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Dimethocaine, also known as DMC or larocaine, is a compound with a stimulatory effect. This effect resembles that of cocaine, although dimethocaine appears to be less potent. Just like cocaine, dimethocaine is addictive due to its stimulation of the reward pathway in the brain. However, dimethocaine is a legal cocaine replacement in some countries and is even listed by the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) under the category “synthetic cocaine derivatives”. The structure of dimethocaine, being a 4-aminobenzoic acid ester, resembles that of procaine. It is found as a white powder at room temperature. Buy Dimethocaine (DMC) larocain
When a product sold online in the UK in June 2010, advertised as dimethocaine was tested, it was found to be a mixture of caffeine and lidocaine, and the lack of any dopaminergic stimulant ingredient in such mixes may explain the limited recreational effects reported by many users. Other samples tested have however been shown to contain genuine dimethocaine, and one branded “bath salt” product containing primarily dimethocaine as the active ingredient, was noted to have been particularly subject to abuse by intravenous drug users in Ireland. Buy Dimethocaine (DMC) larocain
- CAS No: 94-15-5
Larocaine; NSC 68927;Brn 2215967;DiMethocine;Dimethocaine;553-63-9 (Hydrochloride);3-Diethylamino-2,2-dimethylpropyl 4-aminobenzoate;(3-Diethylamino-2,2-dimethyl)propyl 4-aminobenzoat;p-Aminobenzoic acid 3-(diethylamino)-2,2-dimethylpropyl;3-(Diethylamino)-2,2-dimethyl-1-propanol p-aminobenzoate Buy DMC Dimethocaine CAS 94-15-5
- China Export:From 2018.11 to 2019.11, total export volume of Dimethocaine from China was 104,569,403KG while total export value was $249,619,259. The biggest proportion of exporting volume in the last 12 months was 10.70% in 2019.07. Buy Dimethocaine (DMC) larocain
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Cocaine-like discriminative stimulus effects of procaine
Dimethocaine, a synthetic cocaine derivative: studies on its in vitro metabolism catalyzed by P450s and NAT2
Dimethocaine (DMC), a synthetic derivative of cocaine, is distributed and consumed as “new psychoactive substance” (NPS) without any safety testing at the forefront. It is mainly metabolized by N-acetylation, N-deethylation or hydroxylation. Therefore, the aim of the presented study was to determine the human NAT and P450 isozymes involved in this major metabolic steps, to measure the kinetics of the reactions, and to estimate the contribution on in vivo hepatic clearance. For these studies, cDNA-expressed NATs and P450s were used and formation of metabolites after incubation was measured using LC-MS or LC-MS(n). For N-acetylation, NAT2 could be shown to be the only isoform catalyzing the reaction in vitro hence assuming to be the only relevant enzyme for in vivo acetylation. Kinetic profiles of all P450 catalyzed metabolite formations followed classic Michaelis-Menten behavior with enzyme affinities (Km values) between 3.6 and 220 μM. Using the relative activity factor approach, the net clearances for deethylation of DMC were calculated to be 3% for P450 1A2, 1% for 2C19, <1% for 2D6, and 96% for 3A4. The net clearances for hydroxylation of DMC were calculated to be 32% for P450 1A2, 5% for 2C19, 51% for 2D6, and 12% for 3A4. Furthermore, these data were confirmed by chemical inhibition tests in human liver microsomes. As DMC is metabolized via two main steps and different P450 isoforms were involved in the hepatic clearance of DMC, a clinically relevant interaction with single P450 inhibitors should not be expected. However, a slow acetylation phenotype or inhibition of NAT2 could lead to decreased N-acetylation and hence leading to an increased risk of side effects caused by this arylamine. Buy DMC Dimethocaine CAS 94-15-5
Dimethocaine, a synthetic cocaine analogue: studies on its in-vivo metabolism and its detectability in urine by means of a rat model and liquid chromatography-linear ion-trap (high-resolution) mass spectrometry
