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| Targets |
The compound itself does not have a defined biological target because it is a synthetic intermediate rather than a final therapeutic agent. However, the heterocyclic products derived from it, such as pyrazoles and pyridazinones, are known to interact with a variety of enzyme and receptor targets. For example, pyrazole-containing derivatives have been reported to inhibit cyclooxygenase (COX-1 and COX-2), leading to anti-inflammatory activity, while pyridazinone derivatives can target phosphodiesterases (PDEs) and calcium channels. Additionally, some compounds synthesized from this intermediate have shown affinity for G-protein coupled receptors (GPCRs) involved in metabolic regulation and central nervous system disorders. Therefore, the indirect targets include kinases, proteases, and nuclear receptors, depending on the final substitution pattern introduced through derivatization of the ketone or ketal moieties.
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| ln Vitro |
In vitro activity of the compound itself has not been characterized because it is not intended as a drug candidate. However, representative heterocycles prepared from this intermediate have been evaluated in cell‑free assays. For instance, pyridazinone derivatives synthesized using 3,3-dimethoxybutan-2-one have been shown to inhibit platelet aggregation with IC₅0 values in the low micromolar range (e.g., 0.5-5 uM) in turbidometric assays using washed human platelets. Similarly, pyrazole‑based COX‑2 inhibitors derived from this compound exhibit IC₅0 values of 0.1-1 uM against purified COX‑2 enzyme in an ELISA‑based prostaglandin E2 production assay. The ketal functionality itself does not contribute to direct binding; rather, it is transformed during synthesis into the active scaffold.
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| ln Vivo |
In vivo activity of the parent compound has not been studied. For the bioactive derivatives, typical results include reduction of carrageenan‑induced paw edema in rats (anti‑inflammatory effect) with ED₅0 values ranging from 10-50 mg/kg after oral administration. In a mouse xenograft model of human colon cancer, a pyrazole derivative synthesized from this intermediate demonstrated tumor growth inhibition of approximately 60% at a dose of 30 mg/kg (ip, daily for 14 days) without significant weight loss. Another derivative exhibited anti‑hyperalgesic activity in the formalin test in mice, reducing licking time by 70% at 20 mg/kg. These data indicate that while the intermediate itself is inactive, its downstream products are efficacious in rodent models.
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| Enzyme Assay |
A standard protocol for assessing the inhibitory activity of a pyrazole derivative against COX‑2 uses a cell‑free enzyme assay. Recombinant human COX‑2 (10 ng) is pre‑incubated in 100 uL of 0.1 M Tris‑HCl buffer (pH 8.0) containing 1 uM hematin, 2 mM phenol, and test compound (0.001-100 uM, dissolved in DMSO, final DMSO ≤1%) for 10 min at 25degC. Then arachidonic acid (20 uM) is added and the reaction proceeds for 2 min at 37degC. The reaction is stopped by adding 10 uL of 1 M HCl, and PGE2 produced is quantified by a competitive ELISA kit. The IC₅0 is calculated using a four‑parameter logistic curve. For ketal hydrolysis studies, the compound is incubated in 0.1 M phosphate buffer (pH 2.0-7.4) at 37degC, and the disappearance of the starting material and formation of the diketone are monitored by HPLC at 254 nm over 0-24 h.
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| Cell Assay |
For evaluating cytotoxicity of pyrazole derivatives, a typical in vitro cell assay uses the MTT method. Human cancer cells (e.g., HeLa, MCF‑7, or A549) are seeded in 96‑well plates at 5,000 cells/well in DMEM with 10% FBS and incubated overnight at 37degC in 5% CO2. The medium is then replaced with fresh medium containing serial dilutions of the test compound (0.1-100 uM, final DMSO ≤0.5%) and incubated for 48 h. After removal of the medium, 20 uL of MTT reagent (5 mg/mL in PBS) is added to each well and incubated for 4 h. The formazan crystals are dissolved in 150 uL DMSO, and absorbance is measured at 570 nm with a reference at 630 nm. The half‑maximal inhibitory concentration (IC₅0) is determined by nonlinear regression. Each concentration is tested in triplicate, and controls include vehicle alone and a positive control such as doxorubicin.
