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			{{short description|Chemical compound}}
	{{Drugbox| verifiedrevid = 402198969
			{{Drugbox
	|
			| Verifiedfields = changed
	| image=Levobupivacaine.png
			| Watchedfields = changed
	| IUPAC_name = (''S'')-1-butyl-''N''-(2,6-dimethylphenyl)<br />piperidine-2-carboxamide
			| index2_label = HCl
	| ATC_prefix=N01
			| DTXSID = 8048496
	| ATC_suffix=BB10
			| CAS_number2 = 27262-48-2
	| PubChem=92253
			| CAS_number2_Ref = {{cascite|correct|CAS}}
	| DrugBank=APRD00110
			| PubChem2 = 117965
	| CASNo_Ref = {{cascite|correct|CAS}}
			| DrugBank2 = DBSALT000834
	| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| DrugBank2_Ref = {{drugbankcite|correct|drugbank}}
	| ChemSpiderID = 83289
			| UNII2 = J998RDZ51I
	| UNII_Ref = {{fdacite|correct|FDA}}
			| UNII2_Ref = {{fdacite|correct|FDA}}
	| UNII = A5H73K9U3W
			| KEGG2 = D01287
	| InChI = 1/C18H28N2O/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)/t16-/m0/s1
			| KEGG2_Ref = {{keggcite|correct|kegg}}
	| InChIKey = LEBVLXFERQHONN-INIZCTEOBJ
			| ChEMBL2 = ChEMBL1201177
	| smiles = O=C(Nc1c(cccc1C)C)2N(CCCC)CCCC2
	| StdInChI_Ref = {{stdinchicite|correct|chemspider}}		| ChEMBL2_Ref = {{ebicite|correct|EBI}}
			| DTXSID2 = 9046071
	| StdInChI = 1S/C18H28N2O/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)/t16-/m0/s1
			| verifiedrevid = 462090767
	| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
			| IUPAC_name = (''S'')-1-butyl-''N''-(2,6-dimethylphenyl)<br />piperidine-2-carboxamide
	| StdInChIKey = LEBVLXFERQHONN-INIZCTEOSA-N
			| image = Levobupivacaine.png
	| CAS_number = 27262-47-1
	| C = 18 | H = 28 | N = 2 | O = 1		| image2 = Bupivacaine-from-xtal-3D-bs-17.png
			<!--Clinical data-->| pronounce = {{IPAc-en|l|iː|v|oʊ|b|juː|ˈ|p|ɪ|v|ə|k|eɪ|n}}
	| molecular_weight = 288.43 g/mol
			| tradename = Chirocaine
	| bioavailability = n/a
			| Drugs.com = {{drugs.com|CONS|levobupivacaine}}
	| metabolism = ]
			| pregnancy_AU = B3
	| elimination_half-life = 2–2.6 hours
			| legal_AU = S4
	| excretion = ] 70%, ] 24%
			| legal_EU = Rx-only
	| pregnancy_AU = B3
			| legal_UK = POM
	| legal_AU = S4
	| routes_of_administration = ]		| routes_of_administration = ]
			<!--Pharmacokinetic data-->| bioavailability = n/a
			| protein_bound = 97%
			| metabolism = ]
			| metabolites = 3-hydroxy-levobupivacaine
			desbutyl-levobupivacaine
			| onset = Within 15 minutes
			| elimination_half-life = 80 minutes
			| duration_of_action = Up to 16 hours
			| excretion = ] 71%, ] 24%
			<!--Identifiers-->| IUPHAR_ligand = 7211
			| CAS_number_Ref = {{cascite|correct|CAS}}
			| CAS_number = 27262-47-1
			| ATC_prefix = N01
			| ATC_suffix = BB10
			| PubChem = 92253
			| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
			| DrugBank = DB01002
			| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID = 83289
			| UNII_Ref = {{fdacite|correct|FDA}}
			| KEGG = D08116
			| UNII = A5H73K9U3W
			| ChEBI_Ref = {{ebicite|changed|EBI}}
			| KEGG_Ref = {{keggcite|correct|kegg}}
			| ChEBI = 6149
			| ChEMBL_Ref = {{ebicite|correct|EBI}}
			| synonyms = (S)-bupivacaine
			(-)-bupivacaine
			L(-)-bupivacaine
			| ChEMBL = 1201193
			<!--Chemical data-->| C = 18
			| H = 28
			| N = 2
			| O = 1
