| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| 10g | |||
| Other Sizes |
Purity: ≥98%
Levobupivacaine HCl [also known as (S)-(-)-Bupivacaine; Chirocaine, Novabupi], the hydrochloride salt of Levobupivacaine which is the pure S(-)-enantiomer of bupivacaine, is a reversible neuronal sodium channel inhibitor. Levobupivacaine has been used as a long-acting local anesthetic. Levobupivacaine is an amide-type local anaesthetic that acts via blockade of voltage-sensitive ion channels in neuronal membranes, preventing transmission of nerve impulses.
| Targets |
Voltage-gated sodium channels (for regional anaesthesia and pain management) [1]
- miR-489-3p/SLC7A11 signaling pathway (for ferroptosis induction in gastric cancer) [2] - N-methyl-D-aspartate (NMDA) receptor-related targets (for excitotoxic neuronal death regulation)[3] |
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| ln Vitro |
Levobupivacaine (0–4 mM; 24 h) inhibits the viability of HGC27 and SGC7901 cells but has no effect on GES-1 cell viability[2]. Levobupivacaine (2 mM; 24, 48, or 72 h) increases the inhibitory effect of Erastin on the viability of HGC27 and SGC7901 cells; it also raises the levels of iron, Fe2+, and lipid reactive oxygen species[2]. Levobupivacaine (2 mM; 24 h) raises the levels of iron and Fe2+ in HGC27 and SGC7901 cells and improves the expression of miR-489-3p[2].
Levobupivacaine HCl inhibits voltage-gated sodium channels in neuronal membranes, blocking sodium ion influx and suppressing nerve impulse conduction, which is the basis for its regional anaesthetic and analgesic effects [1] - In human gastric cancer cell lines, Levobupivacaine HCl induces ferroptosis by regulating the miR-489-3p/SLC7A11 signaling pathway: it upregulates miR-489-3p expression, which directly targets and downregulates SLC7A11, leading to decreased glutathione (GSH) synthesis, increased lipid peroxidation, and ultimately gastric cancer cell death [2] - In primary cultured cortical neurons, Levobupivacaine HCl reduces excitotoxic neuronal death induced by NMDA exposure; compared with racemic bupivacaine, it shows comparable neuroprotective effects at relevant concentrations [3] |
| ln Vivo |
Levobupivacaine (40 μmol/kg; IP; once daily for 25 days) increases the buildup of lipid ROS while markedly inhibiting the development of SGC7901 cells[2]. When used in small doses, levofloxacin (5 or 36 mg/kg; IP; single dosage) prolongs the latency to partial seizures and inhibits the onset of generalized seizures; when used in large doses, it shortens the latency to N-methyl-d-aspartate (NMDA)-induced seizures and intensifies seizures[3].
In animal models and clinical settings, Levobupivacaine HCl exerts dose-dependent regional anaesthetic effects when administered via epidural, spinal, peripheral nerve block, or local infiltration routes, with analgesic duration matching or exceeding that of racemic bupivacaine [1] - In NMDA-induced seizure mice, Levobupivacaine HCl pretreatment reduces the severity and duration of seizures, and attenuates NMDA-mediated excitotoxic neuronal damage in brain tissues, showing similar neuroprotective potency to racemic bupivacaine [3] |
| Enzyme Assay |
For voltage-gated sodium channel activity assay: Neuronal membrane preparations or isolated neurons are used, and sodium channel currents are recorded using patch-clamp technique. Levobupivacaine HCl is applied at gradient concentrations, and changes in current amplitude and gating properties are analyzed to evaluate blocking efficiency [1]
- For SLC7A11 activity assay: Gastric cancer cell lysates are prepared, and SLC7A11 transport activity is measured by detecting GSH synthesis efficiency. Levobupivacaine HCl is incubated with the lysates, and changes in GSH levels are quantified to reflect SLC7A11 inhibition [2] |
| Cell Assay |
Cell Viability Assay[2]
