PropofolCAS# 2078-54-8 |
2D Structure
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Number of papers citing our products
Cas No. | 2078-54-8 | SDF | Download SDF |
PubChem ID | 4943 | Appearance | Powder |
Formula | C12H18O | M.Wt | 178.3 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | 2,6-di(propan-2-yl)phenol | ||
SMILES | CC(C)C1=C(C(=CC=C1)C(C)C)O | ||
Standard InChIKey | OLBCVFGFOZPWHH-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C12H18O/c1-8(2)10-6-5-7-11(9(3)4)12(10)13/h5-9,13H,1-4H3 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Intravenous general anesthetic and hypnotic with a mode of action which includes potentiation of GABA-mediated inhibitory synaptic transmission, direct activation of the GABAA receptor and inhibition of glutamate receptor mediated excitatory synaptic transmission. Also potentiates P2X4 receptor-mediated currents in P2X4-HEK293 cells. |
Propofol Dilution Calculator
Propofol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 5.6085 mL | 28.0426 mL | 56.0852 mL | 112.1705 mL | 140.2131 mL |
5 mM | 1.1217 mL | 5.6085 mL | 11.217 mL | 22.4341 mL | 28.0426 mL |
10 mM | 0.5609 mL | 2.8043 mL | 5.6085 mL | 11.217 mL | 14.0213 mL |
50 mM | 0.1122 mL | 0.5609 mL | 1.1217 mL | 2.2434 mL | 2.8043 mL |
100 mM | 0.0561 mL | 0.2804 mL | 0.5609 mL | 1.1217 mL | 1.4021 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Systematic review and meta-analysis of propofol versus barbiturates for controlling refractory status epilepticus.[Pubmed:30954065]
BMC Neurol. 2019 Apr 6;19(1):55.
BACKGROUND: Several studies have compared the efficacy and safety of Propofol and barbiturates in the treatment of refractory status epilepticus (RSE). This study aims to quantitatively assess the advantages and disadvantages of Propofol and barbiturates in controlling RSE. METHODS: We searched for studies with relevant data from the PubMed, Embase, Ovid, Cochrane Library, Springer Link, Web of Science, and China National Knowledge Infrastructure databases. By calculating odds ratios and standardized mean differences with 95% confidence intervals, we assessed the disease control rate (DCR), case fatality rate (CFR), average control time (ACT), average tracheal intubation placement time (ATIPT), and incidence of hypotension between Propofol and barbiturates in treating RSE. RESULTS: Seven studies with 261 patients were included in this analysis. Meta-analysis revealed that the DCR of Propofol was higher than that of barbiturates (p < 0.001) and that the CFR (p = 0.382) between the two treatment did not significantly differ in controlling RSE. Propofol shortened the ACT (p < 0.001) of RSE and reduced the ATIPT (p < 0.001) of patients with RSE more extensively than did barbiturates and did not increase the incidence of hypotension (p = 0.737). CONCLUSIONS: In comparison with barbiturates, Propofol can control RSE and shorten ATIPT in a more efficient and timely manner. Moreover, the drug does not increase the incidence of hypotension and CFR.
Identifying drugs that bind selectively to intersubunit general anesthetic sites in the alpha1beta3gamma2 GABAAR transmembrane domain.[Pubmed:30952799]
Mol Pharmacol. 2019 Apr 5. pii: mol.118.114975.
GABAA receptors (GABAARs) are targets for important classes of clinical agents (e.g. anxiolytics, anticonvulsants and general anesthetics) that act as positive allosteric modulators (PAMs). Previously, using photoreactive analogs of etomidate ([(3)H]azietomidate) and mephobarbital ([(3)H]R-mTFD-MPAB), we identified two homologous but pharmacologically distinct classes of general anesthetic binding sites in the alpha1beta3gamma2 GABAAR transmembrane domain at beta(+)-alpha(-) (beta(+)-sites) and alpha(+)-beta(-)/gamma(+)-beta(-) (beta(-)-sites) subunit interfaces. We now use competition photolabeling with [(3)H]azietomidate and [(3)H]R-mTFD-MPAB to identify para-substituted Propofol analogs and other drugs that bind selectively to intersubunit anesthetic sites. Propofol and 4-chloro-Propofol bind with 5-fold selectivity to beta(+), while derivatives with bulkier lipophilic substitutions [4-(tert-butyl)-Propofol and 4-(hydroxyl(phenyl)methyl)-Propofol] bind with ~10-fold higher affinity to beta(-) sites. Similar to R-mTFD-MPAB and Propofol, these drugs bind in the presence of GABA with similar affinity to the alpha(+)-beta(-) and gamma(+)-beta(-) sites. However, we discovered four compounds that bind with different affinities to the two beta(-) interface sites. Two of these bind with higher affinity to one of the beta(-) sites than to the beta(+) sites. We deduce that 4-benzoyl-Propofol binds with >100- fold higher affinity to the gamma(+)-beta(-) site than to the alpha(+)-beta(-) or beta(+)-alpha(-) sites, whereas loreclezole, an anticonvulsant, binds with 5- and 100- fold higher affinity to the alpha(+)-beta(-) site than to the beta(+) and gamma(+)-beta(-) sites. These studies provide a first identification of PAMs that bind selectively to a single intersubunit site in the GABAAR transmembrane domain, a property that may facilitate the development of subtype selective GABAAR PAMs.
Propofol inhibits pancreatic cancer progress under hypoxia via ADAM8.[Pubmed:30945470]
J Hepatobiliary Pancreat Sci. 2019 Apr 4.
BACKGROUND: To investigate the potential anti-tumoral properties of Propofol in pancreatic cancer and elucidate the underlying mechanisms. METHODS: The relative expression of ADAM8 in response to hypoxia in Panc1 cells was analyzed by western blotting. The enzymatic activity was determined by fluorescence release from PEPDAB013 decomposition. Cell growth was measured via cell counting and cell viability was measured using CCK-8 kit. Cell migrative capacity was evaluated by transwell and adhesion assay. The relative abundance of angiogenesis-related markers including PDGF-AA, angionenin, endothelin-1 and VEGF were determined by real-time PCR and western blotting. The anti-tumoral activity of Propofol was investigated with Panc1-derived xenograft mice model. RESULTS: ADAM8 was significantly induced by hypoxia and efficiently inhibited by co-treatment with Propofol. Propofol suppressed proliferation and compromised viability of Panc1 cells. In addition, the migrative capacity was greatly inhibited by Propofol dosage. Comprehensive profiling of angiogenesis-related markers demonstrated that Propofol remarkably suppressed neovascularization response in Panc1 cells under hypoxia. We further uncovered that Propofol administration via subcutaneous injection delayed xenograft tumor progression. CONCLUSION: Propofol specifically inhibited ADAM8 expression and activation in response to hypoxia in pancreatic cancer, and held great values for therapeutic effects. This article is protected by copyright. All rights reserved.