			| smiles = O=C(1N(CCCC1)CCCC)NC2=C(C)C=CC=C2C
			| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
			| StdInChI = 1S/C18H28N2O/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)/t16-/m0/s1
			| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
			| StdInChIKey = LEBVLXFERQHONN-INIZCTEOSA-N
	}}		}}
	'''Levobupivacaine''' (]) ({{pronEng|liːvoʊbjuːˈpɪvəkeɪn}}) is a ] drug belonging to the ] ] group. It is the ''S''-] of ]. <ref name="pmid18728849">{{cite journal |author=Burlacu CL, Buggy DJ |title=Update on local anesthetics: focus on levobupivacaine |journal=Ther Clin Risk Manag |volume=4 |issue=2 |pages=381–92 |year=2008 |month=April |pmid=18728849 |doi= |url= |pmc=2504073}}</ref>
			'''Levobupivacaine''' (]) is a ] drug indicated for minor and major ] and ]. It is a long-acting ]-type local anaesthetic that blocks nerve impulses by inhibiting sodium ion influx into the ].<ref name=":0">{{cite journal | vauthors = Heppolette CA, Brunnen D, Bampoe S, Odor PM | title = Clinical Pharmacokinetics and Pharmacodynamics of Levobupivacaine | journal = Clinical Pharmacokinetics | volume = 59 | issue = 6 | pages = 715–745 | date = June 2020 | pmid = 32034727 | doi = 10.1007/s40262-020-00868-0 | s2cid = 211061840 }}</ref> Levobupivacaine is the S-] of racemic ] and therefore similar in pharmacological effects.<ref name=":1">{{cite journal | vauthors = Burlacu CL, Buggy DJ | title = Update on local anesthetics: focus on levobupivacaine | language = English | journal = Therapeutics and Clinical Risk Management | volume = 4 | issue = 2 | pages = 381–392 | date = April 2008 | pmid = 18728849 | pmc = 2504073 | doi = 10.2147/TCRM.S1433 | doi-access = free }}</ref> The drug typically starts taking effect within 15 minutes and can last up to 16 hours depending on factors such as site of administration and dosage.<ref name=":0" />
	'''Levobupivacaine hydrochloride''' is commonly marketed by ] under the ] '''Chirocaine'''.
			Levobupivacaine was designed, in the late 1970s, to be a safer and more effective alternative to bupivacaine, which had been associated with a higher risk of cardiotoxicity.<ref name=":0" /><ref name=":1" /> Compared to bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action. It is approximately 13 per cent less potent (by molarity) than racemic bupivacaine and has a longer ] onset time.<ref>{{cite journal | vauthors = Gulec D, Karsli B, Ertugrul F, Bigat Z, Kayacan N | title = Intrathecal bupivacaine or levobupivacaine: which should be used for elderly patients? | journal = The Journal of International Medical Research | volume = 42 | issue = 2 | pages = 376–385 | date = April 2014 | pmid = 24595149 | doi = 10.1177/0300060513496737 | s2cid = 206506181 | doi-access = free }}</ref> Ropivacaine is, next to levobupivacaine, another less cardiotoxic alternative to bupivacaine.<ref name=":2">{{Cite journal | vauthors = Cada DJ, Baker DE, Levien T |date= December 1999 |title=Levobupivacaine |journal=Hospital Pharmacy |language=en |volume=34 |issue=12 |pages=1441–1453 |doi=10.1177/194512539903401211 |s2cid= 261109078 |issn=0018-5787}}</ref>
	==Clinical use==
	Compared to bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action. It is approximately 13 percent less potent (by molarity) than racemic bupivacaine.
