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ABSTRACTS: SOFT-TIAFT 1998 Page I Editor's note: The numbers before each title refer to the number assigned in the 1998 SOFT/TIAFT meeting program. The material has been reformatted for this printing. El'ery effort has been made to maintain the accuracy ofthe abstracts. Joseph R. Monforte, Ph.D., DABFT, ToxTalk Editor 4: Safety Of Buprenorphine: Ceiling For Cardio-Respiratory And Subjective Effects At High IV Doses Marilyn A. Huestis, Annie Umbricht, Kenzie L. Preston, and Edward J. Cone, NIDA Intramural Research Program, 5500 Nathan Shock Dr., Baltimore, MD 21224. Buprenorphine (BUP), a partial 11 agonist and K antagonist, is under development for treatment of opioid dependence. The present study was conducted to test the safety and abuse potential of intravenous (IV) BUP in the range of doses used for maintenance treatment. Concerns have been raised about the potential acute health risk ofbuprenorphine if diverted and used by the IV route at doses equivalent to those used for maintenance. Subjective effects ofBUP SL (12 mg) and IV/SL placebo (in random order) and BUP IV (2, 4, 8, 12, and 16 mg in increasing dose order) were evaluated in separate sessions in this single-blind, double-dummy study. Data were collected from 6 non-dependent male opioid abusers. Safety parameters included continuous monitoring of vital signs and oxygen saturation for 3 h after drug administration and additional collections over the next 72 h. Subjective measures included visual analog scales of global drug effects, ARCI subscales, and adjective rating scales. An increase in Systolic Blood Pressure for the 8 mg IV dose (+ 13.5 mm Hg) as .~\ compared to placebo was the only statistically significant change in blood pressure, heart rate or oxygen saturation among the 7 drug conditions. The mean maximum decrease in O2 saturation was greatest for the 8 mg IV dose (-7.3%). The main side effects were sedation, mild. irritability, nausea, and itching. One subject did not receive the 16 mg IV dose because of severe nausea, which persisted for 24 hours (28 to 72 hr on some measures). Subjective measures included visual analog scales of global drug effects, ARCI subscales, and adjective rating scales. All active BUP conditions produced increases in positive subjective measures compared to placebo, including high, drug effect, good effects, drug liking, opioid agonist adjective rating scale, and MEG scale of the ARCL Peak effects occurred I to 1.5 h after IV doses and 3 to 6 h after SL BUP. Duration of action was 24 hours or longer. Effects did not increase in an orderly dose-related manner; on many measures, the magnitude of effect was not different among all active doses. The effects of 16 mg IV tended to be less than those of 12 mg IV and varied in comparison to other active doses. Buprenorphine appears to have a ceiling for cardio-respiratory and subjective effects and a high safety margin when administered by the IV route in the absence of other drugs. Key Words: Buprenorphine lntrm'enous Abuse Liability 5: Disposition of Heroin and Metabolites in Multiple Biological Matrices after Low Dose Oral Heroin Administration in Humans Amanda 1. Jenkins*, and Edward 1. Cone, Addiction Research Center, IRP, NIDA, NIH, Baltimore, MD 21224 U.S.A. Clinical data regarding the disposition of heroin and metabolites after oral heroin administration is limited to case reports of overdoses by "body packers". We conducted a controlled clinical study during which nine healthy male volunteers with a history of heroin use were administered 10 mg heroin hydrochloride in the form of a gelatin capsule. Blood and saliva specimens were collected prior to drug administration and periodically thereafter up to 24 hours. All urine specimens were collected. Specimens were analyzed by solid phase extraction followed by gas chromatography/mass spectrometry for heroin, 6-acetylmorphine and morphine. The assay