Voltage-gated sodium ion channels in neuronal cell membranes. Mepivacaine Hydrochloride binds to specific voltage-gated sodium ion channels, inhibiting both sodium influx and membrane depolarization. This prevents the generation and conduction of nerve impulses, resulting in local anesthesia. The compound is an amide-type local anesthetic, related chemically and pharmacologically to lidocaine and bupivacaine.

Mepivacaine hydrochloride inhibits sodium influx and membrane depolarization by binding to particular voltage-gated sodium channels in the membranes of neuronal cells. This leads to reversible sensory loss and a blockage in the beginning and conduction of nerve impulses. This medication acts more quickly and lasts for a moderate amount of time when compared to other local anesthetics [2]. Compared to procaine, mepivacaine hydrochloride acts more quickly at first and for a longer amount of time in the middle [3]. Preferential usage-dependent blockage of Na(v)1.8 is demonstrated by mepivacaine hydrochloride, while TTX Na(+) channels are preferred by S(-)-bupivacaine [4].
Mepivacaine Hydrochloride demonstrates local anesthetic activity in vitro by blocking voltage-gated sodium channels in neuronal preparations. The compound inhibits sodium influx and membrane depolarization in a concentration-dependent manner. Its potency and efficacy have been characterized in electrophysiological studies using isolated nerve preparations.

In vivo, Mepivacaine Hydrochloride is used clinically as a local anesthetic for infiltration anesthesia, peripheral nerve blocks, and dental anesthesia. It provides rapid onset and moderate duration of anesthesia. The compound is effective for minor surgical procedures and dental treatments. Its effects are reversible and localized to the site of administration.

In vitro assays for Mepivacaine Hydrochloride typically involve electrophysiological recordings from isolated nerve preparations or cells expressing voltage-gated sodium channels. The compound is applied at varying concentrations, and sodium currents are measured using patch-clamp techniques. IC50 values for sodium channel inhibition are determined from dose-response curves. Binding assays may also be performed using radiolabeled ligands.

Cellular assays for Mepivacaine Hydrochloride involve culturing neuronal cells or cells expressing voltage-gated sodium channels. Cells are treated with Mepivacaine Hydrochloride at varying concentrations. Sodium influx is measured using fluorescent indicators or patch-clamp electrophysiology. Membrane depolarization is assessed using voltage-sensitive dyes. The compound's ability to inhibit neuronal excitation is evaluated.

In vivo animal studies for Mepivacaine Hydrochloride are typically conducted in rodent models to assess local anesthetic efficacy. The compound is administered via local infiltration or nerve block. Anesthetic onset, duration, and potency are assessed by measuring responses to painful stimuli. Dosing regimens vary depending on the study. The oral LD50 in mice has been determined in toxicological studies.

Mepivacaine Hydrochloride is administered via local infiltration, peripheral nerve block, or epidural injection. It has a molecular weight of 282.81 and a molecular formula of C15H23ClN2O. The compound is rapidly absorbed from the injection site and metabolized in the liver. It is excreted via the renal route. Detailed pharmacokinetic parameters have been characterized in clinical studies.