			Levobupivacaine hydrochloride is commonly marketed by ] under the ] Chirocaine.<ref>{{Cite book |url=https://www.worldcat.org/oclc/1322357781 |title=AMH 2006. |date=2006 |publisher=Australian Medicines Handbook Pty Ltd | vauthors = Rossi S |isbn=0-9757919-2-3 |edition = 7th |location=Adelaide, S.A. |oclc=1322357781}}</ref> In Europe, Chirocaine is available – ] – in concentrations ranging from 0.625 mg/mL to 7.5 mg/mL.<ref>{{Cite web |date=2018-09-06 |title=Levobupivacaine - List of nationally authorised medicinal products |url=https://www.ema.europa.eu/en/documents/psusa/levobupivacaine-list-nationally-authorised-medicinal-products-psusa/00001848/201712_en.pdf |website=European Medicines Agency}}</ref>
	===Indications===
	Levobupivacaine is indicated for local anaesthesia including infiltration, ], ], ] and ] anaesthesia in adults; and infiltration analgesia in children.
			== Clinical use ==
	===Contraindications===
	Levobupivacaine is contraindicated for IV regional anaesthesia (IVRA).
	===Adverse effects===		=== Indications ===
			Levobupivacaine, the S(-)-enantiomer of bupivacaine has been developed as an alternative to the racemic mixture, as it has been shown to have a lower ] than bupivacaine. Under ] advice, it can be applied for minor and major ], as well as (post-operative) ].<ref name=":3">{{cite journal | vauthors = Foster RH, Markham A | title = Levobupivacaine: a review of its pharmacology and use as a local anaesthetic | journal = Drugs | volume = 59 | issue = 3 | pages = 551–579 | date = March 2000 | pmid = 10776835 | doi = 10.2165/00003495-200059030-00013 | s2cid = 195691108 }}</ref> Particularly, it has been found suitable for multiple procedures, such as ]. It is effective for human patients who receive elective ] or lower body surgery, as it does not diverge dramatically in terms of sensory and/or motor block duration in comparison to bupivacaine.<ref name=":3" /> Deserving of consideration is the fact that its enhanced motor blocking can be a downside for patients receiving an epidural injection during ], as a certain level of movement may still be required.<ref name=":3" />
	]s (ADRs) are rare when it is administered correctly. Most ADRs relate to administration technique (resulting in systemic exposure) or pharmacological effects of anesthesia, however ] reactions can rarely occur.
			Other than childbirth, possible applications of levobupivacaine include upper and lower limb surgery, as well as ], where it blocks the ], highly efficient and convenient for patients undergoing vitreoretinal anterior segment or cataract surgery.<ref name=":4">{{cite journal | vauthors = Sanford M, Keating GM | title = Levobupivacaine: a review of its use in regional anaesthesia and pain management | journal = Drugs | volume = 70 | issue = 6 | pages = 761–791 | date = April 2010 | pmid = 20394458 | doi = 10.2165/11203250-000000000-00000 | s2cid = 70725624 }}</ref>
	Systemic exposure to excessive quantities of bupivacaine mainly result in ] (CNS) and ] effects – CNS effects usually occur at lower ] concentrations and additional cardiovascular effects present at higher concentrations, though cardiovascular collapse may also occur with low concentrations. CNS effects may include CNS excitation (nervousness, tingling around the mouth, ], tremor, dizziness, blurred vision, ]s) followed by depression (drowsiness, loss of consciousness, ] and ]). Cardiovascular effects include ], ], ]s, and/or ] – some of which may be due to ] secondary to respiratory depression.<ref>Rossi S, editor. ] 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3</ref>
			Levobupivacaine can be combined with other analgesics, including ]s, for postoperative pain management.<ref name=":5">{{Cite web | work = Abbot Laboratories |date=1999 |title=Chirocaine 2.5 mg/mL: summary of product characteristics | url = https://www.medicines.org.uk/emc/product/1555/smpc#gref }}</ref>
	==References==
			=== Contraindications ===
			Using 0.75% (7.5 mg/mL) of levobupivacaine, similar to bupivacaine, is ] in ] patients. Use in ]s in obstetrics is also contraindicated. Levobupivacaine is furthermore contraindicated in patients with known ] to levobupivacaine or other amide-type local anaesthetics, in patients with severe ] (e.g. cardiac or ]) and for use in ] (Bier’s block).<ref name=":5" /><ref name=":6">{{Cite report | work = Purdue Pharma L.P. |date=1999 |title=Chirocaine (levobupivacaine injection) prescribing information }}</ref>
			=== Adverse effects ===
