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| Targets |
DCVC targets the inflammatory cytokine pathway, specifically inhibiting the release of pro-inflammatory cytokines including interleukin-1beta (IL-1beta), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha). These cytokines are key mediators of the inflammatory response, and their inhibition represents a mechanism for anti-inflammatory activity. The compound has been shown to inhibit TNF-alpha, a major pro-inflammatory cytokine involved in systemic inflammation. The molecular target of DCVC is not a single receptor or enzyme but rather the signaling pathways that lead to cytokine production and release in response to pathogenic stimulation. DCVC's activity is concentration-dependent, with significant inhibition observed at concentrations ranging from 5 to 50 microM. As a TCE metabolite, DCVC also interacts with cellular pathways involved in nephrotoxicity and immunotoxicity.
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| ln Vitro |
The trichlorethylene (TCE) metabolite S-(1,2-dichlorovinyl)-l-was used to treat placental adventitia, either in the presence or absence of lipopolysaccharide (LPS) or lipoteichoic acid (LTA). To mimic infection, cysteine (DCVC) was incubated in combination for 4, 8, and 24 hours. Furthermore, membranes were cocultured with group B Streptococcus (GBS) and DCVC. As early as 4 hours, DCVC (5-50μM) significantly inhibited the release of LTA, LPS, and GBS-stimulated cytokines in tissue culture. A concentration-dependent manner is observed in DCVC's inhibition of pathogen-stimulated cytokine (IL-1β, IL-8, and TNF-α) release [1].
DCVC demonstrates potent in vitro anti-inflammatory activity by inhibiting pathogen-stimulated pro-inflammatory cytokine release. In tissue culture experiments, DCVC (5-50 microM) significantly inhibits the release of LTA-, LPS-, and GBS-stimulated cytokines as early as 4 hours of treatment. The inhibition of pathogen-stimulated cytokines (IL-1beta, IL-8, and TNF-alpha) by DCVC is concentration-dependent. In studies using placental membrane tissue cultures exposed to lipopolysaccharide (LPS) or lipoteichoic acid (LTA) to simulate infection, DCVC co-incubation for 4, 8, and 24 hours effectively reduced cytokine release. Additionally, membranes co-cultured with Group B Streptococcus (GBS) and DCVC showed reduced inflammatory responses. The compound's anti-inflammatory effects are observed at concentrations that are not cytotoxic to the tissue cultures, indicating a specific anti-inflammatory mechanism rather than general cytotoxicity. |
| ln Vivo |
In vivo activity of DCVC has been studied primarily in the context of its role as a TCE metabolite and its toxicological effects. While the compound exhibits anti-inflammatory activity in vitro, its in vivo effects are complex due to its role in TCE metabolism and toxicity. DCVC is known to contribute to TCE-induced kidney toxicity through bioactivation pathways involving cysteine conjugate beta-lyase. The compound's in vivo behavior is influenced by its metabolism and disposition in the body. Comprehensive in vivo efficacy studies specifically evaluating DCVC as an anti-inflammatory agent are limited, as the compound is primarily studied as a toxicological metabolite rather than a therapeutic candidate. Its effects on cytokine inhibition observed in vitro have not been extensively validated in animal models of inflammation.
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| Enzyme Assay |
In vitro enzyme/receptor binding assays for DCVC are not standard, as the compound is a metabolite rather than a traditional enzyme inhibitor or receptor ligand. However, the compound's structure and properties can be characterized using analytical chemistry methods. High-performance liquid chromatography (HPLC) and mass spectrometry are used to verify the molecular weight (216.09 g/mol) and chemical composition (C5H7Cl2NO2S). The compound's purity (typically ≥98%) is confirmed by HPLC and NMR analysis. Stability studies may be performed by incubating DCVC in various buffer systems and analyzing degradation products over time. The compound's logP (2.108) and other physicochemical properties can be determined using standard methods. Binding studies to specific proteins or transporters have not been extensively reported for DCVC.
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| Cell Assay |
In vitro cellular assays for DCVC are performed using tissue cultures stimulated with pathogens or inflammatory stimuli. Placental membrane explants or other tissue cultures are treated with DCVC (typically 5-50 microM) in the presence or absence of lipopolysaccharide (LPS), lipoteichoic acid (LTA), or Group B Streptococcus (GBS) to simulate infection. Following co-incubation for 4, 8, and 24 hours, culture supernatants are collected and cytokine levels (IL-1beta, IL-8, and TNF-alpha) are measured using enzyme-linked immunosorbent assays (ELISA). Cytotoxicity is assessed in parallel using lactate dehydrogenase (LDH) release assays or MTT assays to ensure that observed cytokine inhibition is not due to cell death. The concentration-dependent inhibition of cytokine release is determined by testing multiple DCVC concentrations. Results are typically expressed as percent inhibition of cytokine release compared to pathogen-stimulated controls.
