Delving into the Latest Updates on Copper Gluconate/Disulfiram with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

DSF-Cu, Dicopp, Disulfiram/copper gluconate

+ [2]

Target

ADHs

Mechanism

ADHs inhibitors(Alcohol dehydrogenases inhibitors)

Therapeutic Areas

NeoplasmsNervous System DiseasesSkin and Musculoskeletal Diseases+ [1]

Active Indication

Breast CancerGlioblastoma

Inactive Indication

Recurrent GlioblastomaMetastatic Pancreatic Cancer

Originator Organization

CANTEX, Inc.

Active Organization

CANTEX, Inc.

Inactive Organization

Cantex Pharmaceuticals, Inc.

Drug Highest PhasePhase 2

First Approval Date-

Regulation-

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Structure/Sequence

Molecular FormulaC12H22CuO14

InChIKeyOCUCCJIRFHNWBP-IYEMJOQQSA-L

CAS Registry527-09-3

View All Structures (2)

This is an open-label Phase 2 Pilot study to evaluate Disulfiram + Copper Gluconate in patients metastatic pancreatic cancer whose CA-19-9 levels rise while receiving nab-paclitaxel (Abraxane) plus gemcitabine (Gemzar) or FOLFIRINOX or single-agent gemcitabine (Gemzar). Patient must have received a minimum of 8 weeks of treatment and have rising CA-19-9 levels in the absence of radiographic evidence of progression.

Start Date17 Oct 2019

Sponsor / Collaborator

Scottsdale Healthcare Corp.

[+1]

NCT03034135

/ CompletedPhase 2

A Phase II, Multicenter, Open-Label, Single-Arm Study to Evaluate the Safety, Tolerability, and Efficacy of DIsulfiram and Copper Gluconate in Recurrent Glioblastoma

This study of DSF-Cu in combination with TMZ for recurrent GBM will evaluate the antitumor effect in patients who have recurrent GBM. Patients will take DSF-Cu daily during their routine standard of care with TMZ therapy for approximately 6 months. Patients will be evaluated for response every 8 weeks. Patients will be followed up 2 years after the last dose of DSF-Cu.

Start Date09 Mar 2017

Sponsor / Collaborator

Cantex Pharmaceuticals, Inc.

100 Clinical Results associated with Copper Gluconate/Disulfiram

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100 Translational Medicine associated with Copper Gluconate/Disulfiram

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100 Patents (Medical) associated with Copper Gluconate/Disulfiram

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634

Literatures (Medical) associated with Copper Gluconate/Disulfiram

01 Dec 2025·Lung

Disulfiram Alleviates MTX-Induced Pulmonary Fibrosis by Inhibiting EMT in Type 2 Alveolar Epithelial Cells

Article

Author: Ma, Ziyi ; Zhang, Linyi ; Lan, Kai ; Li, Rong ; Wu, Xiaohui ; Wang, Chunyang ; Xu, Hong ; Chen, Min ; Zhang, Zhaohua

PURPOSEMethotrexate (MTX)-induced pulmonary fibrosis is associated with high morbidity and mortality, with limited treatment options available. This study investigates whether disulfiram (DSF) can mitigate MTX-induced pulmonary fibrosis and explores the underlying mechanisms.METHODSEight-week-old male mice were divided into control, DSF, MTX, and MTX+DSF groups and treated for 8 weeks. Weight, food, and water intake were monitored. Post-treatment, lung tissues were analyzed using HE and Masson staining, and electron microscopy. Real-time qPCR and ELISA were employed to assess inflammatory markers such as IL-1β and TNF-α in lung tissues and serum. PCR, ELISA, and Western blot were used for fibrotic markers including Col1α1, α-SMA, and hydroxyproline. Type 2 alveolar epithelial cell line MLE12 cells were similarly grouped, followed by RNA sequencing and bioinformatics analysis to elucidate the mechanisms by which DSF exerts anti-MTX-induced pulmonary fibrosis effects. ELISA and Western blot were used to measure E-cadherin and α-SMA expression.RESULTSDSF significantly reduced MTX-induced alveolar septal thickening, pulmonary fibrosis, and inflammatory cell infiltration. It also decreased the expression of inflammatory factors IL-1β and TNF-α, as well as the expression of Col1α1, α-SMA, and others. RNA-seq revealed that DSF induces changes in multiple signaling pathways associated with pulmonary fibrosis, particularly in extracellular matrix-related genes. ELISA and Western blot showed decreased E-cadherin and increased α-SMA in the MTX group, which was partially restored with DSF treatment.CONCLUSIONDSF alleviates MTX-induced pulmonary fibrosis by reducing epithelial-mesenchymal transition (EMT) in type 2 alveolar epithelial cells. Disulfiram shows potential as a therapeutic agent for MTX-induced pulmonary fibrosis.