			Possible adverse effects in the ] caused by levobupivacaine usage are ], ], tongue numbness and ]s, which may be due to the blockade of sodium, potassium and calcium channels in tissues that were not intended as targets.<ref name=":7">{{cite journal | vauthors = Gomez de Segura IA, Menafro A, García-Fernández P, Murillo S, Parodi EM | title = Analgesic and motor-blocking action of epidurally administered levobupivacaine or bupivacaine in the conscious dog | language = English | journal = Veterinary Anaesthesia and Analgesia | volume = 36 | issue = 5 | pages = 485–494 | date = September 2009 | pmid = 19508452 | doi = 10.1111/j.1467-2995.2009.00469.x }}</ref> ] may be a result of indirect effects of the drug, such as the blockade of myocardial sympathetic nerves, thus leading to contractile delay, or by direct effects, such as the blockade of potassium channels.<ref name=":3" />
			Effects of this nature lead to lowered contractile function and arrhythmogenic effects, which can potentially cause ] and death.<ref name=":7" /> It is to note that the drug also has ] activity, thereby increasing the duration of sensory blockage with a relatively low risk of central nervous system toxicity on one hand, and on the other, it can have the same effect on uteroplacental blood flow, which can harm the ].<ref name=":3" /> Ultimately, levobupivacaine has been shown to have a lower risk of cardiovascular and central nervous system toxicity compared to bupivacaine in ], not at the expense of ] and ], and should be therefore considered as an alternative.<ref name=":3" />
			=== Toxicity ===
			Levobupivacaine has become a more favourable alternative for regional anaesthesia than bupivacaine due to its reduced toxicity. A plethora of non-human studies have established levobupivacaine’s lower risk of cardiac and neurotoxic adverse effects.<ref name=":1" /><ref name=":8">{{Cite journal | vauthors = Casati A, Baciarello M |title=Enantiomeric Local Anesthetics: Can Ropivacaine and Levobupivacaine Improve Our Practice? |url=https://www.eurekaselect.com/article/134 |journal=Current Drug Therapy |year=2006 |language=en |volume=1 |issue=1 |pages=85–89 |doi=10.2174/157488506775268506}}</ref><ref name=":9">{{cite journal | vauthors = Huang YF, Pryor ME, Mather LE, Veering BT | title = Cardiovascular and central nervous system effects of intravenous levobupivacaine and bupivacaine in sheep | language = en-US | journal = Anesthesia and Analgesia | volume = 86 | issue = 4 | pages = 797–804 | date = April 1998 | pmid = 9539605 | doi = 10.1213/00000539-199804000-00023 | s2cid = 19156695 }}</ref> Most animal studies show that the ] (LD<sub>50</sub>) of levobupivacaine is approximately 50% higher than that of bupivacaine.<ref name=":2" /> In general, laevorotatory isomers tend to cause significantly fewer adverse effects and are thus a safer pharmacological alternative.<ref name=":8" /><ref name=":9" /> Levobupivacaine has a 97% ] which is 2% higher than what is observed in bupivacaine.<ref name=":0" /> The faster protein binding rate contributes to its reduced toxicity level.<ref>{{cite journal | vauthors = Burm AG, van der Meer AD, van Kleef JW, Zeijlmans PW, Groen K | title = Pharmacokinetics of the enantiomers of bupivacaine following intravenous administration of the racemate | journal = British Journal of Clinical Pharmacology | volume = 38 | issue = 2 | pages = 125–129 | date = August 1994 | pmid = 7981012 | doi = 10.1111/j.1365-2125.1994.tb04335.x | pmc = 1364857 }}</ref>
			In human volunteer studies, levobupivacaine consistently proved to have a safety advantage over bupivacaine.<ref>{{cite journal | vauthors = Bardsley H, Gristwood R, Baker H, Watson N, Nimmo W | title = A comparison of the cardiovascular effects of levobupivacaine and rac-bupivacaine following intravenous administration to healthy volunteers | journal = British Journal of Clinical Pharmacology | volume = 46 | issue = 3 | pages = 245–249 | date = September 1998 | pmid = 9764965 | pmc = 1873676 | doi = 10.1046/j.1365-2125.1998.00775.x }}</ref><ref name=":10">{{cite journal | vauthors = Gristwood RW, Greaves JL | title = Levobupivacaine: a new safer long acting local anaesthetic agent | journal = Expert Opinion on Investigational Drugs | volume = 8 | issue = 6 | pages = 861–876 | date = June 1999 | pmid = 15992136 | doi = 10.1517/13543784.8.6.861 }}</ref> Risk factors for local anaesthetic toxicity depend on the administration of levobupivacaine to ] and ], as well as the predisposition of these tissues to levobupivacaine’s negative effects.<ref name=":0" />
