(S)-(+)-Ketamine hydrochlorideCAS# 33643-47-9 |
2D Structure
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Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 33643-47-9 | SDF | Download SDF |
PubChem ID | 44632368 | Appearance | Powder |
Formula | C13H17Cl2NO | M.Wt | 274.19 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water and to 100 mM in DMSO | ||
Chemical Name | (2S)-2-(2-chlorophenyl)-2-(methylamino)cyclohexan-1-one;hydrochloride | ||
SMILES | CNC1(CCCCC1=O)C2=CC=CC=C2Cl.Cl | ||
Standard InChIKey | VCMGMSHEPQENPE-ZOWNYOTGSA-N | ||
Standard InChI | InChI=1S/C13H16ClNO.ClH/c1-15-13(9-5-4-8-12(13)16)10-6-2-3-7-11(10)14;/h2-3,6-7,15H,4-5,8-9H2,1H3;1H/t13-;/m0./s1 | ||
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 | NMDA receptor antagonist. Displays neuroprotective efficacy in vitro. Racemate also available. |
(S)-(+)-Ketamine hydrochloride Dilution Calculator
(S)-(+)-Ketamine hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.6471 mL | 18.2355 mL | 36.4711 mL | 72.9421 mL | 91.1777 mL |
5 mM | 0.7294 mL | 3.6471 mL | 7.2942 mL | 14.5884 mL | 18.2355 mL |
10 mM | 0.3647 mL | 1.8236 mL | 3.6471 mL | 7.2942 mL | 9.1178 mL |
50 mM | 0.0729 mL | 0.3647 mL | 0.7294 mL | 1.4588 mL | 1.8236 mL |
100 mM | 0.0365 mL | 0.1824 mL | 0.3647 mL | 0.7294 mL | 0.9118 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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Terahertz spectroscopic investigation of S-(+)-ketamine hydrochloride and vibrational assignment by density functional theory.[Pubmed:20187612]
J Phys Chem A. 2010 Apr 1;114(12):4364-74.
The terahertz (THz) spectrum of (S)-(+)-Ketamine hydrochloride has been investigated from 10 to 100 cm(-1) (0.3-3.0 THz) at both liquid-nitrogen (78 K) and room (294 K) temperatures. Complete solid-state density functional theory structural analyses and normal-mode analyses are performed using a single hybrid density functional (B3LYP) and three generalized gradient approximation density functionals (BLYP, PBE, PW91). An assignment of the eight features present in the well-resolved cryogenic spectrum is provided based upon solid-state predictions at a PW91/6-31G(d,p) level of theory. The simulations predict that a total of 13 infrared-active vibrational modes contribute to the THz spectrum with 26.4% of the spectral intensity originating from external lattice vibrations.
Low dose of S+-ketamine prevents long-term potentiation in pain pathways under strong opioid analgesia in the rat spinal cord in vivo.[Pubmed:16113037]
Br J Anaesth. 2005 Oct;95(4):518-23.
BACKGROUND: micro-Opioid receptor (MOR) agonists are strong antinociceptive drugs. Low, but not high doses of the MOR agonist fentanyl prevent synaptic long-term potentiation (LTP) in pain pathways. Block of spinal N-methyl-D-aspartate (NMDA) receptors prevent central sensitization. Here we tested whether the NMDA receptor antagonist S(+)-ketamine reduces C-fibre-evoked potentials and prevents induction of LTP despite high doses of fentanyl. METHODS: C-fibre-evoked field potentials were recorded in the superficial laminae I/II of the rat lumbar spinal cord. High-frequency stimulation (HFS) was applied to the sciatic nerve at C-fibre strength to induce LTP. S(+)-ketamine 5 mg kg(-1) was given 1 h before or after HFS. S(+)-ketamine 5 mg kg(-1) and fentanyl as a bolus (40 microg kg(-1)) followed by an infusion (96 microg kg(-1) h(-1)) were given before HFS to test the action of the combination of these drugs. RESULTS: HFS potentiated C-fibre-evoked field potentials to mean 173 (sem 15)% of control (n=7) for at least 1 h. Low-dose S(+)-ketamine given before HFS blocked the induction of LTP. S(+)-ketamine given after HFS had no effect on the maintenance of LTP. Low-dose S(+)-ketamine prevented induction of LTP under fentanyl-infusion. CONCLUSIONS: Low-dose S(+)-ketamine does not affect C-fibre-evoked potentials alone but blocks LTP induction in pain pathways. In contrast, high doses of opioids strongly reduce C-fibre-evoked potentials, but do not fully prevent LTP induction. In this animal study the combination of S(+)-ketamine with fentanyl reveals both a reduction of C-fibre-evoked potentials and prevention of LTP and seem therefore a better choice for perioperative pain management compared with the sole administration.
Neuroprotection of S(+) ketamine isomer in global forebrain ischemia.[Pubmed:11406122]
Brain Res. 2001 Jun 22;904(2):245-51.
The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist ketamine can block the action of excitotoxic amino acids in the central nervous system. S(+) ketamine has a 2-3 times higher anesthetic potency compared with the ketamine-racemate and also shows a higher neuroprotective efficacy in vitro. To determine the neuroprotective activity of S(+) ketamine compared with its R(-) stereoisomer in vivo, we examined the functional and neurohistological outcome in rats treated 15 min after global forebrain ischemia with S(+) ketamine in different dosages compared with R(-) ketamine. Influence of the treatment on regional cerebral blood flow (rCBF) and cortical oxygen saturation (HbO2) was monitored over 1 h after the ischemia using laser doppler flowmetry and microphotospectrometry respectively. Sixty and ninety mg/kg of S(+) ketamine but not R(-) ketamine significantly reduced neuronal cell loss in the cortex compared with the saline treated group. No significant neuroprotection was observed in the hippocampus. Although no significant change in rCBF was found, S(+) ketamine restored the cortical HbO2 to preischemic values. These results indicate that S(+) ketamine in higher dosages can reduce neuronal damage in the cortex after cerebral ischemia, possibly by improving the ratio of oxygen supply to consumption in the postischemic tissue.
Comparative pharmacology of the optical isomers of ketamine in mice.[Pubmed:658124]
Eur J Pharmacol. 1978 May 1;49(1):15-23.
Relative pharmacological potencies of the optical isomers of ketamine have been estimated in ICR mice. The (+)-isomer was 3X more potent than (-)-ketamine as an analgesic using the phenylquinone writhing test, only 1.5X more potent in terms of hypnotic activity and 1.8X more potent in causing locomotor stimulation. At equianalgesic doses (+)-ketamine caused less stimulation of locomotor activity than the (-)-isomer. These potency differences did not appear to be due to differences in biodisposition although stereoselective metabolism was demonstrated in vivo. Analgesia induced by ketamine was reversed by 10 mg/kg of naloxone.