had a limit of quantitation (LOQ) of I ng/ml for each analyte. The total morphine concentration also was measured in the urine specimens. December 1998 ABSTRACTS: SOFT-TIAFT 1998 Page 2 Blood Heroin and 6~acetylmorphine were not detected in blood after ingestion. Morphine was first detected 7.5 to 30 minutes after drug administration with peak concentrations ranging from 2.2-15 ng/ml (mean=7.7 ng/ml, N=9), achieved 7.5 minutes to 4 hours later. Morphine concentrations declined thereafter, reaching the assay LOQ by 1-12 hours. Saliva No analytes were detected in saliva after oral heroin administration. Urine Heroin and 6-acetylmorphine were not detected in urine. Morphine was detected in the first void after drug administration for each subject (Mean time ofvoid= 2.35 h, N=9). Peak free morphine concentrations ranging from 172-491 ng/ml were achieved at an average of 4.2 hours after drug administration. Peak levels typically occurred in the 1st.3 rd voids. Peak total morphine concentrations ranging from 4317-12580 ng/ml were achiev~d at a~ average of 4.6 hours after drug administration. The time to the first negative sample for free morphine averaged 33.2 hours (Range:=: 21.5-54.7 h) with total morphine being detectable in 6/9 subjects at the last collected void at 68-75 hours. The time to the first total morphine negative for the remaining 3 subjects ranged between 53.1-77.9 hours. These data indicate that after low dose administration of heroin by the oral route, heroin and 6-acetylmorphine are not detected in blood, saliva or urine. However, measurable concentrations of free and total morphine are excreted in the urine for approximately 30 and 53 hours, respectively. Key Words: Heroin. Oral Administration. Blood. Saliva. Urine 6: The Role of Ethanol in the Etiology of Heroin-Related Deaths. Evidence for Pharmaco­ kinetic Interactions between Heroin and Alcohol Aldo Polettini*, Angelo Groppi, and Maria Montagna, Department ofLegal Medicine and Public Health, University of Pavia, Via Forlanini, 12, 27100 PAVIA, Italy In order to evaluate the significance of pharmacokinetic interactions between heroin and alcohol in the etiology of heroin related deaths (HRD), the blood concentrations of ethanol (BAC), offree morphine (FM) and of total morphine ~, (TM), as well as the total morphine concentrations in urine and bile were examined in a population of 39 lethal cases. The cases were included in the records of the Department of Legal Medicine and Public Health, University of Pavia in the period January 1997 - April 1998. Morphine was determined using the DPC Coat-A-Count radioimmunoassay with or without enzymatic hydrolysis. The cause ofdeath was attributed to either heroin or associated heroin-ethanol intoxication. Cases were arbitrarily divided in two groups according to BAC «1000 mgll, LE, and >1000 mg/l, HE). The differences in the FM and TM concentrations in blood, bile, and urine, and in the FMffM ratios between the two groups were statistically evaluated (Mann-Whitney U test). A similar statistical evaluation was carried out on the data published by Goldberger et a1. (J. Anal. Toxicol., 18, 1994,22-28) who studied the disposition of heroin and its metabolites (6-acetylmorphine, free morphine) in blood and urine in 23 lethal cases attributed to either heroin or heroin and alcohol intoxication. In this case the following variables in the LE and HE groups were compared: FM, TM, 6~acetyl-morphine concentration in blood (A), the FMI(FM+A) ratio, the FMlTM ratio, the urinary concentration of heroin (UH), 6-acetylmorphine (UA) and free morphine (UFM), and the UFMI(UFM+UH+UA) ratio. Statistical analyses ofdata indicated that high BAC inhibits the hydrolysis of6-acetymorphine to morphine (FMI(FM+A), p = 0.0025) and that the percentage of inhibition is correlated to BAC (r = 0.67). High BAC was also found to significantly decrease glucuronidation (FMffM, p = 0.0129), and the excretion offree and conjugated