01 Mar 2025·Journal of Colloid and Interface Science

A novel reactive oxygen species nano-amplifier for tumor-targeted photoacoustic imaging and synergistic therapy

Article

Author: Fan, Yadi ; Zhang, Li ; Yang, Mo ; Yang, Zhe ; Wong, Chun-Yuen

Intracellular redox homeostasis and the type of exogenous Fenton reagent play crucial roles in determining the efficacy of chemodynamic therapy (CDT). Herein, we succeeded for the first time in preparing ultrasmall copper sulfide (CuS) nanodots (1-2 nm)-embedded hollow mesoporous organosilica nanoparticle (HMON), which served as an ideal nanocarrier to load both 3-amino-1,2,4-triazole (3-AT) and disulfiram (DSF) after folate-polyethylene glycol-silane (FA-PEG-Silane) modification. The as-prepared nanoplatform (3-AT/DSF@CuS/HMON-FA, denoted as ADCuSi-FA) was found to regulate intracellular redox homeostasis once internalized by 4T1 cells, showing rapid glutathione (GSH)-responsive 3-AT, DSF and Cu⁺ ions release. Specifically, 3-AT restrained the endogenous hydrogen peroxide (H₂O₂) consumption by suppressing catalase (CAT) activity, thereby augmenting hydroxyl radical (OH) generation via Cu⁺-based Fenton-like reaction. DSF, upon complexation with Cu²⁺, exhibited enhanced chemotherapeutic efficacy, while the by-product Cu⁺ ions further boosted the efficacy of CDT. Additionally, CuS nanodots enabled near-infrared-II (NIR-II) photothermal therapy (PTT) and facilitated photoacoustic (PA) imaging, with the ensuing hyperthermia expediting the CDT process. As expected, the tumor growth was dramatically inhibited with PTT/chemotherapy co-synergized CDT. This work offers an innovative paradigm for cooperative cancer treatment as well as new insights into the fabrication of biodegradable inorganic/organic hybrid materials.

01 Feb 2025·Cancer Letters

Disulfiram impairs USP21-mediated MOF-K257 deubiquitination to inhibit esophageal squamous cell carcinoma progression

Article

Author: Zhu, Yilin ; Sui, Huacong ; Zhang, Yifan ; Mu, Ning ; Zhao, Xiaogang ; Jiang, Yunfeng ; Zhao, Yunpeng ; Tian, Zhongxian ; Fan, Guangyan ; Yang, Lingxiao ; Ding, Yi ; Hong, Yilang ; Song, Xiangqing ; Wang, Jiaxu ; Li, Peichao ; Zhao, Shuyong ; Cui, Xiujie

Disulfiram (DSF), primarily applied in the therapy for alcohol addiction, has been demonstrated to possess the promising capability of anti-tumor in many human cancers, including esophageal squamous cell carcinoma (ESCC). To date, almost all studies about DSF in ESCC are focusing on investigating either drug combinations or nanoparticle-based delivery systems. However, the exact molecular mechanisms mediating the response to DSF in ESCC are totally unknown. An increasing number of studies reported that aberrant expression of acetylation-related genes is closely involved in regulating the response of cancer cells to anti-tumor drugs. Here, we defined DSF-sensitive and -resistant cells by measuring the half-maximal inhibitory concentration (IC₅₀) of DSF in four ESCC cell lines, followed by detecting the protein expression of nine dysregulated histone acetyltransferase (HAT) genes in ESCC. Our results demonstrate that MOF is responsible for the sensitivity to DSF in ESCC cells. Consistently, DSF treatment markedly abolished MOF-driving ESCC progression and Wnt/β-Catenin signaling activation. Interestingly, DSF decreased MOF protein expression via the ubiquitin-proteasome system. Further exploration verified the essential role of USP21, among three candidates (USP2, USP21, and USP10), in DSF-mediated MOF protein levels. Mechanistically, USP21 binds to MOF protein and decreases the ubiquitination of its K257 site, while DSF notably impedes MOF-mediated ESCC malignant progression and Wnt/β-Catenin signaling activation by blocking USP21-governed MOF-K257 deubiquitination. In conclusion, our study elucidates the USP21/MOF-K257 axis regulating the response to DSF in ESCC, which provides novel and key evidence for the clinical application of DSF in individualized therapy for ESCC patients.