Dimethocaine (DMC, larocaine), a synthetic derivative of cocaine, is a widely distributed “legal high” consumed as a “new psychoactive substance” (NPS) without any safety testing, for example studies of metabolism. Therefore, the purpose of this work was to study its in-vivo and in-vitro metabolism by use of liquid chromatography-(high resolution) mass spectrometry (LC-HRMS(n)). DMC was administered to male Wistar rats (20 mg kg(-1)) and their urine was extracted either by solid-phase extraction after enzymatic cleavage of conjugates or by use of protein precipitation (PP). The metabolites were separated and identified by LC-HRMS(n). The main phase I reactions were ester hydrolysis, deethylation, hydroxylation of the aromatic system, and a combination of these. The main phase II reaction was N-acetylation of the p-aminobenzoic acid part of the unchanged parent compound and of several phase I metabolites. The metabolites identified were then used for identification of DMC in rat urine after application of a common user’s dose. By use of GC-MS and LC-MS(n) standard urine-screening approaches (SUSAs), DMC and its metabolites could be detected in the urine samples. Buy DMC Dimethocaine CAS 94-15-5
Human esterases such as the human carboxylesterases (hCES) are important for the catalytic ester hydrolysis of xenobiotics and they play an important role in the detoxification of drugs (e.g., cocaine) but also in the activation of prodrugs (e.g., ramipril). Therefore, the aim of the presented study was to characterize the enzyme-catalyzed ester hydrolysis of ten drugs (cocaine, dimethocaine, ethylphenidate, 4-fluoro-3α-tropacocaine, 4-fluoro-3β-tropacocaine, heroin, methylphenidate, mitragynine, ramipril, and thebacon) by different esterase-containing systems (recombinant hCES1b, hCES1c, and hCES2, pooled human liver microsomes, pooled human liver S9 fraction, and pooled human plasma). Michaelis-Menten kinetic studies were done using in vitro incubations with the aforementioned enzyme-containing systems and LC coupled to ion trap MS for analysis. Ramipril and heroin were used as known model substrates to ensure reliable incubation conditions. The hydrolysis reactions followed classic Michaelis-Menten kinetics with exception of cocaine and 4-fluoro-3α-tropacocaine, for which hydrolysis rate was too low for reliable modeling. The substrates were mainly metabolized by the following enzymes systems: cocaine, hCES1c; dimethocaine, human plasma esterases; ethylphenidate, hCES1c; 4-fluoro-3β-tropacocaine, human plasma esterases; heroin, hCES2; methylphenidate, hCES1c; mitragynine, hCES1c; ramipril, hCES1b; thebacon, hCES2. Compounds bearing a small alcohol part and a larger acyl part showed higher affinity to hCES1 while those with a large alcohol part showed higher affinity to hCES2. The collected data are important for prediction of drug-drug or drug-food interactions as well as for individual variations in metabolism of drugs of abuse due to enzyme polymorphisms.
The effects of selected local anesthetics on in vitro and in vivo measurements of dopamine transporter activity were determined to investigate the role of local anesthetic activity in the neuronal actions of cocaine. Cocaine inhibited [3H]2-beta-carbomethoxy-3-beta-(4-fluorophenyl)tropane 1.5-naphthalenedisulfonate (CFT) binding and [3H]dopamine uptake with estimated Ki and IC50 values of 0.6 microM and 0.7 micorM, respectively. Of the local anesthetics tested, only dimethocaine showed full displacement of CFT binding (0-30 microM tested) and full inhibition of dopamine uptake (0-100 microM tested). Dimethocaine was only slightly less potent than cocaine with an estimated Ki of 1.4 micorM and an IC50 value of 1.2 microM for [3H]CFT binding and dopamine uptake. At a maximum concentration of 100 microM, the ester containing local anesthetics procaine, tetracaine, piperocaine and the amide containing local anesthetic dibucaine and bupivacaine partially inhibited dopamine uptake by 47-70%. The ester containing local anesthetic propoxycaine and the amide containing local anesthetics prilocaine, etidocaine, procainamide, and lidocaine inhibited dopamine uptake by 8-30% at 100 microM. A 10 min administration of cocaine, dimethocaine, or procaine in the dialysis solution produced dose-dependent, reversible increases in endogenous dopamine efflux from the striata of awake rats. Cocaine and dimethocaine produced similar 12-fold increases in dialysate dopamine at concentrations of 0.1 mM and 1 mM respectively. Procaine (10 mM) produced a 6-fold increase in dialysate dopamine while lidocaine (1 mM) produced a reproducible and reversible decrease (30%). These results show that the cocaine-like actions of certain local anesthetics such as dimethocaine and procaine result from their direct actions of dopamine uptake inhibitors.