Cell Types: GES-1, HGC27 and SGC790 Tested Concentrations: 0, 0.5, 1, 2 and 4 mM Incubation Duration: 24 h Experimental Results: Did not affect the viability of normal gastric epithelial GES-1 cell lines but inhibited the viability of HGC27 and SGC7901 cells in a dose-dependent manner. Cell Viability Assay[2] Cell Types: HGC27 and SGC7901 (incubated with 5 μM erastin) Tested Concentrations: 2 mM Incubation Duration: 24, 48 or 72 h Experimental Results: Enhanced erastin-induced inhibitory impact on HGC27 and SGC7901 cell viabilities; induced the levels of Fe2+, iron, and lipid ROS. RT-PCR[2] Cell Types: HGC27 and SGC7901 (incubated with 5 μM erastin) Tested Concentrations: 2 mM Incubation Duration: 24 h Experimental Results: Enhanced the expression of miR-489-3p in HGC27 and SGC7901 cells, increased the levels of Fe2+ and iron. Gastric cancer cell ferroptosis assay: Gastric cancer cells are seeded and cultured to logarithmic phase, then treated with Levobupivacaine HCl at different concentrations (range not specified in public data) for 24-72 hours. Cell viability is detected by CCK-8 assay; lipid peroxidation is measured using a lipid reactive oxygen species (ROS) probe; GSH levels are determined by colorimetric assay; miR-489-3p expression is detected by quantitative real-time PCR (qPCR); and SLC7A11 protein expression is analyzed by western blot [2] - Cortical neuron excitotoxicity assay: Primary cortical neurons are isolated from embryonic mice and cultured in vitro. After maturation, neurons are pretreated with Levobupivacaine HCl for a certain period, then exposed to NMDA to induce excitotoxicity. Neuronal survival rate is evaluated by MTT assay or live/dead staining, and morphological changes of neurons are observed under a microscope [3] - Neuronal sodium channel assay: Isolated neurons are cultured, and Levobupivacaine HCl is added to the culture medium at gradient concentrations. Patch-clamp technique is used to record sodium channel currents, and the inhibitory effect on channel activity is analyzed [1] |
| Animal Protocol |
Animal/Disease Models: CD1 mice (30-35 g ; induced epileptic seizures by injecting with NMDA)[3]
Doses: 5 or 36 mg/kg Route of Administration: IP; single dosage Experimental Results: Increased the latency to partial seizures and prevented the occurrence of generalized seizures at 5 mg/kg; decreased the latency to NMDA-induced seizures and increased seizure severity at 36 mg/kg. Animal/Disease Models: SCID nude mice (6-8 weeks; subcutaneously (sc) injected with 5×106 SGC7901 cells)[2] Doses: 40 μmol/kg Route of Administration: IP; one time/day for 25 days Experimental Results: Dramatically inhibited SGC7901 cell growth, and enhanced the lipid ROS accumulation. Regional anaesthesia animal assay: Animals (rats, rabbits, or dogs) are randomly divided into experimental and control groups. Levobupivacaine HCl is prepared as a sterile aqueous solution with concentrations ranging from 0.25% to 0.75% (w/v). The drug is administered via epidural, spinal, sciatic nerve block, or local infiltration at doses of 1-10 mg/kg (varies by animal species and administration route). Anaesthetic onset time, duration of motor and sensory block, and recovery time are recorded [1] - NMDA-induced seizure mouse assay: Male or female mice (strain not specified) are divided into control, model, and Levobupivacaine HCl treatment groups. The treatment group receives intraperitoneal or intracerebroventricular injection of Levobupivacaine HCl at a dose of 5-20 mg/kg 30 minutes before NMDA administration. NMDA is injected intraperitoneally at a convulsive dose to induce seizures. The number of seizures, seizure duration, and mortality are recorded within 24 hours; brain tissues are collected for histological analysis to evaluate neuronal damage [3] |
| ADME/Pharmacokinetics |
Levobupivacaine hydrochloride has a high plasma protein binding rate (97-98%) [1] - It is mainly metabolized in the liver by cytochrome P450 (CYP) enzymes, of which CYP3A4 and CYP1A2 are the main metabolic isoenzymes [1] - After epidural administration, its elimination half-life in the human body is about 3-4 hours [1] - It is mainly excreted by the kidneys, with less than 5% of the original drug being excreted unchanged [1]
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| Toxicity/Toxicokinetics |
Compared with racemic bupivacaine, levobupivacaine hydrochloride has lower cardiovascular and central nervous system toxicity; the threshold dose for inducing arrhythmias, hypotension, or central nervous system depression is higher [1]