1

News (Medical) associated with Copper Gluconate/Disulfiram

14 Sep 2021

·www.biospace.com

Cantex Pharmaceuticals Announces Sale of Equity Interest in Chimerix, Inc.

WESTON, Fla., Sept. 14, 2021 /PRNewswire/ -- Cantex Pharmaceuticals ("Cantex") today announced that it has sold 6.5 million shares of Chimerix, Inc., in brokerage transactions at a price of $5.75 per share, less brokerage commissions and fees. About Cantex Pharmaceuticals Cantex Pharmaceuticals, Inc. is a privately-held, clinical stage pharmaceutical company focused on the transformation of known drugs into innovative products with blockbuster potential. Cantex is currently developing novel cancer treatments. Cantex's pipeline consists of three product candidates in Phase 2 and Phase 3 development for diseases with significant unmet medical needs: Azeliragon for life-threatening and disabling complications of cancer, Dicopp® for hematologic malignancies, and DSTAT, licensed to Chimerix, Inc., as a first-line therapy of acute myeloid leukemia. For more information, please visit . Cantex Contacts Investors: Stephen G. Marcus, M.D. (954) 315-3660 smarcus@cantex.com or Media: Jason Rando Tiberend Strategic Advisors (917) 930-6346 jrando@tiberend.com

100 Deals associated with Copper Gluconate/Disulfiram

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R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Breast Cancer	Phase 2	-	CANTEX, Inc.	-
Glioblastoma	Phase 2	-	CANTEX, Inc.	-
Metastatic Pancreatic Cancer	Discovery	US	Cantex Pharmaceuticals, Inc.	17 Oct 2019
Recurrent Glioblastoma	Discovery	US	Cantex Pharmaceuticals, Inc.	09 Mar 2017

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03714555 (CTgov)	Phase 2	Metastatic Pancreatic Cancer	1	AE Assessment+nab-paclitaxel+disulfiram/copper gluconate+Gemzar+Disulfiram+gemcitabine+Copper Gluconate (Nab-Paclitaxel/Gemcitabine + DSF/Cu)	tmxnsvfids(gnxwetfyvu) = lvattwpxgn ufoppfkomx (noizuoaofm, mgmqxsgygy - yknnpfnfpw) View more	-	18 Oct 2023
				AE Assessment+nab-paclitaxel+disulfiram/copper gluconate+Gemzar+Disulfiram+gemcitabine+Copper Gluconate (FOLFIRINOX +DSF/Cu)	tmxnsvfids(gnxwetfyvu) = jonwwcrhme ufoppfkomx (noizuoaofm, udxvimonrs - qisqjivhcf) View more
NCT03034135 (ACTR-21, CTgov)	Phase 2	Recurrent Glioblastoma	23	Temozolomide (TMZ)+Disulfiram/Copper	(vdtlvdhqri) = frltmzhxhp wdcyxklurv (tvrfuxxhgu, umhdpyijnw - cynidyovsx) View more	-	13 Sep 2021
EXTH-61 (SNO2020)	Not Applicable	Recurrent Medulloblastoma ALDH \| Nestin- \| CD133-positive	-	Disulfiram	nthfcgumhh(asdswhoeig) = DSF/Cu++ induced cell death (increased AnnV/PI, cleaved-Poly(ADP-ribose)polymerase fraction, and Apoptosis Inducing Factor on WB/FC/IF, in vitro and ex vivo) through NPL4 accumulation in cell nucleus and intracellular buildup of poly-ubiquitylated proteins qzjlvikunc (eyduuiedvn ) View more	Positive	09 Nov 2020
				Copper
PDTM-06 (SNO2019)	Not Applicable	Medulloblastoma	24	Disulfiram-Copper (DSF-Cu++)	vefsihaupf(iuorbyxjta) = ebtmmpydte xlsmwtiytj (ojeccmskzh )	Positive	11 Nov 2019
				Disulfiram-Copper (Control (No treatment))	vefsihaupf(iuorbyxjta) = nxwiznkwoi xlsmwtiytj (ojeccmskzh )