The effects of cocaine on dopaminergic function in the rat were compared with those of other local anesthetics having an esteratic linkage (dimethocaine, procaine) or an amide linkage (lidocaine). By means of reverse-phase HPLC with electrochemical detection and gas chromatography-mass spectrometry, levels of dopamine (DA) and its metabolites 3-methoxytyramine (3-MT) and dihydroxyphenylacetic acid were quantified in the striatum, nucleus accumbens and prefrontal cortex after i.p. injection of the drugs or saline. Time course and dose response studies determined the effects of the drugs on these parameters of dopaminergic function. These studies provide strong evidence that the three esteratic local anesthetics cocaine, dimethocaine and procaine all increase the synaptic presence of DA, as reflected in increased levels of 3-MT and the ratio of 3-MT to DA, in the striatum, nucleus accumbens and prefrontal cortex. Surprisingly, procaine had an equal or greater effect than cocaine and dimethocaine on 3-MT levels and the ratio 3-MT/DA. The effects of these drugs on dihydroxyphenylacetic acid, an indicator of intraneuronal metabolism of DA, were more variable. However, the amidergic local anesthetic lidocaine did not affect DA metabolism. Although the exact mechanisms behind the dopaminergic activities of procaine and dimethocaine remain unknown, it is clear that these drugs, as well as cocaine, activate dopaminergic systems in the intact animal.
The present study evaluated the effects of dimethocaine and procaine, esteratic local anesthetics, on locomotor activity, conditioned place preference and on the elevated plus-maze test of anxiety in mice, behavioral tests believed to be sensitive to cocaine action. Acute administration of dimethocaine (10-40 mg/kg, IP) significantly increased locomotor activity and time spent on the drug-paired side and reduced the relative number of entries and time spent on the open arms of the plus-maze in mice. Procaine (20-50 mg/kg, IP) failed to affect these responses. These data demonstrate the locomotor stimulant, reinforcing and anxiogenic actions of dimethocaine similar to those reported for cocaine in animals. In addition, these findings support a role for dopaminergic activity, rather than local anesthetic action, in the behavioral effects caused by dimethocaine.
Post-training intracerebroventricular administration of procaine (20 micrograms/microliter) and dimethocaine (10 or 20 micrograms/microliter), local anesthetics of the ester class, prolonged the latency (s) in the retention test of male and female 3-month-old Swiss albino mice (25-35 g body weight; N = 140) in the elevated plus-maze (mean +/- SEM for 10 male mice: control = 41.2 +/- 8.1; procaine = 78.5 +/- 10.3; 10 micrograms/microliter dimethocaine = 58.7 +/- 12.3; 20 micrograms/microliter dimethocaine = 109.6 +/- 5.73; for 10 female mice: control = 34.8 +/- 5.8; procaine = 55.3 +/- 13.4; 10 micrograms/microliter dimethocaine = 59.9 +/- 12.3 and 20 micrograms/microliter dimethocaine = 61.3 +/- 11.1). However, lidocaine (10 or 20 micrograms/microliter), an amide class type of local anesthetic, failed to influence this parameter. Local anesthetics at the dose range used did not affect the motor coordination of mice exposed to the rota-rod test. These results suggest that procaine and dimethocaine impair some memory process(es) in the plus-maze test. These findings are interpreted in terms of non-anesthetic mechanisms of action of these drugs on memory impairment and also confirm the validity of the elevated plus-maze for the evaluation of drugs affecting learning and memory in mice.
