2969 T3D2927 Cocaine An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [PubChem] 50-36-2 446220 C17H21NO4 303.147060 White powder. 98°C 1800 mg/L (at 22°C) Cocaine is absorbed from all sites of application, including mucous membranes and gastrointestinal mucosa. By oral or intra-nasal route, 60 to 80% of cocaine is absorbed. Cocaine produces anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. This is achieved by reversibly binding to and inactivating sodium channels. Sodium influx through these channels is necessary for the depolarization of nerve cell membranes and subsequent propagation of impulses along the course of the nerve. Cocaine is the only local anesthetic with vasoconstrictive properties. This is a result of its blockade of norepinephrine reuptake in the autonomic nervous system. Cocaine binds differentially to the dopamine, serotonin, and norepinephrine transport proteins and directly prevents the re-uptake of dopamine, serotonin, and norepinephrine into pre-synaptic neurons. Its effect on dopamine levels is most responsible for the addictive property of cocaine. Hepatic. Cocaine is metabolized to benzoylecgonine and ecgonine methyl ester, which are both excreted in the urine. In the presence of alcohol, a further active metabolite, cocaethylene is formed, and is more toxic then cocaine itself. Half Life: 1 hour Oral mouse LD<sub>50</sub> = 96 mg/kg LD50: 95.1 mg/kg (i.p, mouse) (L1860) No indication of carcinogenicity to humans (not listed by IARC). Cocaine (KOE-kane) is a local anesthetic. It is applied to certain areas of the body (for example, the nose, mouth, or throat) to cause loss of feeling. This allows some kinds of examinations or surgery to be done without causing pain. (L1505) Continued use produces insomnia, hyperactivity, anxiousness, agitation and malnutrition. Overdoses can be lethal. Intense agitation, convulsions, hypertension, rhythm disturbance, coronary insufficiency, hyperthermia, rhabdomyolysis, and renal impairment. The specific treatment of acute cocaine poisoning is the intravenous administration of a short-acting barbiturate or diazepam. Artificial respiration may be necessary. It is important to limit absorption of the drug. If entrance of the drug into circulation can be checked, and respiratory exchange maintained, the prognosis is favorable since cocaine is eliminated fairly rapidly. (L1712) 2009-07-21T20:27:56Z 2014-12-24T20:25:53Z Cocaine C01416 27958 CPD-9776 Cocaine DB00907 COC true [H][C@@]12CC[C@@]([H])(N1C)[C@@]([H])(C(=O)OC)[C@]([H])(C2)OC(=O)C1=CC=CC=C1 C17H21NO4 InChI=1S/C17H21NO4/c1-18-12-8-9-13(18)15(17(20)21-2)14(10-12)22-16(19)11-6-4-3-5-7-11/h3-7,12-15H,8-10H2,1-2H3/t12-,13+,14-,15+/m0/s1 InChIKey=ZPUCINDJVBIVPJ-LJISPDSOSA-N 303.3529 303.147058165 Exogenous Solid 2.3 HMDB15043 CHEMBL120901 10194104 <p>Nobuyuki Shigetoh, Hiroshi Nakayama, Jinsei Miyazaki, Tadayasu Mitsumata, &#8220;Labelling colors for detecting cocaine or methamphetamine, method of preparing the same and detector for cocaine or methamphetamine.&#8221; U.S. Patent US5571727, issued October, 1981.</p>