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| Animal Protocol |
In vivo animal studies for DCVC have primarily focused on its toxicological effects as a TCE metabolite rather than its anti-inflammatory activity. Animal models of TCE exposure are used to study the metabolism and toxicity of DCVC. Rodents are administered TCE or DCVC via oral gavage, intraperitoneal injection, or inhalation, and tissues (particularly kidney and liver) are examined for signs of toxicity. Biomarkers of kidney injury, such as urinary N-acetyl-beta-D-glucosaminidase (NAG) and kidney injury molecule-1 (KIM-1), are measured. Histopathological examination of kidney tissues is performed to assess tubular damage. Cytokine levels in serum or tissue homogenates may be measured to assess inflammatory responses. However, comprehensive efficacy studies evaluating DCVC as an anti-inflammatory therapeutic in animal models have not been widely reported.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of DCVC are primarily understood through studies of TCE metabolism. Following TCE exposure, DCVC is formed in the liver and transported to the kidney, where it undergoes further metabolism. The compound is a substrate for cysteine conjugate beta-lyase, an enzyme that cleaves the cysteine conjugate to generate reactive intermediates responsible for nephrotoxicity. DCVC is polar and water-soluble due to its amino acid structure, which influences its distribution and elimination. The compound is eliminated primarily through urinary excretion. Its half-life in biological systems is influenced by the activity of beta-lyase and other metabolic enzymes. Comprehensive pharmacokinetic parameters such as volume of distribution, clearance, and oral bioavailability have not been extensively characterized for DCVC as a standalone compound.
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| Toxicity/Toxicokinetics |
DCVC exhibits significant toxicity, primarily as a nephrotoxicant, due to its role as a TCE metabolite. The compound is bioactivated by cysteine conjugate beta-lyase in the kidney to generate reactive sulfur-containing intermediates that covalently bind to cellular proteins and cause mitochondrial dysfunction. This bioactivation pathway leads to selective proximal tubular necrosis and is a well-established mechanism of TCE-induced nephrotoxicity. The compound is also immunotoxic, contributing to TCE-induced immune dysfunction. In vitro, DCVC shows concentration-dependent inhibition of cytokine release at 5-50 microM without significant cytotoxicity. However, at higher concentrations or with prolonged exposure, DCVC can be cytotoxic. The compound is strictly for research use and is not intended for human therapeutic applications. Comprehensive toxicological characterization including genotoxicity and carcinogenicity studies has been conducted as part of TCE toxicology research.
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| References |
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| Additional Infomation |
S-(1,2-dichlorovinyl)-L-cysteine is an L-α-amino acid formed by replacing the hydrogen atom bonded to the sulfur atom in L-cysteine with 1,2-dichlorovinyl. It is an organochlorine compound, a monocarboxylic acid, an L-cysteine thioether, and a non-protein-derived L-α-amino acid.
DCVC is the S-(1,2-dichlorovinyl) conjugate of L-cysteine and a major metabolite of the industrial solvent trichloroethylene (TCE). It is formed through glutathione conjugation of TCE followed by enzymatic cleavage to the cysteine conjugate. The compound has a molecular formula of C5H7Cl2NO2S and a molecular weight of 216.09 g/mol. DCVC exhibits anti-inflammatory activity by inhibiting the release of pro-inflammatory cytokines IL-1beta, IL-8, and TNF-alpha from pathogen-stimulated tissue cultures. However, it is also a known nephrotoxicant and immunotoxicant, contributing to TCE-induced kidney toxicity and immune dysfunction. The compound's dual role as both an anti-inflammatory agent and a toxic metabolite highlights the complexity of its biological activity. DCVC is not a therapeutic agent and has not entered clinical trials. It is available from research chemical suppliers for non-clinical research purposes only. |
| Molecular Formula |
C5H7NO2SCL2
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|---|---|
| Molecular Weight |
216.08558
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| Exact Mass |
214.957
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| CAS # |
13419-46-0
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| PubChem CID |
6433207
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| Appearance |
White to off-white solid powder
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| Density |
1.544g/cm3
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| Boiling Point |
339.7ºC at 760mmHg
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| Flash Point |
159.2ºC
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| Vapour Pressure |
1.66E-05mmHg at 25°C
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| Index of Refraction |
1.6
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| LogP |
2.108
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
11
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| Complexity |
174
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C([C@@H](C(=O)O)N)S/C(=C/Cl)/Cl
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| InChi Key |
PJIHCWJOTSJIPQ-AGFFZDDWSA-N
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| InChi Code |
InChI=1S/C5H7Cl2NO2S/c6-1-4(7)11-2-3(8)5(9)10/h1,3H,2,8H2,(H,9,10)/b4-1+/t3-/m0/s1
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| Chemical Name |
(2R)-2-amino-3-[(Z)-1,2-dichloroethenyl]sulfanylpropanoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~2.5 mg/mL (~11.57 mM)
H2O : ~1.034 mg/mL (~4.79 mM) |
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| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.6277 mL | 23.1385 mL | 46.2770 mL | |
| 5 mM | 0.9255 mL | 4.6277 mL | 9.2554 mL | |
| 10 mM | 0.4628 mL | 2.3139 mL | 4.6277 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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