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]

Levobupivacaine（0–4 mM；24 h）抑制 HGC27 和 SGC7901 细胞的活力，但对 GES-1 细胞的活力没有影响[2]。 Levobupivacaine（2 mM；24、48 或 72 小时）可增加 Erastin 对 HGC27 和 SGC7901 细胞活力的抑制作用；它还会提高铁、Fe2+ 和脂质活性氧的水平[2]。 Levobupivacaine（2 mM；24 h）可提高 HGC27 和 SGC7901 细胞中铁和 Fe2+ 的水平，并改善 miR-489-3p 的表达[2]。

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盐酸左旋布比卡因（Levobupivacaine HCl） 抑制神经元细胞膜上的电压门控钠通道，阻断钠离子内流并抑制神经冲动传导，这是其发挥区域麻醉和镇痛作用的基础 [1]
- 在人胃癌细胞系中，盐酸左旋布比卡因（Levobupivacaine HCl） 通过调控miR-489-3p/SLC7A11信号通路诱导铁死亡：上调miR-489-3p表达，该microRNA直接靶向并下调SLC7A11，导致谷胱甘肽（GSH）合成减少、脂质过氧化水平升高，最终导致胃癌细胞死亡 [2]
- 在原代培养的皮质神经元中，盐酸左旋布比卡因（Levobupivacaine HCl） 可减少NMDA暴露诱导的兴奋性毒性神经元死亡；与消旋布比卡因相比，其在相关浓度下表现出相当的神经保护作用 [3]

Levobupivacaine（40 μmol/kg；IP；每日一次，持续 25 天）可增加脂质 ROS 的积累，同时显着抑制 SGC7901 细胞的发育[2]。小剂量使用时，左氧氟沙星（5 或 36 mg/kg；IP；单剂量）可延长部分性癫痫发作的潜伏期并抑制全身性癫痫发作；当大剂量使用时，它会缩短 N-甲基-d-天冬氨酸 (NMDA) 诱发的癫痫发作潜伏期并加剧癫痫发作[3]。

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在动物模型和临床场景中，盐酸左旋布比卡因（Levobupivacaine HCl） 经硬膜外、脊髓、周围神经阻滞或局部浸润给药时，呈现剂量依赖性区域麻醉效果，镇痛持续时间与消旋布比卡因相当或更长 [1]
- 在NMDA诱导癫痫的小鼠中，盐酸左旋布比卡因（Levobupivacaine HCl） 预处理可降低癫痫发作的严重程度和持续时间，并减轻脑组织中NMDA介导的兴奋性毒性神经元损伤，其神经保护效力与消旋布比卡因相似 [3]

电压门控钠通道活性测定：采用神经元细胞膜制备物或分离的神经元，通过膜片钳技术记录钠通道电流。将盐酸左旋布比卡因（Levobupivacaine HCl） 以梯度浓度应用，分析电流幅度和门控特性的变化，以评估阻断效率 [1]
- SLC7A11活性测定：制备胃癌细胞裂解液，通过检测GSH合成效率来衡量SLC7A11的转运活性。将盐酸左旋布比卡因（Levobupivacaine HCl） 与裂解液共同孵育，定量检测GSH水平变化以反映SLC7A11的抑制情况 [2]

细胞活力测定[2]
细胞类型： GES-1、HGC27 和 SGC790
测试浓度： 0、0.5、1、2 和 4 mM
孵育时间： 24 h
实验结果：不影响正常胃上皮GES-1细胞系的活力，但抑制HGC27和SGC7901细胞的活力以剂量依赖性方式。

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细胞活力测定[2]
细胞类型： HGC27 和 SGC7901（与 5 μMerastin 一起孵育）
测试浓度： 2 mM
孵育时间：24、48或72小时
实验结果：增强erastin诱导的对HGC27和SGC7901细胞活力的抑制作用；诱导 Fe2+、铁和脂质 ROS 的水平。

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RT-PCR[2]
细胞类型： HGC27 和 SGC7901（与 5 μMerastin 一起孵育）
测试浓度： 2 mM
孵育时间： 24 h
实验结果：增强HGC27和SGC7901细胞中miR-489-3p的表达，增加Fe2+和铁的水平。

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胃癌细胞铁死亡测定：将胃癌细胞接种培养至对数生长期，用不同浓度（公开数据未明确具体范围）的盐酸左旋布比卡因（Levobupivacaine HCl） 处理24-72小时。采用CCK-8法检测细胞活力；使用脂质活性氧（ROS）探针检测脂质过氧化水平；通过比色法测定GSH含量；采用实时荧光定量PCR（qPCR）检测miR-489-3p表达；通过western blot分析SLC7A11蛋白表达 [2]
- 皮质神经元兴奋性毒性测定：从胚胎小鼠中分离原代皮质神经元并进行体外培养。神经元成熟后，用盐酸左旋布比卡因（Levobupivacaine HCl） 预处理一定时间，再用NMDA诱导兴奋性毒性。通过MTT法或活/死染色评估神经元存活率，在显微镜下观察神经元形态变化 [3]
- 神经元钠通道测定：培养分离的神经元，在培养基中加入梯度浓度的盐酸左旋布比卡因（Levobupivacaine HCl）。采用膜片钳技术记录钠通道电流，分析对通道活性的抑制作用 [1]

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.

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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.

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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]

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]

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]

[1]. Levobupivacaine: a review of its use in regional anaesthesia and pain management. Drugs. 2010 Apr 16;70(6):761-91.

[2]. Levobupivacaine Induces Ferroptosis by miR-489-3p/SLC7A11 Signaling in Gastric Cancer. Front Pharmacol. 2021 Jun 9;12:681338.

[3]. Comparative effects of levobupivacaine and racemic bupivacaine on excitotoxic neuronal death in culture and N-methyl-D-aspartate-induced seizures in mice. Eur J Pharmacol. 2005 Aug 22;518(2-3):111-5.

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].

C18H28N2O.HCL

324.89

324.196

27262-48-2

Levobupivacaine;27262-47-1

117965

White to off-white solid powder

423.4ºC at 760 mmHg

254 °C (dec.)(lit.)

209.9ºC

2.24E-07mmHg at 25°C

4.74

23.55

2

2

5

22

321

1

CCCCN1CCCC[C@H]1C(=O)NC2=C(C=CC=C2C)C.Cl

SIEYLFHKZGLBNX-NTISSMGPSA-N

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

(2S)-1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 3 mg/mL (9.23 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 30.0 mg/mL 澄清的 DMSO 储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL 生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 3 mg/mL (9.23 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 30.0 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。