Cocaine and several other local anesthetics were tested for their ability to induce rotational behavior in rats with unilateral 6-hydroxydopamine lesions of substantia nigra. Acute administration of bupivacaine, chloroprocaine, etidocaine, lidocaine, mepivacaine, procaine or tetracaine failed to induce active rotation in this sensitive assay of dopamine agonist activity. On the other hand, cocaine or dimethocaine treatment induced active rotation directed ipsilaterally to the lesioned side, indicating indirect dopamine agonist activity. Repeated administration of cocaine or dimethocaine at 1-week intervals resulted in increased rotational response (i.e., sensitization) while there was no suggestion of sensitization or induction of rotational behavior after weekly repeated administration of procaine or tetracaine. Daily administration of mepivacaine, procaine or tetracaine for 5 days also failed to induce rotation. Dimethocaine thus was found similar to cocaine and different from the other local anesthetics tested both in terms of frank stimulant activity and development of sensitization upon repeated administration.
A number of esteratic local anesthetics serve as positive reinforcers and produce cocaine-like discriminative stimulus effects in animals. It has been suggested that the affinity of these compounds for a site on the dopamine transporter, and not their local anesthetic actions, is responsible for these abuse-related behavioral effects. In the present study, three local anesthetics previously shown to be self-administered in animals were examined in squirrel monkeys trained to discriminate cocaine (0.3 mg/kg) from saline in a two-lever, food-reinforced procedure. Dimethocaine (0.1-3.0 mg/kg) fully and dose-dependently substituted for cocaine. Doses of dimethocaine (1.7 mg/kg) and cocaine (0.3 mg/kg) which produced full (> 80%) substitution for cocaine were administered in combination with the dopamine D1 receptor antagonist SCH 39166 ((-)-trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H -benzo [d]naphtho-(2,1-b)azepine) and the dopamine D2 receptor antagonist raclopride (both at 0.003-0.03 mg/kg). SCH 39166 fully blocked the cocaine-like discriminative stimulus effects of dimethocaine and cocaine, but raclopride produced only partial antagonism of cocaine-lever selection. In addition, there was some evidence that raclopride blocked cocaine-lever responding produced by a lower dose of dimethocaine. In substitution studies, neither procaine (1-10 mg/kg) nor chloroprocaine (1-30 mg/kg) produced cocaine-like effects. These results support a role for dopamine in the behavioral effects of some local anesthetics.
1. Different local anesthetics were tested for analgesic activity in three antinociceptive models, the acetic acid-induced abdominal constriction, tail-flick and hot plate tests in the mouse. 2. In the abdominal constriction test, subcutaneous, SC, injection of lidocaine (10, 20 or 30 mg/kg) and dimethocaine (5, 10 or 20 mg/kg) induced dose-dependent antinociceptive responses. Procaine (20, 30 or 50 mg/kg) was also able to reduce the response to noxious chemical stimuli. 3. The IP injection of lidocaine and dimethocaine significantly inhibited the tail-flick and paw-licking hot plate responses; procaine was weak or inactive in these tests, in which heat was the noxious stimulus. 4. Taken together, these results suggest that antinociception produced by systemically administered lidocaine and dimethocaine at nontoxic doses in mice is due, at least in part, to their central effects.
What is dimethocaine?
Dimethocaine’s structure and chemical composition of dimethocaine is an ester of 4-aminobenzoic acid, similar to that of procaine. Also called DMC or lidocaine is a chemical that produces a stimulatory impact. Like cocaine, dimethocaine is addicting because it stimulates the brain’s reward pathway. Dimethocaine is an approved substitute for cocaine in certain countries. It has been recognized in the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) under the heading “synthetic cocaine derivatives”. The chemical structure of dimethocaine, a 4-aminobenzoic acid ester, is similar to procaine. It appears as a white powder at temperatures of room temperature.
Uses of dimethocaine
Dimethocaine (DMC, lidocaine) is a synthetic version of cocaine and is a well-known “legal high” used as a “new psychoactive drug” (NPS). Initially was utilized in the 1930s to be an anesthetic. It was used primarily in ophthalmology, dentistry, and the field of otolaryngology. The drug blocks dopamine transporter and has the potential to be abused. Dimethocaine is to be used for research and forensic reasons.