heroin metabolites. According to these results, we advance the hypothesis that pharmacokinetic interactions between heroin and ethanol do occur in the organism of individuals exposed to high doses of these substances. Keywords: heroin. ethanol. interaction 7: Heroin Metabolites in the Blood of Car Drivers. Maciej lBogusz, Wiebke FrUchtnicht, Rolf-Dieter Maier, Institute of Forensic Medicine, Aachen University of Technology, D-52057 Aachen, Germany~' The purpose ofthe study was to test whether the determination ofall possible heroin metabolites in blood may bring new information facilitating the correlation between the symptoms and analy1ical findings. ToxTaik Volume 22. No.4 December 1998 ABSTRACTS: SOFT-TIAFT 1998 Page 3 ~, In the presented pilot phase 40 cases were analyzed from the period Febmary 1997 to May 1998. On the basis of circumstantial infonnation two groups were formed: "road traffic offenses" or "drivers" (n = 14) and "other offenses" (n = 26). As a sources of this infonnation the police and court files and the results of medical examination before the blood sampling were used. Blood concentrations of morphine, M3G, M6G, 6MAM, codeine and C6G were determined by HPLC-APCI-MS. Other relevant drugs (cocaine, cannabinoids, amphetamines, benzodiazepines etc.) were analyzed by LC-MS or GC-MS after immunoassay screening. In both groups polydrug use was observed: only one "driver" and three "other offenders" had solely morphine and morphine metabolites in their blood. In all other cases, one to three additional drugs (cocaine, cannabinoids, methadone, amphetamines, benzodiazepines, ethanol) were detected. The concentrations of morphine and its active metabolite M6G in the group of "drivers" ranged from 3 to 80 IlgIL and 8 to 248 IlgIL, respectively. In the group of"other offenders" morphine concentrations were 1 to 95 JlgIL and M6G 15 to 278 JlgIL. The detennination of M6G as active heroin/morphine metabolite may bring new information concerning the exposition to opiates particularly in the view of new German law defining the mere presence of some drugs of abuse such as heroin or morphine in the blood of a driver as an offense.
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  • United States Patent (19) 11 Patent Number: 5,925,634 Olney (45) Date of Patent: *Jul

    United States Patent (19) 11 Patent Number: 5,925,634 Olney (45) Date of Patent: *Jul

    USOO5925634A United States Patent (19) 11 Patent Number: 5,925,634 Olney (45) Date of Patent: *Jul. 20, 1999 54 USE OF IBOGAINE FOR TREATING Green, P.G., et al., “Antinociception opioids and the cholin NEUROPATHIC PAIN ergic system,” Progress in Neurobiology 26: 119-146 (1986). 75 Inventor: John W. Olney, Ladue, Mo. Harsing, L.G., et al., “Evidence that ibogaine releases dopamine from the cytoplasmic pool in isolated mouse 73 Assignee: Washington University, St. Louis, Mo. striatum.” J. Neural. Transm. Gen. Sect. 96: 215–25 (1994). Popik, P., et al., “The putative anti-addictive drug ibogaine * Notice: This patent is Subject to a terminal dis is a competitive inhibitor of H MK-801 binging to the claimer. NMD receptor complex, Psychopharmacology 114: 672–674 (1994). 21 Appl. No.: 08/854,979 Sershen, H., et al., “Ibogaine antagonizes cocaine-induced 22 Filed: May 13, 1997 locomotor stimulation in mice,” Life Sci 50: 1079–1086 (1992). Related U.S. Application Data Sershen, H., et al., “Ibogaine reduces preference for cocaine consumption in C57BL/6By mice,” Pharmacol Biochem 60 Division of application No. 08/398,731, Mar. 6, 1995, Pat. No. 5,629,307, which is a continuation-in-part of application Behav 47: 13–19 (1994). No. 07/877,839, May 1, 1992, which is a continuation-in Sershen, H., “Effect of ibogaine on Serotonergic and dopam part of application No. 07/467,139, Jan. 18, 1990, aban inergic interactions in Striatum from mice and rats, Neu doned, which is a continuation-in-part of application No. rochem. Res. 19: 1463-1464 (1994).