Dequalinium Chloride targets mitochondria in carcinoma cells, acting as a mitochondrial poison by blocking mitochondrial enzymes, specifically the mitochondrial enzyme F1-ATPase via direct binding and subsequent inhibition. It also inhibits protein kinase C (PKC). [1]
Dequalinium Chloride targets multiple cellular components. It is a selective blocker of apamin-sensitive K+ channels. It also functions as an antagonist of α7 nAChR. As a cationic, lipophilic compound, it acts as a mitochondrial poison. This multi-target profile contributes to its broad antimicrobial activity and its effects on cellular ion channels and mitochondrial function. It exhibits broad bactericidal and fungicidal activity.

Dequalinium chloride (DECA) is a cationic, lipophilic compound with structure similar to the dye rhodamine 123. DECA is selectively accumulated and retained within the mitochondria of carcinoma cells where it acts as a mitochondrial poison by blocking mitochondrial enzymes which can then disrupt cellular energy production, eventually resulting in cell death. Dequalinium Chloride is a blocker of ganglionic transmission (EC50 = 2 μM). Dequalinium is a potent inhibitor of apamin-sensitive K+ channels in hepatocytes and of nicotinic responses in skeletal muscle. Dequalinium blocks angiotensin II-evoked K+ loss with an IC50 of 1.5 μM and also inhibited125I - monoiodoapamin binding with Ki of 1.1 μM. Dequalinium produces a rapid and reversible inhibition of the slow apamin-sensitive component of the afterhyperpolarization (AHP) which follows a single action potential in cultured rat sympathetic neurons. Dequalinium Chloride (DECA) is a dicationic lipophilic PKC inhibitor. When exposed to UV light, DECA covalently binds to and irreversibly inhibits PKCα and PKCβ.
Cell Assay: DECA, as a mitochondrial poison, is an agent with capable of potentiating the effects of tumor necrosis factor against ovarian cancer cell lines.

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Dequalinium Chloride was previously shown by the authors to synergize the in vitro antitumor effects of tumor necrosis factor (TNF) against a panel of human ovarian cancer cell lines. However, no detailed in vitro experimental data (e.g., IC50, cell viability, apoptosis) are presented in this paper. The combination of Dequalinium Chloride and TNF resulted in enhanced tumor cell killing in vitro, as referenced from earlier studies (Manetta et al., 1990, 1991). [1]
In vitro, Dequalinium Chloride exhibits broad bactericidal and fungicidal activity. It is a selective blocker of apamin-sensitive K+ channels. It also functions as an antagonist of α7 nAChR. Its activity as a mitochondrial poison has been characterized in various cell-based assays. These in vitro studies confirm its diverse mechanisms of action and its potential as an antimicrobial agent. It is used in wound dressings and for mouth infections.

In mice bearing bladder MB49 tumors, Dequalinium chloride (2 mg/kg/d, i.p.) displays anticarcinoma activity with T/C of 210%.
In the PA-1 human ovarian cancer xenograft model, treatment with single-agent Dequalinium Chloride (5 mg/kg every other day, IP) initiated 3 days post-tumor injection increased animal survival by 37% (P=0.002) compared to controls. When treatment was delayed until day 7 (histologically confirmed tumor), single-agent Dequalinium Chloride increased survival by 23% (P=0.04). In the UCI-101 ovarian tumor model (initiated day 6), single-agent Dequalinium Chloride increased survival by 28% (P=0.04). Sequential treatment with Dequalinium Chloride followed by TNF resulted in survival increases of 45% (PA-1, day 3, P=0.0002), 23% (PA-1, day 7, P=0.04), and 41% (UCI-101, P=0.003). No statistical differences were detected between single-agent Dequalinium Chloride and combination DECA+TNF except in the UCI-101 model, where the apparent potentiation was due to the stimulatory effects of TNF alone. [1]
In vivo, Dequalinium Chloride is used topically as a bacteriostat in wound dressings and for mouth infections. It has been used in the treatment of vaginal infections. However, its use may cause skin ulceration. Its systemic effects are limited due to its topical application. Its efficacy as an antimicrobial agent has been demonstrated in clinical settings. It is not intended for systemic use.

The paper mentions that Dequalinium Chloride inhibits the mitochondrial enzyme F1-ATPase by direct binding (citing Zhou and Allison, 1988),[1]
Non-cellular assays for Dequalinium Chloride are not typically performed, as its mechanism involves interaction with ion channels and mitochondria rather than direct enzyme inhibition. However, its binding to apamin-sensitive K+ channels can be studied using radioligand binding assays with membrane preparations. Its antagonism of α7 nAChR can be assessed using electrophysiological techniques in oocytes or other expression systems. These assays are essential for characterizing its receptor and channel interactions.

The authors reference previous in vitro work showing that Dequalinium Chloride synergizes with TNF and interferon-gamma against human ovarian cancer cell lines, but the present paper focuses on in vivo studies and does not include any original cell-based experimental procedures or results. [1]
In vitro cell-based assays for Dequalinium Chloride are conducted using various cell types to assess its antimicrobial activity and its effects on ion channels and mitochondria. For example, its antimicrobial activity can be assessed using bacterial and fungal culture systems. Its effects on K+ channels can be studied in cells expressing these channels. Its mitochondrial toxicity can be assessed by measuring mitochondrial membrane potential or ATP levels. These experiments are crucial for confirming its mechanisms of action.