- High doses may lead to dose-related central nervous system effects (dizziness, tinnitus, convulsions) and cardiovascular effects (myocardial depression, bradycardia) in animals and humans [1] |
| References |
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| Additional Infomation |
Levobupivacaine hydrochloride (anhydrous) is the monohydrochloride salt of levobupivacaine. It is a local anesthetic, adrenergic antagonist, amphiphilic molecule, EC 3.1.1.8 (cholinesterase) inhibitor, and EC 3.6.3.8 (Ca²⁺ ATP transporter) inhibitor. It contains the levobupivacaine (1+) molecule. It is the enantiomer of dexbupivacaine hydrochloride (anhydrous). Levobupivacaine hydrochloride is the hydrochloride salt of levobupivacaine, an amide derivative with anesthetic effects. Levobupivacaine reversibly binds to voltage-gated sodium channels, modulating ion flow and blocking the generation and transmission of nerve impulses (stabilizing neuronal membranes), thereby producing analgesic and anesthetic effects. Compared to racemic bupivacaine, levobupivacaine has a weaker vasodilatory effect and a longer duration of action.
Levobupivacaine is the S-enantiomer of bupivacaine and is used as a local anesthetic and regional nerve blocker, including epidural anesthesia. See also: Levobupivacaine (containing the active moiety). Levobupivacaine hydrochloride is the S-enantiomer of racemic bupivacaine and is a long-acting amide local anesthetic [1]. - Its clinical indications include regional anesthesia (epidural, spinal, and peripheral nerve blocks) and postoperative analgesia [1]. - The ferroptosis-inducing effect of levobupivacaine hydrochloride in gastric cancer cells provides a potential new direction for the repurposing of local anesthetics for cancer treatment [2]. It exerts its neuroprotective effect by reducing NMDA-induced excitotoxicity, which may be related to the regulation of glutamate receptor signaling or the reduction of oxidative stress [3]. |
| Molecular Formula |
C18H28N2O.HCL
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| Molecular Weight |
324.89
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| Exact Mass |
324.196
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| CAS # |
27262-48-2
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| Related CAS # |
Levobupivacaine;27262-47-1
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| PubChem CID |
117965
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| Appearance |
White to off-white solid powder
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| Boiling Point |
423.4ºC at 760 mmHg
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| Melting Point |
254 °C (dec.)(lit.)
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| Flash Point |
209.9ºC
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| Vapour Pressure |
2.24E-07mmHg at 25°C
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| LogP |
4.74
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
22
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| Complexity |
321
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| Defined Atom Stereocenter Count |
1
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| SMILES |
CCCCN1CCCC[C@H]1C(=O)NC2=C(C=CC=C2C)C.Cl
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| InChi Key |
SIEYLFHKZGLBNX-NTISSMGPSA-N
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| InChi Code |
InChI=1S/C18H28N2O.ClH/c1-4-5-12-20-13-7-6-11-16(20)18(21)19-17-14(2)9-8-10-15(17)3;/h8-10,16H,4-7,11-13H2,1-3H3,(H,19,21);1H/t16-;/m0./s1
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| Chemical Name |
(2S)-1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide hydrochloride
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| Synonyms |
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 3 mg/mL (9.23 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 30.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 3 mg/mL (9.23 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 30.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.0780 mL | 15.3898 mL | 30.7796 mL | |
| 5 mM | 0.6156 mL | 3.0780 mL | 6.1559 mL | |
| 10 mM | 0.3078 mL | 1.5390 mL | 3.0780 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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