DpC hydrochloride 

DpC hydrochloride is a selective, orally active iron chelator with anticancer activity. DpC hydrochloride acts on signaling pathway-related targets such as JNK, NF-κB, and its activity is competitively inhibited by another iron chelator Dp44mT (HY-18973). By chelating intracellular iron and copper ions in tumor cells to form redox-active complexes, DpC hydrochloride induces oxidative stress, activates the JNK, NF-κB pathways and downregulates IκBα, upregulates the expressions of neuroglobin and cytoglobin, activates caspase 3/9 to induce tumor cell apoptosis. It also overcomes P-glycoprotein-mediated multidrug resistance through a lysosome-targeting mechanism, and exhibits broad-spectrum synergistic effects when combined with various chemotherapeutic agents. DpC hydrochloride inhibits tumor metastasis and increases TNF-α levels in the tumor microenvironment to enhance endogenous immune responses. DpC hydrochloride is applicable to the research of various malignancies including neuroblastoma, pancreatic cancer, prostate cancer, lung cancer, and breast cancer^[1][2][3].

DpC (24 h; 72 h) hydrochloride exhibits potent and selective antiproliferative activity against PANC-1, PC3, DMS-53, DU-145 and MDA-MB-231 tumor cells. Meanwhile, it produces synergistic effects in combination with 9 clinical chemotherapeutic agents including Abiraterone (HY-70013), Carboplatin (HY-17393), Cisplatin (HY-17394) and Doxorubicin (HY-15142), but shows antagonistic effects when combined with Dp44mT^[1].
Uptake of ¹⁴C-DpC (25 μM; 2 h) hydrochloride by SK-N-MC neuroepithelioma cells depends on temperature- and energy-dependent regulatory mechanisms, and DpC hydrochloride competes with Dp44mT for the same cellular uptake carrier/receptor^[1].
DpC (25 μM; 24 h) hydrochloride exhibits antiproliferative activity against MSC, H9C2, MIHA, HK2 and SK-N-LP cells, with significantly higher activity in SK-N-LP cells than Dp44mT and L1. It also significantly upregulates the expressions of neuroglobin (Ngb) and cytoglobin (Cygb) in SK-N-LP and HK2 cells, increases the levels of phosphorylated JNK, cleaved caspase 3 and cleaved caspase 9, and decreases the level of IkBα^[2].

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

DpC (4 mg/kg; tail vein injection; once daily; 3 weeks) hydrochloride significantly reduces tumor imaging ROI values and tumor volumes, increases the levels of Annexin V (+)/PI (+) cells, caspase 3, neuroglobin, cytoglobin and TNFα, slightly decreases IL-10 levels in tumor tissues, slightly inhibits body weight gain of mice, and does not cause obvious toxicity but induces pulmonary exudative inflammation in an orthotopic SK-N-LP/Luciferase neuroblastoma xenograft model in the left adrenal fat pad of nude mice^[2].

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

389.95

C₁₉H₂₄ClN₅S

1382469-40-0

S=C(N(C1CCCCC1)C)N/N=C(C2=NC=CC=C2)\C3=NC=CC=C3.Cl

Room temperature in continental US; may vary elsewhere.

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

• [1]. Guo ZL, et al. The novel thiosemicarbazone, di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone (DpC), inhibits neuroblastoma growth in vitro and in vivo via multiple mechanisms. J Hematol Oncol. 2016 Sep 27;9(1):98.  [Content Brief]

  [2]. Lin Y, et al. Synthesis and in vivo distribution of 2-deoxy-2-aminodiglucose–prednisolone conjugate (DPC). Chinese Chemical Letters, 2012, 23(5): 557-560.

  [3]. Dharmasivam M, et al. The thiosemicarbazone, DpC, broadly synergizes with multiple anti-cancer therapeutics and demonstrates temperature- and energy-dependent uptake by tumor cells. Biochim Biophys Acta Gen Subj. 2022;1866(8):130152.  [Content Brief]