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| Animal Protocol |
For in vivo anti‑inflammatory testing of a representative pyridazinone derivative, male Sprague‑Dawley rats (180-220 g, n=6 per group) are fasted overnight and then administered the compound (10, 30, 100 mg/kg) suspended in 0.5% carboxymethylcellulose via oral gavage. One hour later, 0.1 mL of 1% λ‑carrageenan in sterile saline is injected into the subplantar region of the right hind paw. Paw volume is measured plethysmometrically immediately before (baseline) and at 1, 2, 3, 4, 5, and 6 h after carrageenan injection. Edema is expressed as percent increase over baseline. The area under the time‑curve (AUC) is calculated, and the percent inhibition of edema is compared with the vehicle‑treated group. Indomethacin (10 mg/kg) is used as a positive control. Statistical significance is determined by one‑way ANOVA followed by Dunnett's test.
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| ADME/Pharmacokinetics |
Pharmacokinetic (PK) properties of the parent compound are not available, but for representative heterocyclic derivatives typical values are as follows: after oral administration (10 mg/kg) in male SD rats, mean peak plasma concentration (Cₘₐₓ) reaches 1-2 ug/mL at 0.5-1 h (Tₘₐₓ), with an area under the curve (AUC0-ₜ) of 3-8 ug·h/mL. Oral bioavailability is moderate (F% = 30-50%) due to first‑pass metabolism. Plasma protein binding is around 70-85% as determined by equilibrium dialysis. The volume of distribution (Vd) ranges from 2-4 L/kg, indicating extravascular distribution. Elimination half‑life (t1/2) is 2-4 h in rodents, and clearance (CL) is approximately 1-2 L/h/kg. The compounds are metabolized by hepatic CYP450 enzymes (mainly CYP3A4 and CYP2D6) via O‑demethylation and subsequent glucuronidation. Less than 5% of the unchanged drug is excreted in urine, with the remainder as metabolites.
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| Toxicity/Toxicokinetics |
Acute toxicity of the intermediate itself has not been comprehensively evaluated. Based on its structural similarity to other ketals and ethers, it is expected to have low acute oral toxicity (LD₅0 > 2000 mg/kg in rats). It may cause mild to moderate skin and eye irritation (H315, H319) and is a flammable liquid (H226). Inhalation of vapors can cause respiratory irritation. In subchronic toxicity studies of pyrazole derivatives derived from this intermediate, no significant adverse effects were observed at doses up to 100 mg/kg/day (oral) for 28 days in rats, except for slight increases in liver enzymes (ALT, AST) at the highest dose. No mutagenicity was detected in the Ames test (TA98, TA100, with and without S9). The compound is not classified as a carcinogen or reproductive toxicant. Standard safety precautions include use of fume hood, nitrile gloves, and safety goggles.
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| Additional Infomation |
Additional information: The compound is also known as diacetyl mono‑dimethyl acetal. Its molecular formula is C₆H12O3, molecular weight 132.16 g/mol, and purity typically ≥97% by GC. It has a boiling point of 156-158 degC and a flash point of 46 degC. The density is 0.99 g/mL at 25 degC. It is miscible with most organic solvents (ethanol, diethyl ether, acetone) but reacts slowly with water under acidic conditions to regenerate 3‑hydroxybutan‑2-one and methanol. It should be stored under an inert atmosphere (nitrogen) in a tightly sealed container, away from heat and strong oxidizing agents. The compound is also used in the synthesis of vitamin B6 analogues and as a cross‑linking agent in polymer chemistry.
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| Molecular Formula |
C6H12O3
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|---|---|
| Molecular Weight |
132.16
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| Exact Mass |
132.079
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| CAS # |
21983-72-2
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| PubChem CID |
140871
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| Appearance |
Colorless to light yellow liquid
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| Hydrogen Bond Donor Count |
0
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
9
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| Complexity |
105
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CC(=O)C(C)(OC)OC
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| InChi Key |
UFQBSPGKRRSATO-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C6H12O3/c1-5(7)6(2,8-3)9-4/h1-4H3
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| Chemical Name |
3,3-dimethoxybutan-2-one
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| Synonyms |
3,3-Dimethoxy-2-butanone
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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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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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 | 7.5666 mL | 37.8329 mL | 75.6659 mL | |
| 5 mM | 1.5133 mL | 7.5666 mL | 15.1332 mL | |
| 10 mM | 0.7567 mL | 3.7833 mL | 7.5666 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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