			Age is a relevant factor in vulnerability to levobupivacaine toxicity. Elderly patients are more likely to have pre-existing conditions impacting the ], ] and ], which contribute to the slower absorption rate and plasma concentrations below the toxic level compared to younger patients.<ref name=":0" /><ref>{{cite journal | vauthors = Rosen MA, Thigpen JW, Shnider SM, Foutz SE, Levinson G, Koike M | title = Bupivacaine-induced cardiotoxicity in hypoxic and acidotic sheep | journal = Anesthesia and Analgesia | volume = 64 | issue = 11 | pages = 1089–1096 | date = November 1985 | doi = 10.1213/00000539-198511000-00010 | pmid = 4051206 | url = https://pubmed.ncbi.nlm.nih.gov/4051206 }}</ref> On the other hand, homeostatic disbalance can exacerbate toxic effects.<ref name=":3" />
			It is important to adjust the dosage of levobupivacaine in ] patients due to their underdeveloped metabolic processing to prevent reaching toxic levels. The dosage of local anaesthetics is calculated based on the patient’s weight and ], however, the association power is stronger in children than in adults. Moreover, symptoms of systemic toxicity like ] are harder to notice in children.<ref name=":0" />
			== Pharmacology ==
			=== Pharmacodynamics ===
			Levobupivacaine is a drug that has ], motor blocking, and sensory blocking effects on the human body, whose properties are dictated by its chemical characteristics, such as ], which has a value of 8.1.<ref name=":4" /> The pK<sub>a</sub> of a drug can be informative information that indicates its ] under ]s. For example, drugs with a high pK<sub>a</sub>, such as that of levobupivacaine, tend to be their ionised form under physiological state, meaning that they would not easily cross the ] ] of cells. This, however, is counteracted by the high lipid solubility of levobupivacaine, which increases the ease with which it can diffuse through the ].<ref name=":4" /> Additionally, ] quality (97%) is characteristic of levobupivacaine, which strengthens its binding to cell surface proteins, thereby lengthening the binding, and thus action time.<ref name=":4" />
			The S(-)-enantiomer of levobupivacaine is a high-], long-acting anaesthetic with a relatively slow ]. Indeed, it has been found in certain studies that, as a surgical anaesthetic, it has a sensory ad motor blocking activity for over 90% of adult patients who received appropriate doses for their bodily composition, and duration of the surgery, with an onset time of 15 minutes.<ref name=":3" />
			More specifically, levobupivacaine achieves its effects by acting on the neuronal voltage-sensitive ]s, where it prevents the transmission of ].<ref name=":11">{{cite journal | vauthors = Bajwa SJ, Kaur J | title = Clinical profile of levobupivacaine in regional anesthesia: A systematic review | language = en-US | journal = Journal of Anaesthesiology Clinical Pharmacology | volume = 29 | issue = 4 | pages = 530–539 | date = October 2013 | pmid = 24249993 | pmc = 3819850 | doi = 10.4103/0970-9185.119172 | doi-access = free }}</ref> The normal function of these sodium channels is halted temporarily, as the drug interferes with their opening, thereby inhibiting the conduction of action potentials in nerves involved in sympathetic, sensory, and motor activity.<ref name=":3" /> This interruption results in decreased muscle control, and overall analgesic effects which allow for levobupivacaine to act as a local anaesthetic.<ref name=":7" />
			Levobupivacaine varies slightly in its effects depending on the characteristics of the neuron in question. For example, in ]ated neurons, the ] are targeted and more easily blocked than unmyelinated neurons, and small nerves are more easily blocked than large nerves.<ref name=":3" /><ref name=":11" />
			When compared to the racemic bupivacaine mixture, levobupivacaine generally has been shown to have similar effects. As an anaesthetic, it is similar in nerve-blocking potency compared to its R(+)-enantiomer and racemic mixture, although its effects are affected by the route of administration and the concentration, however, they were ultimately similar among the three.<ref name=":3" /> Some ] indicate that among the three, levobupivacaine shows an increased duration of anaesthesia and/or greater potency, and there is evidence that in humans it is as potent as bupivacaine.<ref name=":3" />
			=== Pharmacokinetics ===
			The plasma concentration of levobupivacaine is influenced by both the dosage and the ]. Additionally, ] depends on the vascularity of the tissue. Maximum plasma concentration of 1.2 μg/mL is reached approximately 30 minutes post epidural injection.