The history of dimethocaine
The Hoffmann-La Roche company first created Dimethocaine in 1930. It was then sold under the trade name lidocaine. The 1930s saw dimethocaine gain recognition in the US as a local anesthetic. Like procaine, cocaine is used in procedures, particularly in the fields of ophthalmology, dentistry, and otolaryngology. However, by the 1940s, it was withdrawn from the market due to its psychoactive effects and the risk of dependence. Dimethocaine has been abused in recent times for the psychoactive effects it has. It is advertised as a substitute for cocaine to avoid legal issues.
|Synthesis Method Details||Design of the Synthesis Pathway
Dimethocaine can be synthesized by a multi-step process involving the reaction of piperidine with 4-chlorobenzoic acid to form 4-chlorobenzoylpiperidine. This intermediate is then reacted with 2-dimethylaminoethanol to form dimethocaine.Starting Materials
Piperidine, 4-chlorobenzoic acid, 2-dimethylaminoethanol, Sodium hydroxide, Hydrochloric acid, Diethyl ether, MethanolReaction
Step 1: Piperidine is reacted with 4-chlorobenzoic acid in the presence of sodium hydroxide and diethyl ether to form 4-chlorobenzoylpiperidine.
Step 2: The resulting intermediate is then reacted with 2-dimethylaminoethanol in the presence of hydrochloric acid and methanol to form dimethocaine.
Step 3: The product is then purified by recrystallization or chromatography.
|Molecular Weight||278.39 g/mol|
|IUPAC Name||[3-(diethylamino)-2,2-dimethylpropyl] 4-aminobenzoate|
|Other CAS RN||94-15-5|
|Purity||>98% (or refer to the Certificate of Analysis)|
|Related CAS||553-63-9 (hydrochloride)|
|Shelf Life||>3 years if stored properly|
|Solubility||Soluble in DMSO|
|Storage||Dry, dark and at 0 – 4 C for short term (days to weeks) or -20 C for long term (months to years).|
|Origin of Product||United States|
1: Meyer MR, Lindauer C, Maurer HH. Dimethocaine, a synthetic cocaine derivative: studies on its in vitro metabolism catalyzed by P450s and NAT2. Toxicol Lett. 2014 Feb 10;225(1):139-46. doi: 10.1016/j.toxlet.2013.11.033. Epub 2013 Dec 3. PubMed PMID: 24309420. 2: Meyer MR, Lindauer C, Welter J, Maurer HH. Dimethocaine, a synthetic cocaine analogue: studies on its in-vivo metabolism and its detectability in urine by means of a rat model and liquid chromatography-linear ion-trap (high-resolution) mass spectrometry. Anal Bioanal Chem. 2014 Mar;406(7):1845-54. doi: 10.1007/s00216-013-7539-0. Epub 2014 Jan 22. PubMed PMID: 24448968. 3: Rigon AR, Takahashi RN. The effects of systemic procaine, lidocaine and dimethocaine on nociception in mice. Gen Pharmacol. 1996 Jun;27(4):647-50. PubMed PMID: 8853299. 4: Graham JH, Balster RL. Cocaine-like discriminative stimulus effects of procaine, dimethocaine and lidocaine in rats. Psychopharmacology (Berl). 1993;110(3):287-94. PubMed PMID: 7831421. 5: Rigon AR, Takahashi RN. Stimulant activities of dimethocaine in mice: reinforcing and anxiogenic effects. Psychopharmacology (Berl). 1996 Oct;127(4):323-7. PubMed PMID: 8923567. 6: Woodward JJ, Compton DM, Balster RL, Martin BR. In vitro and in vivo effects of cocaine and selected local anesthetics on the dopamine transporter. Eur J Pharmacol. 1995 Apr 13;277(1):7-13. PubMed PMID: 7635175. 