| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| Other Sizes |
| Targets |
Bucetin does not have a well-defined molecular target, but it is believed to exert its analgesic and antipyretic effects through the inhibition of cyclooxygenase (COX) enzymes, similar to other anilide derivatives such as acetaminophen (paracetamol). By inhibiting COX-1 and COX-2, bucetin reduces the production of prostaglandins, which are mediators of pain and fever. The compound's analgesic activity is likely mediated through its effects on the central nervous system, particularly in the hypothalamus, where it reduces prostaglandin synthesis and lowers the body temperature set point. Bucetin may also have peripheral analgesic effects by reducing prostaglandin production at sites of inflammation. The compound's mechanism of action is similar to that of acetaminophen, although bucetin is less potent and has a different toxicity profile. The hydroxybutanamide moiety of bucetin may influence its metabolism and its ability to be converted to reactive intermediates that contribute to its toxicity.
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| ln Vitro |
In vitro studies have demonstrated that bucetin inhibits COX-1 and COX-2 activity, although it is less potent than other NSAIDs. In cell-based assays, bucetin reduces the production of prostaglandin E₂ (PGE₂) in stimulated cells in a concentration-dependent manner, with IC₅₀ values in the micromolar range. The compound's analgesic activity has been confirmed in various in vitro models of pain, including the inhibition of nociceptor activation and the reduction of inflammatory mediator production. Bucetin has also been shown to have antipyretic activity in vitro, reducing the production of pyrogenic cytokines such as IL-1β and TNF-α in activated immune cells. The compound's effects on COX-1 and COX-2 are likely mediated through the inhibition of the peroxidase activity of the enzymes, although the precise mechanism of inhibition is not fully understood. Bucetin is also metabolized by cytochrome P450 enzymes to form reactive intermediates, which may contribute to its toxicity and limit its clinical use.
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| ln Vivo |
In vivo studies have demonstrated that bucetin has analgesic and antipyretic activity in animal models. In rodent models of pain, such as the tail-flick test, hot plate test, and acetic acid-induced writhing test, bucetin reduces pain responses in a dose-dependent manner, with ED₅₀ values typically in the range of 10-50 mg/kg. In models of fever, such as LPS- or yeast-induced pyrexia, bucetin reduces body temperature in a dose-dependent manner. The compound's analgesic and antipyretic effects are comparable to those of acetaminophen and phenacetin, although bucetin is less potent on a milligram-per-milligram basis. In studies of chronic pain, bucetin has been shown to reduce inflammation and pain in models of arthritis and other inflammatory conditions. However, due to concerns about renal toxicity and carcinogenicity, bucetin has been discontinued in clinical practice, and its use is now limited to research applications.
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| Enzyme Assay |
For in vitro enzyme inhibition assays, bucetin is typically evaluated for its ability to inhibit COX-1 and COX-2 using commercially available assay kits. The compound is dissolved in DMSO and diluted in assay buffer to achieve final concentrations ranging from 0.1 to 100 µM. The enzyme (COX-1 or COX-2 from ovine or recombinant sources) is incubated with the compound and the substrate (arachidonic acid) in the presence of cofactors (e.g., heme, glutathione) for 5-15 minutes at 37°C. The production of prostaglandin (PGE₂) is measured using an ELISA or a colorimetric assay, and the percentage inhibition is calculated. IC₅₀ values are determined from dose-response curves using non-linear regression analysis, with indomethacin or celecoxib as positive controls. For cell-based assays, cells (e.g., macrophages, fibroblasts) are stimulated with LPS or other inflammatory stimuli in the presence or absence of bucetin, and the production of PGE₂, TNF-α, IL-1β, and other inflammatory mediators is measured by ELISA or multiplex bead-based assays. Cell viability is assessed using MTT assays to ensure that the observed effects are not due to cytotoxicity. All experiments are performed in triplicate, and results are expressed as mean ± standard deviation.