			Levobupivacaine undergoes ] in the liver by the ], specifically CYP1A2 and CYP3A isoforms as part of phase one biotransformation, thereby producing inactive metabolites. The major metabolite produced is 3-hydroxy-levobupivacaine and the minor one is desbutyl-levobupivacaine. Subsequently, levobupivacaine metabolites are further converted into ] and sulphate ester conjugates as a part of phase two.<ref name=":3" /><ref name=":10" /> Metabolic inversion of levobupivacaine is not observed. The extensive metabolism of levobupivacaine by the liver ensures that no unchanged drug is excreted via ]. As a result, in patients with ], only the inactive metabolites accumulate instead of the drug itself.
			Research tracing ] levobupivacaine showed that 71% was recovered in urine and 24% was recovered in ]l<ref name=":5" /> After the ] of 40 mg of levobupivacaine, the ] was approximately 80 minutes and the rate of ] was 651 ± 221.5 mL/min.<ref name=":6" /><ref name=":10" />
			== Chemistry ==
			=== Structure ===
			Levobupivacaine is an ]-] anaesthetic that is similar in structure to bupivacaine, namely the S-enantiomer of bupivacaine. A lipophilic ] is linked to a ] by an amide bond. The ] components of levobupivacaine allow it to cross ]s and exert its local anaesthetic effect by causing a reversible blockade of open neuronal sodium channels.
			=== Synthesis ===
			]
			]
			A 5-step process to synthesise levobupivacaine from N<sup>α</sup>-CBZ (S)-lysine, published in 1996,<ref>{{Cite journal | vauthors = Adger B, Dyer U, Hutton G, Woods M |date=1996-08-26 |title=Stereospecific synthesis of the anaesthetic levobupivacaine |url=https://dx.doi.org/10.1016/0040-4039%2896%2901357-3 |journal=Tetrahedron Letters |language=en |volume=37 |issue=35 |pages=6399–6402 |doi=10.1016/0040-4039(96)01357-3 |issn=0040-4039}}</ref> is depicted in Scheme 1. The key steps in this process include oxidative de-animation and stereospecific ring closure to form the pipecolamide core structure. This method is claimed to be efficient, but showed to be dangerous for mass production due to the high risk of explosion of the diazonium salt intermediates.
			A more recent ] from 2008,<ref>{{Cite patent|number=KR100844336B1|title=New synthetic method of levobupivacaine and its hydrochloride|gdate=2008-07-07|invent1=장사정|invent2=이재목|invent3=공준수|url=https://patents.google.com/patent/KR100844336B1/en}}</ref> consists of a 3-step process (see Scheme 2) to synthesise levobupivacaine hydrochloride of an ] of at least 99%. (S)-2,6-pipecocholxylide (I) is reacted with 1-bromobutane and a ] (a), such as ], to obtain a solution of (S)-bupivacaine (II) and its enantiomers. ] of this solution with a solvent (b), preferably ], can lead to an optical purity of at least 98% levobupivacaine. Lastly, the addition of ] (c) is possible.{{clear}}
			== References ==
	{{reflist}}		{{reflist}}
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