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
There is currently no information regarding the use of mepivacaine during lactation. Given the low levels of other local anesthetics in breast milk, a single dose of mepivacaine during lactation is unlikely to have adverse effects on breastfed infants. However, other medications may be preferred, especially when breastfeeding newborns or preterm infants.
Mepivacaine administered to mothers as a local anesthetic during labor has been reported to affect initial breastfeeding behavior in some infants, but not weight gain in the first 5 days postpartum. Although research on mepivacaine is limited, it appears that with good breastfeeding support, epidural local anesthetics, whether or not combined with fentanyl or its derivatives, have little or no adverse effects on breastfeeding success. Labor analgesia may delay the onset of lactation. More research is needed to clarify the impact of mepivacaine use during labor on breastfeeding outcomes.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
A study compared the effects of epidural analgesia using mepivacaine, bupivacaine, and lidocaine during normal labor. The results showed no difference in weight change among the three groups of breastfed infants in the first five days postpartum. Overall weight gain was within the normal range in all groups.
Of the six infants who received mepivacaine pudendal nerve block within one hour before delivery, four started breastfeeding later and had fewer initial milk volumes than 10 infants who did not receive anesthesia during delivery. The long-term consequences of these differences have not been reported.
A national survey of women and their infants from late pregnancy to 12 months postpartum compared the time to lactroogenesis II in mothers who received and did not receive analgesia during labor. Drug categories included: spinal or epidural anesthesia alone, spinal or epidural anesthesia combined with other drugs, and other analgesics alone. Women who received any type of labor analgesia were approximately twice as likely to experience a delay in the second stage of lactation (>72 hours) compared to women who did not receive labor analgesia.
Mepivacaine Hydrochloride is generally well-tolerated but can cause side effects typical of local anesthetics, including central nervous system excitation or depression, cardiovascular effects, and allergic reactions. It is contraindicated in patients with a history of hypersensitivity to amide-type local anesthetics. The compound is approved for clinical use as a local anesthetic.

[1]. ECMO for Cardiac Rescue after Accidental Intravenous Mepivacaine Application. Case Rep Pediatr. 2012;2012:491692.

[2]. mepivacaine hydrochloride.

[3]. Pharmacokinetics of the enantiomers of mepivacaine after intravenous administration of the racemate in volunteers. Anesth Analg, 1997. 84(1): p. 85-9.

[4]. Leffler, A., J. Reckzeh, and C. Nau, Block of sensory neuronal Na+ channels by the secreolytic ambroxol is associated with an interaction with local anesthetic binding sites. Eur J Pharmacol, 2010. 630(1-3): p. 19-28.

Mepivacaine hydrochloride is the hydrochloride salt of mepivacaine and is used as a local anesthetic. It is a piperidine carboxamide compound with local anesthetic effects. Its function is related to that of mepivacaine. Mepivacaine hydrochloride is the hydrochloride form of mepivacaine, an amide derivative with local anesthetic properties. At the injection site, mepivacaine hydrochloride acts by binding to specific sodium ion channels on the neuronal cell membrane, thereby inhibiting sodium ion influx. This leads to nerve impulse conduction blockade, ultimately resulting in loss of sensation. Mepivacaine is a local anesthetic with a chemical structure related to bupivacaine but pharmacologically related to lidocaine. It is suitable for infiltration anesthesia, nerve blocks, and epidural anesthesia. Mepivacaine is only effective when used locally in large doses and therefore should not be used via this route. (Excerpt from AMA Drug Evaluation, 1994, p. 168) See also: mepivacaine (with active fraction); levonorepinephrine; mepivacaine hydrochloride (component).
Mepivacaine Hydrochloride is an amide-type local anesthetic used for infiltration anesthesia, peripheral nerve blocks, and dental anesthesia. It binds to voltage-gated sodium channels, inhibiting sodium influx and membrane depolarization. The compound is available as a prescription medication and is approved for clinical use in many countries. It is also known by the brand names Carbocaine and Scandicain.

C15H23CLN2O

282.8089

282.149

1722-62-9

(+)-Mepivacaine;24358-84-7;Mepivacaine;96-88-8

66070

White to off-white solid powder

383.1ºC at 760 mmHg

255-257ºC (dec.)

185.5ºC

4.52E-06mmHg at 25°C

3.539

2

2

2

19

282

0

RETIMRUQNCDCQB-UHFFFAOYSA-N

InChI=1S/C15H22N2O.ClH/c1-11-7-6-8-12(2)14(11)16-15(18)13-9-4-5-10-17(13)3;/h6-8,13H,4-5,9-10H2,1-3H3,(H,16,18);1H

N-(2,6-dimethylphenyl)-1-methylpiperidine-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

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

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

H2O : ~100 mg/mL (~353.59 mM)

Solubility in Formulation 1: 100 mg/mL (353.59 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)