7: Blatt SL, Takahashi RN. Memory-impairing effects of local anesthetics in an elevated plus-maze test in mice. Braz J Med Biol Res. 1998 Apr;31(4):555-9. PubMed PMID: 9698809. 8: Mansbach RS, Jortani SA, Balster RL. Discriminative stimulus effects of esteratic local anesthetics in squirrel monkeys. Eur J Pharmacol. 1995 Feb 14;274(1-3):167-73. PubMed PMID: 7768269. 9: Wilcox KM, Kimmel HL, Lindsey KP, Votaw JR, Goodman MM, Howell LL. In vivo comparison of the reinforcing and dopamine transporter effects of local anesthetics in rhesus monkeys. Synapse. 2005 Dec 15;58(4):220-8. PubMed PMID: 16206183. 10: Meyer MR, Schütz A, Maurer HH. Contribution of human esterases to the metabolism of selected drugs of abuse. Toxicol Lett. 2015 Jan 5;232(1):159-66. doi: 10.1016/j.toxlet.2014.10.026. Epub 2014 Oct 24. PubMed PMID: 25445008. 11: Graham JH 3rd, Maher JR, Robinson SE. The effect of cocaine and other local anesthetics on central dopaminergic neurotransmission. J Pharmacol Exp Ther. 1995 Aug;274(2):707-17. PubMed PMID: 7636732. 12: Silverman PB. Cocaine and local anesthetics: stimulant activity in rats with nigral lesions. Psychopharmacology (Berl). 1990;102(2):269-72. PubMed PMID: 1980374. 13: Acton WJ, Lanza M, Agarwal B, Jürschik S, Sulzer P, Breiev K, Jordan A, Hartungen E, Hanel G, Märk L, Mayhew CA, Märk TD. Headspace analysis of new psychoactive substances using a Selective Reagent Ionisation-Time of Flight-Mass Spectrometer. Int J Mass Spectrom. 2014 Mar 1;360:28-38. PubMed PMID: 25844048; PubMed Central PMCID: PMC4375562. 14: Lew R, Grigoriadis DE, Sharkey J, Kuhar MJ. Dopamine transporter: solubilization from dog caudate nucleus. Synapse. 1989;3(4):372-5. PubMed PMID: 2740994. 15: Sharkey J, Ritz MC, Schenden JA, Hanson RC, Kuhar MJ. Cocaine inhibits muscarinic cholinergic receptors in heart and brain. J Pharmacol Exp Ther. 1988 Sep;246(3):1048-52. PubMed PMID: 3047364. 16: Wilcox KM, Rowlett JK, Paul IA, Ordway GA, Woolverton WL. On the relationship between the dopamine transporter and the reinforcing effects of local anesthetics in rhesus monkeys: practical and theoretical concerns. Psychopharmacology (Berl). 2000 Dec;153(1):139-47. PubMed PMID: 11255924. 17: Wilcox KM, Paul IA, Woolverton WL. Comparison between dopamine transporter affinity and self-administration potency of local anesthetics in rhesus monkeys. Eur J Pharmacol. 1999 Feb 19;367(2-3):175-81. PubMed PMID: 10078990. 18: Tella SR, Goldberg SR. Subtle differences in the discriminative stimulus effects of cocaine and GBR-12909. Prog Neuropsychopharmacol Biol Psychiatry. 2001 Apr;25(3):639-56. PubMed PMID: 11371002. 19: Woolverton WL, Balster RL. Effects of local anesthetics on fixed-interval responding in rhesus monkeys. Pharmacol Biochem Behav. 1983 Mar;18(3):383-7. PubMed PMID: 6835995. 20: Wilcox KM, Paul IA, Ordway GA, Woolverton WL. Role of the dopamine transporter and the sodium channel in the cocaine-like discriminative stimulus effects of local anesthetics in rats. Psychopharmacology (Berl). 2001 Sep;157(3):260-8. PubMed PMID: 11605081
WebCAS RN 94-15-5 Product Name Dimethocaine Molecular Formula C16H26N2O2 Molecular Weight 278.39 g/mol IUPAC Name [3 …
CAS RN: 94-15-5
Molecular Weight: 278.39 g/mol
Molecular Formula: C16H26N2O2
Product Name: Dimethocaine
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