| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C16H29N3O8 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Diethylcarbamazine citrate is an orally active microfilaricidal agent originally used for onchocerciasis and lymphatic filariasis. It reduces eosinophil trafficking to lung tissue and produces anti-allergic effects, lowers serum leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without changing body, liver, or adipose tissue weight. It also enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits development of actinomycetoma lesions, and it can be used in research on bronchial asthma, insulin resistance, and infection[1][2][3]. It is supplied as a white to off-white solid (C16H29N3O8, MW 391.42) at 98.01% purity.
Physical & Chemical Properties
| CAS Number | 1642-54-2 |
|---|---|
| Molecular Formula | C16H29N3O8 |
| Molecular Weight | 391.42 g/mol |
| Purity | 98.01% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O=C(N1CCN(C)CC1)N(CC)CC.O=C(CC(C(O)=O)(O)CC(O)=O)O |
| Target | IL-6 |
| Signaling Pathway | Anti-infection; Apoptosis; Immunology/Inflammation |
| Solubility | In Vitro: H2O: 100 mg/mL (255.48 mM; Requires sonication) DMSO: ≥ 39 mg/mL (99.64 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) * "≥" means soluble, but saturation unknown. |
| Storage | 4°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| H2O | 100 mg/mL (255.48 mM) | requires sonication |
| DMSO | ≥ 39 mg/mL (99.64 mM) | use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
If water is used as the stock solvent, dilute to the working solution and sterilize it through a 0.22 μm filter before use.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (6.39 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (6.39 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.39 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
Rabbit anti-MPCA-BSA polyclonal IgG antibodies cross-react with Diethylcarbamazine (0-40 mM; 60 min) citrate in an inhibition ELISA[1].
In Vivo
In asthmatic mice induced with Ovalbumin, Diethylcarbamazine (12 mg/kg; p.o.) citrate exerts anti-allergic effects, and pre-treatment with 40 mg/kg quercetin significantly potentiates them, as shown by reduced serum Th2 cytokines, BALF IgE, and lung eosinophil markers together with complete resolution of histopathological lung damage[1]. High-fat diet-induced insulin resistance in male Swiss mice is significantly ameliorated by Diethylcarbamazine (12-200 mg/kg; p.o.; twice weekly; 12 weeks) citrate through suppression of adipose tissue inflammation at an optimal dose of 50 mg/kg; body and tissue weights are unaffected, while serum glucose, insulin, and triglycerides, as well as proinflammatory mediators, cyclooxygenase activity in the liver, and nuclear translocation of NF-κBp65, are all significantly reduced[2]. Actinomycetoma development in BALB/c mice is inhibited by Diethylcarbamazine (6 mg/kg; p.o.; daily; 1 week) citrate, with a statistically significant reduction in lesion size; cellular immune responses are also enhanced, including neutrophil production of reactive oxygen intermediates and lymphocyte proliferation[3].
| Animal Model | white albino mice (6 to 8-week-old female, 18-20 g, intradermal sensitization + aerosol exposure Ovalbumin-induced asthma)[1] |
|---|---|
| Dosage | 12 mg/kg |
| Administration | p.o.; |
| Result | Reduced serum IL-4 and IL-5, total BALF IgE and specific anti-ovalbumin IgE, lung tissue EPO and eotaxin2, and reduced inflammatory cell infiltration and thickened alveolar walls compared to untreated asthmatic mice. Showed no significant changes in serum IL-4, IL-5, BALF IgE, lung EPO, or eotaxin2, and similar histopathological improvement compared to DEC alone when preceded by anti-DEC antibody. Showed no significant changes in serum IL-4, IL-5, lung EPO, or eotaxin2, and partial reduction in inflammatory cell infiltration and alveolar wall thickening compared to DEC alone when preceded by 10 mg/kg Quercetin. Significantly reduced serum IL-4 and IL-5, increased IFN-γ/IL-4 ratio to near control levels, decreased total BALF IgE, and reduced inflammatory cell infiltration compared to DEC alone when preceded by 20 mg/kg and 40 mg/kg Quercetin. |
| Animal Model | Swiss mice (male, 5 weeks old, initial 10 g body weight, high-fat diet-induced insulin resistance)[2] |
|---|---|
| Dosage | 12 mg/kg; 50 mg/kg; 200 mg/kg |
| Administration | p.o.; twice weekly; 12 weeks (from 6 to 18 week) |
| Result | Reduced serum glucose levels at all oral glucose tolerance test time points (0, 30, 60, 120 min) with a statistically significant reduction in area under the curve at 50 mg/kg. Reduced serum triglyceride levels at 50 mg/kg. Reduced serum insulin levels and HOMA-IR score at 50 mg/kg. Reduced serum leptin levels at 50 mg/kg. Reduced serum levels of TNF-α, IL-6, and MCP-1 at 50 mg/kg. Significantly reduced liver cyclooxygenase activity at 50 mg/kg. Significantly inhibited nuclear localization of NF-κBp65 with increased cytoplasmic retention at 50 mg/kg. Showed no statistically significant reductions in serum glucose, triglycerides, insulin, HOMA-IR, leptin, TNF-α, IL-6, MCP-1, or liver cyclooxygenase activity relative to untreated high-fat diet-fed mice at 12 mg/kg and 200 mg/kg. Exhibited less potent effects on NF-κBp65 nuclear localization at 12 mg/kg and 200 mg/kg compared to 50 mg/kg. Caused no significant changes to body, adipose tissue, or liver weights at 50 mg/kg. |
| Animal Model | BALB/c (male, 10-12 weeks old, 37-45 g, actinomycetoma model via footpad inoculation with Nocardia brasiliensis)[3] |
|---|---|
| Dosage | 6 mg/kg |
| Administration | p.o.; daily; 1 week |
| Result | Reduced actinomycetoma lesion size with statistical significance compared to untreated infected controls. Resolved fistulae, granule discharge, hyperemia, and erythema by day 20 post-infection, and prevented mycetoma establishment through day 90. Reduced cellular infiltrate, eliminated granuloma layer formation, restored epidermal integrity, and reorganized damaged striated muscle fibers by day 28 post-infection. Enhanced polymorphonuclear neutrophil reactive oxygen intermediate production with statistical significance at day 3 post-infection. Increased lymphocyte proliferation in response to N. brasiliensis cellular crude extract with statistical significance at day 21 post-infection. Increased lymphocyte proliferation in response to concanavalin A with statistical significance at day 28 post-infection. Caused no significant changes in IgG or IgM antibody production against N. brasiliensis P24 antigen. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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