(-)-Bupivacaine

288.43

288.43

1533716-785-6

A5H73K9U3W

DTXSID8048496

N01BB10|N - Nervous system

2933399090

32.34000

3.64

Solid

1.0±0.1 g/cm3

135-137 °C

423.4±45.0 °C at 760 mmHg

209.9±28.7 °C

1.547

9.77e-02 g/L

Refrigerator

Intravenous-rat LD50: 7.2 mg/kg; Intravenous-mouse LD50: 9.6 mg/kg

Thermal decomposition to emit toxic nitrogen oxide fumes

D25 -80.9° (c = 5 in methanol)

8.1None

8.1

UN 2811 6

Xn: Harmful;T+: Very toxic;

The warehouse is ventilated, low temperature and dry; stored separately from food raw materials

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P271, P280, P284, P301+P310, P302+P352, P304+P340, P310, P312, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

highly toxic

LD50: 5.1mg/kg in rabbit, intravenous; 18mg/kg in rabbit, oral; 207mg/kg in rabbit, parenteral; 63mg/kg in rat, subcutaneous (Archives Internationales de Pharmacodynamie et de Therapie. Vol. 200, Pg. 359, 1972.) Levobupivacaine appears to cause less myocardial depression than both bupivacaine and ropivacaine, despite being in higher concentrations.

>97%

For the production of local or regional anesthesia for surgery and obstetrics, and for post-operative pain management|FDA Label

Levobupivacaine, a local anesthetic agent, is indicated for the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures.

Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate. (See all compounds classified as Anesthetics, Local.)

The plasma concentration of levobupivacaine following therapeutic administration depends on dose and also on route of administration, because absorption from the site of administration is affected by the vascularity of the tissue. Peak levels in blood were reached approximately 30 minutes after epidural administration, and doses up to 150 mg resulted in mean C_max levels of up to 1.2 µg/mL.|Following intravenous administration, recovery of the radiolabelled dose of levobupivacaine was essentially quantitative with a mean total of about 95% being recovered in urine and feces in 48 hours. Of this 95%, about 71% was in urine while 24% was in feces.|66.91 ±18.23 L [after intravenous administration of 40 mg in healthy volunteers]|39.06 ±13.29 L/h [after intravenous administration of 40 mg in healthy volunteers]

Levobupivacaine is extensively metabolized with no unchanged levobupivacaine detected in urine or feces. In vitro studies using [14 C] levobupivacaine showed that CYP3A4 isoform and CYP1A2 isoform mediate the metabolism of levobupivacaine to desbutyl levobupivacaine and 3-hydroxy levobupivacaine, respectively. In vivo, the 3-hydroxy levobupivacaine appears to undergo further transformation to glucuronide and sulfate conjugates. Metabolic inversion of levobupivacaine to R(+)-bupivacaine was not evident both in vitro and in vivo.|Levobupivacaine has known human metabolites that include N-(2,6-Dimethylphenyl)piperidine-2-carboxamide.

3.3 hours

Local anesthetics such as Levobupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Specifically, the drug binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization.

Chirocaine