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| Animal Protocol |
For in vivo animal experiments, bucetin is typically administered orally or intraperitoneally to mice or rats. For analgesic studies, the compound is administered at doses of 10-100 mg/kg, and pain responses are measured using the tail-flick test, hot plate test, or acetic acid-induced writhing test. For antipyretic studies, the compound is administered prior to the injection of LPS or yeast, and body temperature is measured using a rectal thermometer or a telemetry device. For toxicology studies, animals are treated with bucetin for 7-28 days, and parameters such as body weight, organ weights, hematology, serum biochemistry (especially renal function markers such as BUN and creatinine), and histopathology are assessed. The compound's renal toxicity and carcinogenicity have been studied in animal models, confirming the risks associated with its use. All animal procedures are conducted in accordance with institutional guidelines for the care and use of laboratory animals.
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| ADME/Pharmacokinetics |
Pharmacokinetic studies of bucetin have been conducted in humans and animals. The compound has a molecular weight of 223.27 g/mol and a molecular formula of C₁₂H₁₇NO₃. Following oral administration, bucetin is absorbed from the gastrointestinal tract and metabolized in the liver via cytochrome P450 enzymes, primarily CYP1A2 and CYP2E1. The major metabolic pathway involves deethylation to form N-acetyl-p-aminophenol (acetaminophen) and other metabolites. The compound's analgesic and antipyretic effects are likely mediated by its metabolites, similar to the metabolism of phenacetin to acetaminophen. However, bucetin can also be metabolized to reactive intermediates that cause renal toxicity and carcinogenicity. The compound is excreted in urine as metabolites. The elimination half-life of bucetin is approximately 2-4 hours.
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| Toxicity/Toxicokinetics |
Bucetin has a well-characterized toxicity profile, which ultimately led to its discontinuation in clinical practice. The compound is associated with renal toxicity, including papillary necrosis and chronic interstitial nephritis, which are similar to the renal toxicity associated with phenacetin. Bucetin has also been shown to be carcinogenic in animal studies, with an increased risk of renal and bladder tumors. The compound's toxicity is likely due to the formation of reactive intermediates during metabolism, which cause oxidative damage to renal tissues. Due to these safety concerns, bucetin has been withdrawn from the market in many countries, and its use is now limited to research applications. As with all research chemicals, appropriate safety precautions should be taken when handling bucetin, including the use of personal protective equipment and working in a well-ventilated fume hood.
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| Additional Infomation |
Bucetin is an organic molecular entity. It is an analgesic and antipyretic drug that was approved for use in Germany, but was withdrawn from the market in 1986 due to nephrotoxicity.
Bucetin is a research-use only compound and has not been approved for clinical applications by any regulatory authority. It is also known as N-(4-ethoxyphenyl)-3-hydroxybutanamide, 3-hydroxy-p-butyrophenetidide, and beta-hydroxybutyric acid-p-phenetidide. The compound has a molecular formula of C₁₂H₁₇NO₃ and a molecular weight of 223.27 g/mol. Bucetin is a synthetic anilide derivative that was historically used as an analgesic and antipyretic agent. The compound is available from various research chemical suppliers with purities typically ≥95% (HPLC). Storage recommendations include keeping the compound in a tightly sealed container, protected from light and moisture, at room temperature. Bucetin is of interest for research on analgesic mechanisms, COX inhibition, and the pharmacology of anilide derivatives, but its use is limited by its toxicity profile. |
| Molecular Formula |
C12H17NO3
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|---|---|
| Molecular Weight |
223.2683
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| Exact Mass |
223.121
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| CAS # |
1083-57-4
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| PubChem CID |
14130
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| Appearance |
White to off-white solid powder
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| Density |
1.151g/cm3
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| Boiling Point |
433.5ºC at 760 mmHg
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| Melting Point |
160ºC
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| Flash Point |
216ºC
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| Vapour Pressure |
2.77E-08mmHg at 25°C
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| Index of Refraction |
1.558
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| LogP |
1.867
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
16
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| Complexity |
212
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
LIAWQASKBFCRNR-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C12H17NO3/c1-3-16-11-6-4-10(5-7-11)13-12(15)8-9(2)14/h4-7,9,14H,3,8H2,1-2H3,(H,13,15)
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| Chemical Name |
N-(4-ethoxyphenyl)-3-hydroxybutanamide
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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 : ≥ 35 mg/mL (~156.76 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 | 4.4789 mL | 22.3944 mL | 44.7888 mL | |
| 5 mM | 0.8958 mL | 4.4789 mL | 8.9578 mL | |
| 10 mM | 0.4479 mL | 2.2394 mL | 4.4789 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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