf Proc IEEE Eng Med Biol Soc. 2017 Jul;2017:309-312. doi: 10.1109/EMBC.2017.8036824. PubMed PMID: 29059872.
Moussa RS, Kovacevic Z, Bae DH, Lane DJR, Richardson DR. Transcriptional regulation of the cyclin-dependent kinase inhibitor, p21(CIP1/WAF1), by the chelator, Dp44mT. Biochim Biophys Acta. 2017 Oct 13. pii: S0304-4165(17)30330-6. doi: 10.1016/j.bbagen.2017.10.009. [Epub ahead of print] PubMed PMID: 29032246.
Abayaweera GS, Wang H, Shrestha TB, Yu J, Angle K, Thapa P, Malalasekera AP, Maurmann L, Troyer DL, Bossmann SH. Synergy of Iron Chelators and Therapeutic Peptide Sequences Delivered via a Magnetic Nanocarrier. J Funct Biomater. 2017 Jun 26;8(3). pii: E23. doi: 10.3390/jfb8030023. PubMed PMID: 28672849; PubMed Central PMCID: PMC5618274.
Nam SY, Han NR, Yoon KW, Kim HM, Jeong HJ. Di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT), an anticancer agent, exerts an anti-inflammatory effect in activated human mast cells. Inflamm Res. 2017 Oct;66(10):871-879. doi: 10.1007/s00011-017-1067-x. Epub 2017 Jun 14. PubMed PMID: 28616734.
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