Dissolved in water using a bath sonicator; 2 mg/kg; i.p. injection Mice bearing bladder MB49 tumors

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Female Balb/c athymic nude mice (8-10 weeks old) were used. Ovarian cancer xenografts were established by intraperitoneal (IP) injection of 2.0 × 10^7 PA-1 or UCI-101 human ovarian cancer cells. Dequalinium Chloride was dissolved in sterile water using a water bath sonicator, and subsequent dilutions were prepared in physiological saline containing 0.2% fetal calf serum. For the PA-1 model, treatments were initiated either on day 3 (tumor implantation not histologically confirmed) or day 7 (histologically confirmed microscopic tumor implantation). For the UCI-101 model, treatments began on day 6 (histologically confirmed). Dequalinium Chloride was administered IP at a dose of 5 mg/kg every other day (qod). Combination treatment consisted of Dequalinium Chloride given on day 1, followed by TNF (recombinant human TNF-α, 0.5 μg/mouse) on the subsequent day; animals received only one drug per day. All mice received daily IP injections of either drug or vehicle (saline with 0.2% fetal calf serum, 0.5 ml/mouse) in alternating abdominal quadrants. Drug treatments were discontinued 60 days post-implantation. In the UCI-101 model, drugs were discontinued on day 56 due to observed toxicity. [1]
In vivo animal studies for Dequalinium Chloride are limited due to its primary use as a topical agent. However, its efficacy in treating vaginal infections has been studied in animal models. Topical application of the compound to infected areas is typically used to assess its antimicrobial efficacy. Systemic toxicity studies may be conducted to evaluate its safety profile. However, specific detailed protocols are not extensively documented.

Dequalinium Chloride has a molecular weight of 527.57 g/mol and a molecular formula of C30H40Cl2N4. It is a cationic, lipophilic compound. As a topical agent, its systemic absorption is expected to be minimal. Its pharmacokinetic properties are not extensively documented due to its topical use. It is available for research purposes and as a topical antimicrobial agent.

In the UCI-101 ovarian tumor model, drug treatment (including Dequalinium Chloride alone and in combination with TNF) was discontinued on day 56 due to toxicity, as noted in Figure 3 caption. No other specific toxicity data (e.g., LD50, hepatotoxicity, nephrotoxicity, protein binding) are provided in this paper. [1]
Dequalinium Chloride is generally well-tolerated when used topically, but may cause skin ulceration. Its use in wound dressings and for mouth infections is established. However, comprehensive toxicological data are available from its clinical use as a topical agent. It is not intended for systemic use. As with all chemicals, appropriate safety precautions should be taken when handling Dequalinium Chloride.

Gynecol Oncol.1993;50:38-44;Eur J Pharmacol.1993;236:201-7;Proc Natl Acad Sci U S A.1987;84:5444-8.

Dequalinium chloride is an organochloride, a dichloride of desquinammonia. It has various pharmacological effects, including use as a disinfectant, an inhibitor of mitochondrial NADH:ubiquinone reductase, an antifungal agent, and an antitumor agent. It contains desquinammonia. It is a topical antibacterial agent, available in various salt forms. It can be used in wound dressings and for the treatment of oral infections, and may also have antifungal activity, but may cause skin ulceration. See also: 2,4-dichlorophenoxyacetic acid (note moved to).

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Dequalinium Chloride is a cationic, lipophilic compound structurally similar to rhodamine 123 but with two positive charges. It is used clinically as an antimicrobial agent in mouthwash and vaginal ointments. The compound selectively accumulates in the mitochondria of carcinoma cells due to the high negative membrane electric potential of carcinoma plasma membranes and the high mitochondrial membrane potential. This selectivity provides carcinoma-specific cytotoxicity with reduced normal tissue toxicity. Dequalinium Chloride has been shown to be more effective than cisplatin, 5-fluorouracil, vinblastine, methotrexate, bleomycin, or cyclophosphamide in certain animal models (e.g., MB49 bladder carcinoma, human colon carcinoma CX-1). In a rat colon tumor isograft model, Dequalinium Chloride significantly inhibited primary tumor growth. The compound also demonstrated activity against human ovarian xenografts in athymic mice. Its mechanisms of action include inhibition of mitochondrial ATP synthesis (specifically F1-ATPase), disruption of cellular energy production, and inhibition of protein kinase C and calmodulin. [1]
Dequalinium Chloride is a cationic, lipophilic bis-quinolinium compound with diverse biological activities. It is a selective blocker of apamin-sensitive K+ channels, an antagonist of α7 nAChR, and a mitochondrial poison. It exhibits broad bactericidal and fungicidal activity and is used topically as an antiseptic. It is used in wound dressings and for mouth infections. Dequalinium Chloride is not a systemic drug and is available as a topical antimicrobial agent and research compound.

C30H40N4.2CL

527.57

526.263

522-51-0

10649

Off-white to light yellow solid powder

≥300 °C(lit.)

1.34

2

4

11

36

532

0

[Cl-].[Cl-].[N+]1(=C(C([H])([H])[H])C([H])=C(C2=C([H])C([H])=C([H])C([H])=C12)N([H])[H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[N+]1=C(C([H])([H])[H])C([H])=C(C2=C([H])C([H])=C([H])C([H])=C12)N([H])[H]

LTNZEXKYNRNOGT-UHFFFAOYSA-N

InChI=1S/C30H38N4.2ClH/c1-23-21-27(31)25-15-9-11-17-29(25)33(23)19-13-7-5-3-4-6-8-14-20-34-24(2)22-28(32)26-16-10-12-18-30(26)34;;/h9-12,15-18,21-22,31-32H,3-8,13-14,19-20H2,1-2H3;2*1H

1,1-(decane-1,10-diyl)bis(4-amino-2-methylquinolin-1-ium) chloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)